Glucagon: A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)Dexamethasone: An anti-inflammatory 9-fluoro-glucocorticoid.Urea: A compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids.Argininosuccinate Synthase: An enzyme of the urea cycle that catalyzes the formation of argininosuccinic acid from citrulline and aspartic acid in the presence of ATP. Absence or deficiency of this enzyme causes the metabolic disease CITRULLINEMIA in humans. EC 6.3.4.5.Carbamoyl-Phosphate Synthase (Ammonia): An enzyme that catalyzes the formation of carbamoyl phosphate from ATP, carbon dioxide, and ammonia. This enzyme is specific for arginine biosynthesis or the urea cycle. Absence or lack of this enzyme may cause CARBAMOYL-PHOSPHATE SYNTHASE I DEFICIENCY DISEASE. EC 6.3.4.16.Urea Cycle Disorders, Inborn: Rare congenital metabolism disorders of the urea cycle. The disorders are due to mutations that result in complete (neonatal onset) or partial (childhood or adult onset) inactivity of an enzyme, involved in the urea cycle. Neonatal onset results in clinical features that include irritability, vomiting, lethargy, seizures, NEONATAL HYPOTONIA; RESPIRATORY ALKALOSIS; HYPERAMMONEMIA; coma, and death. Survivors of the neonatal onset and childhood/adult onset disorders share common risks for ENCEPHALOPATHIES, METABOLIC, INBORN; and RESPIRATORY ALKALOSIS due to HYPERAMMONEMIA.Ornithine Carbamoyltransferase: A urea cycle enzyme that catalyzes the formation of orthophosphate and L-citrulline (CITRULLINE) from CARBAMOYL PHOSPHATE and L-ornithine (ORNITHINE). Deficiency of this enzyme may be transmitted as an X-linked trait. EC 2.1.3.3.Myxomatosis, InfectiousSiphonaptera: An order of parasitic, blood-sucking, wingless INSECTS with the common name of fleas.Pulmonary Stretch Receptors: Stretch receptors found in the bronchi and bronchioles. Pulmonary stretch receptors are sensors for a reflex which stops inspiration. In humans, the reflex is protective and is probably not activated during normal respiration.Bibliometrics: The use of statistical methods in the analysis of a body of literature to reveal the historical development of subject fields and patterns of authorship, publication, and use. Formerly called statistical bibliography. (from The ALA Glossary of Library and Information Science, 1983)Publications: Copies of a work or document distributed to the public by sale, rental, lease, or lending. (From ALA Glossary of Library and Information Science, 1983, p181)Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.VietnamArgentinaPubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Biological Science Disciplines: All of the divisions of the natural sciences dealing with the various aspects of the phenomena of life and vital processes. The concept includes anatomy and physiology, biochemistry and biophysics, and the biology of animals, plants, and microorganisms. It should be differentiated from BIOLOGY, one of its subdivisions, concerned specifically with the origin and life processes of living organisms.Chromatin: The material of CHROMOSOMES. It is a complex of DNA; HISTONES; and nonhistone proteins (CHROMOSOMAL PROTEINS, NON-HISTONE) found within the nucleus of a cell.Epigenesis, Genetic: A genetic process by which the adult organism is realized via mechanisms that lead to the restriction in the possible fates of cells, eventually leading to their differentiated state. Mechanisms involved cause heritable changes to cells without changes to DNA sequence such as DNA METHYLATION; HISTONE modification; DNA REPLICATION TIMING; NUCLEOSOME positioning; and heterochromatization which result in selective gene expression or repression.Histones: Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each.Cellular Apoptosis Susceptibility Protein: A nucleocytoplasmic transport protein that binds to ALPHA KARYOPHERINS and RAN GTP BINDING PROTEIN inside the CELL NUCLEUS and participates in their export into CYTOPLASM. It is also associated with the regulation of APOPTOSIS and microtubule assembly.Epigenomics: The systematic study of the global gene expression changes due to EPIGENETIC PROCESSES and not due to DNA base sequence changes.Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing): An enzyme that catalyzes the formation of carbamoyl phosphate from ATP, carbon dioxide, and glutamine. This enzyme is important in the de novo biosynthesis of pyrimidines. EC 6.3.5.5.Ribonucleotide ReductasesNucleosides: Purine or pyrimidine bases attached to a ribose or deoxyribose. (From King & Stansfield, A Dictionary of Genetics, 4th ed)Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.Pyrimidine Nucleosides: Pyrimidines with a RIBOSE attached that can be phosphorylated to PYRIMIDINE NUCLEOTIDES.Pyrimidine Nucleotides: Pyrimidines with a RIBOSE and phosphate attached that can polymerize to form DNA and RNA.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Pyruvaldehyde: An organic compound used often as a reagent in organic synthesis, as a flavoring agent, and in tanning. It has been demonstrated as an intermediate in the metabolism of acetone and its derivatives in isolated cell preparations, in various culture media, and in vivo in certain animals.Markov Chains: A stochastic process such that the conditional probability distribution for a state at any future instant, given the present state, is unaffected by any additional knowledge of the past history of the system.Glucosyltransferases: Enzymes that catalyze the transfer of glucose from a nucleoside diphosphate glucose to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-.Tropaeolum: A plant genus of the family TROPAEOLACEAE. The common nasturtium is a plant that grows 2.4-3.6 m (8-12 feet) tall and has funnel-shaped flowers that are commonly yellow-orange with red spots or stripes and have a long spur that contains sweet nectar. Some species in this genus are called watercress which is also a common name for RORIPPA and NASTURTIUM.Databases, Protein: Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.Lactoylglutathione Lyase: An enzyme that catalyzes the interconversion of methylglyoxal and lactate, with glutathione serving as a coenzyme. EC 4.4.1.5.Proteins: Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.Russia (Pre-1917)Pseudotsuga: A plant genus in the family PINACEAE, order Pinales, class Pinopsida, division Coniferophyta. They are coniferous evergreen trees with long, flat, spirally arranged needles that grow directly from the branch.Alexander Disease: Rare leukoencephalopathy with infantile-onset accumulation of Rosenthal fibers in the subpial, periventricular, and subependymal zones of the brain. Rosenthal fibers are GLIAL FIBRILLARY ACIDIC PROTEIN aggregates found in ASTROCYTES. Juvenile- and adult-onset types show progressive atrophy of the lower brainstem instead. De novo mutations in the GFAP gene are associated with the disease with propensity for paternal inheritance.Douglas' Pouch: A sac or recess formed by a fold of the peritoneum.Fat Body: A nutritional reservoir of fatty tissue found mainly in insects and amphibians.Williams Syndrome: A disorder caused by hemizygous microdeletion of about 28 genes on chromosome 7q11.23, including the ELASTIN gene. Clinical manifestations include SUPRAVALVULAR AORTIC STENOSIS; MENTAL RETARDATION; elfin facies; impaired visuospatial constructive abilities; and transient HYPERCALCEMIA in infancy. The condition affects both sexes, with onset at birth or in early infancy.Stevens-Johnson Syndrome: Rare cutaneous eruption characterized by extensive KERATINOCYTE apoptosis resulting in skin detachment with mucosal involvement. It is often provoked by the use of drugs (e.g., antibiotics and anticonvulsants) or associated with PNEUMONIA, MYCOPLASMA. It is considered a continuum of Toxic Epidermal Necrolysis.Clostridium thermocellum: A species of gram-positive, thermophilic, cellulolytic bacteria in the family Clostridaceae. It degrades and ferments CELLOBIOSE and CELLULOSE to ETHANOL in the CELLULOSOME.Renewable Energy: Forms of energy that are constantly and rapidly renewed by natural processes such as solar, ocean wave, and wind energy. (from McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Biofuels: Hydrocarbon-rich byproducts from the non-fossilized BIOMASS that are combusted to generate energy as opposed to fossilized hydrocarbon deposits (FOSSIL FUELS).Clostridium: A genus of motile or nonmotile gram-positive bacteria of the family Clostridiaceae. Many species have been identified with some being pathogenic. They occur in water, soil, and in the intestinal tract of humans and lower animals.Cellulase: An endocellulase with specificity for the hydrolysis of 1,4-beta-glucosidic linkages in CELLULOSE, lichenin, and cereal beta-glucans.Gram-Positive Asporogenous Rods, Irregular: A group of irregular rod-shaped bacteria that stain gram-positive and do not produce endospores.Metabolic Networks and Pathways: Complex sets of enzymatic reactions connected to each other via their product and substrate metabolites.

*Carbamoyl phosphate synthase II

Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) at the US National Library of Medicine Medical Subject Headings (MeSH) ... glutamine) glutamine-dependent carbamyl phosphate synthetase carbamoyl phosphate synthetase CPS carbon-dioxide:L-glutamine ... Carbamoyl-phosphate synthetase (glutamine-hydrolysing) is also known as: hydrogen-carbonate:L-glutamine amido-ligase (ADP- ... Carbamoyl phosphate synthetase II (EC 6.3.5.5) is an enzyme that catalyzes the reactions that produce carbamoyl phosphate in ...

*List of MeSH codes (D08)

... carbamoyl-phosphate synthase (glutamine-hydrolyzing) MeSH D08.811.464.259.550 --- formate-tetrahydrofolate ligase MeSH D08.811. ... carbamoyl-phosphate synthase (ammonia) MeSH D08.811.464.259.400 --- carbon-nitrogen ligases with glutamine as amide-n-donor ... glutamate synthase MeSH D08.811.913.477.700.500 --- glutamine-fructose-6-phosphate transaminase (isomerizing) MeSH D08.811. ... riboflavin synthase MeSH D08.811.913.225.825 --- spermidine synthase MeSH D08.811.913.225.912 --- spermine synthase MeSH ...

*Ribonucleotide

... by enzyme ribose-phosphate diphosphokinase (PRPS1). PRPP is then converted to 5-phosphoribosylamine (5-PRA) as glutamine ... Phosphodiester bonds, when hydrolyzed, release a considerable amount of free energy. Therefore, nucleic acids tend to ... begins with the conversion of Aspartate to N-Carbamoylaspartate by undergoing a condensation reaction with carbamoyl phosphate ... closure of the second ring structure is carried out by IMP synthase to form IMP, where IMP fate would lead to the formation of ...

*List of EC numbers (EC 4)

... phosphate synthase (glutamine hydrolyzing) EC 4.3.3.7: 4-hydroxy-tetrahydrodipicolinate synthase EC 4.3.99.1: now EC 4.2.1.104 ... carbamoyl-serine ammonia-lyase EC 4.3.1.14: 3-aminobutyryl-CoA ammonia-lyase EC 4.3.1.15: diaminopropionate ammonia-lyase EC ... 11-diene synthase EC 4.2.3.25: S-linalool synthase EC 4.2.3.26: R-linalool synthase EC 4.2.3.27: isoprene synthase EC 4.2.3.28 ... d-cadinene synthase EC 4.2.3.14: pinene synthase EC 4.2.3.15: myrcene synthase EC 4.2.3.16: (4S)-limonene synthase EC 4.2.3.17 ...
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The fasting plasma glucagon level was measured in 39 normal subjects, 13 IDDM and 44 NIDDMpatients. The results showed that the glucagon level in both IDDs and NIDDs was significantly higherthan that in normal subjects (P0.001). In addition, 18 normal subjects and 30 NIDDM patientsunderwent a steamed-bread meal test, and the changes in glucagon level was also studied. The glucagonlevel in NIDDM patients was significantly elevated after the meal (P0.05 or less), but in normalsubjects there was no significant change (P0.05). Whereas the glucagon levels before and after themeal in NIDDs were significantly higher than those in normal subjects (P0.05 or less). The rise ofinsulin/glucagon ratio in NIDDs was retarded and much lower that that in normal subjects (P0.01 orless) The results indicate that there exists dysfunction of islet a-cells in diabetic patients, and it maycontribute to hyperglycemia. Insulin/glucagon ratio may be a more perfect index than sole insulin me-asurement in reflecting the
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Dexamethasone Sodium Phosphate Inj: Dexamethasone belongs to the group of medications known as corticosteroids. It may be used to treat a wide variety of conditions.
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Looking for insulin:glucagon ratio? Find out information about insulin:glucagon ratio. hormone hormone, secretory substance carried from one gland or organ of the body via the bloodstream to more or less specific tissues, where it exerts some... Explanation of insulin:glucagon ratio
Treatment for significant hypoglycemia will depend on how conscious the patient is.. In some circumstances, someone with diabetes may recover sufficiently to be able to treat the hypo themselves.. Though this may not always be the case and therefore its beneficial to treat severe hypoglycemia as an emergency.. If you know how to apply glucagon via a glucagon injection kit, this is a dependable and effective way to raise blood glucose levels of someone sustaining from a severe hypo. If you apply glucagon, ensure the person is in the recovery state as glucagon can commence to vomiting.. If you do not have access to glucagon, call for emergency hospitalization and have a form of sugar ( fruit juice, a sugary drink, glucose tablets ) available in case they recover.. ...
In the study, intranasal glucagon consistently corrected insulin-induced hypoglycemia in adults with type 1 diabetes, meeting the predefined definition of noninferiority to intramuscular injection of glucagon. In the one case in which intranasal glucagon did not meet the study-defined success criteria, hypoglycemia was corrected without any additional intervention but after the time frame for study-defined success. Average glucose concentrations and time to meet the primary end point after intranasal glucagon lagged ∼3 min behind glucose concentrations after intramuscular glucagon, consistent with the glucagon concentrations showing a relative delay in achievement of peak glucagon levels with intranasal glucagon of ∼5 min. Nevertheless, pharmacologic levels of glucagon were present by 5 min after administration by either approach. The slight delay in glycemic response would likely be clinically inconsequential and in many circumstances might be offset by the time required, errors, and ...
Glucagon secretion by pancreatic α-cells is triggered by hypoglycemia and suppressed by high glucose levels; impaired suppression of glucagon secretion is a hallmark of both type 1 and type 2 diabetes. Here, we show that α-cell glucokinase (Gck) plays a role in the control of glucagon secretion. Using mice with α-cell-specific inactivation of Gck (αGckKO mice), we find that glucokinase is required for the glucose-dependent increase in intracellular ATP/ADP ratio and the closure of KATP channels in α-cells and the suppression of glucagon secretion at euglycemic and hyperglycemic levels. αGckKO mice display hyperglucagonemia in the fed state, which is associated with increased hepatic gluconeogenic gene expression and hepatic glucose output capacity. In adult mice, fed hyperglucagonemia is further increased and glucose intolerance develops. Thus, glucokinase governs an α-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon secretion
Pancreatic expression of the glucagon gene depends on multiple transcription factors interacting with at least three DNA control elements: G1, the upstream promoter element, and G2 and G3, two enhancer-like sequences. We report here that the major enhancer of the rat glucagon gene, G2, interacts with three protein complexes, A1, A2, and A3. A2 is detected only in islet cells, and impairment of its binding to mutant G2 causes a marked decrease in transcriptional activity. We identify A1 as hepatocyte nuclear factor 3 beta (HNF-3 beta), a member of the HNF-3 DNA-binding protein family found in abundance in the liver which has been proposed to play a role in the formation of gut-related organs. HNF-3 beta binds G2 on a site which overlaps A2 and acts as a repressor of glucagon gene expression, as demonstrated by mutational analyses of G2 and by cotransfection of HNF-3 beta cDNA along with reporter genes containing G2 into glucagon-producing cells. Our data implicate HNF-3 beta in the control of ...
Hyperglucagonemia is an important factor for type 2 diabetes which contributes to increased hepatic glucose production (Rizza 2010). In spite of this, however, little is known about the role of chronically elevated glucagon levels for β-cell function. A reason for this is the lack of appropriate models of long-term glucagon action, which in part is due to difficulties in administering native glucagon long-term because of poor chemical and physical stability. Therefore, in the current study, we administered a stable glucagon analog (ZP-GA-1) to mice fed a HFD to create a novel model for studying effects of chronic GCGR activation on β-cell function. The HFD fed mice do not develop hyperglucagonemia (Ahlkvist et al. 2013) which allowed us to study the impact of chronic GCGR stimulation on glucose tolerance in a glucose intolerant model without the confounding factor of endogenous hyperglucagonemia. In these mice, 2-week ZP-GA-1 infusion markedly reduced the insulin response to oral glucose. ...
Anti-glucagon antibodies have shown some efficacy in animal models (Brand et al., 1994, 1996; Sørensen et al., 2006a); however, daily injections of high doses of antibodies were required (Sørensen et al., 2006). The lack of long-term efficacy of the antibody on blood glucose lowering is probably due to a compensatory mechanism involving oversecretion of endogenous glucagon in response to the reduction of glucagon receptor signaling. Increases in circulating glucagon levels have been reported with all modalities blocking the glucagon signaling pathway, which presents technical challenges for both small-molecule GCGR inhibitors and glucagon-neutralizing mAb approaches.. Despite rising glucagon levels, treatment with neutralizing hGCGR mAbs maintained glucose-lowering efficacy. These anti-GCGR mAbs have several desirable attributes as potential therapeutic agents compared with previously pursued approaches. First, mAb B showed a higher affinity than glucagon to the GCGR (Kd = 36 pM versus Kd = ...
The diagnosis of Cushings syndrome is usually made clinically. However to differentiate between adrenal cause and pituitary cause, tests may be required. The most common screening test to establish increased serum cortisol levels is to do 24 hours urine estimation of free cortisol. Normally, the levels are between 20-70 µg/sqm, however in case of Cushings syndrome, urinary free cortisol is elevated. To find out the cause, your doctor may do blood ACTH levels and high dose dexamethasone suppression test. In case of pituitary tumors, ACTH levels will be elevated. In case of adrenal tumors, ACTH levels will be decreased. High dose dexamethasone tests consists of given high dose dexamethasone 6 hourly for 48 hours and then doing urinary free cortisol on 2nd day. In case of suppression of secretion of cortisol in urine, it suggests a pituitary cause and in case of non suppression, it suggests adrenal cause ...
Abstract: In addition to its primary role in regulating glucose production from the liver, glucagon has many other actions, reflected by the wide tissue distribution of the glucagon receptor (Gcgr). To investigate the role of glucagon in the regulation of insulin secretion and whole body glucose homeostasis in vivo, we generated mice overexpressing the Gcgr specifically on pancreatic β-cells (RIP-Gcgr). In vivo and in vitro insulin secretion in response to glucagon and glucose was increased 1.7- to 3.9-fold in RIP-Gcgr mice compared with controls. Consistent with the observed increase in insulin release in response to glucagon and glucose, the glucose excursion resulting from both a glucagon challenge and intraperitoneal glucose tolerance test (IPGTT) was significantly reduced in RIP-Gcgr mice compared with controls. However, RIP-Gcgr mice display similar glucose responses to an insulin challenge. β-Cell mass and pancreatic insulin content were also increased (20 and 50%, respectively) in ...
Toxicology Question of the Week. June 13, 2017. How does glucagon ameliorate the hypotension caused by beta-blocker toxicity?. Glucagon is a hormone secreted from pancreatic alpha cells. It has inotropic and chronotropic cardiac effects. When the beta receptor is stimulated, cAMP is increased and calcium influx (via L-type calcium channels) also increases. When the beta receptor is blocked, glucagon stimulates the same subcellular protein to increase cAMP production and increase calcium influx.. Glucagon administration is indicated for hypotension, bradycardia or conduction impairment. It may also be effective in treating hypotension in calcium channel blocker and other overdoses with cardiac toxicity.. IF dose is too high or pushed IV too fast, the patient will vomit. A bolus of 5-10 mg (150 mcg/kg) given over 10 minutes is less likely to have this side effect. Glucagons half-life is 6 minutes so a continuous infusion of 3 mg/hr (50-100 mcg/kg/hr) should follow this bolus.. References:. DeWitt ...
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Glucagon is a hormone that causes increase in blood glucose by promoting breakdown of liver glycogen. Glucagon is used for emergency treatment of severe hypoglycaemia. Administration of therapeutic glucagon as a rescue treatment for severe hypoglycaemia is safe and effective, however, its use is challenging due to its low solubility and very poor stability in liquid solution. Thus, currently available glucagon treatments (rescue kits) are only available in the form of a lyophilised powder, which requires the caregiver to perform a complex multi-step reconstitution procedure prior to administration in this highly stressful emergency situation. The reconstitution procedure leads to handling errors and delayed administration of glucagon, resulting in sub-optimal treatment. This is a significant barrier to the use of these rescue kits with recent usability studies demonstrating that more than 80% of people failed to reconstitute properly and inject the recommended dose of glucagon. As a result, only ...
Treatment of intact hepatocytes with glucagon led to the rapid desensitization of adenylate cyclase, which reached a maximum around 5 min after application of glucagon, after which resensitization ensued. Complete resensitization occurred some 20 min after the addition of glucagon. In hepatocytes which had been preincubated with the cyclic AMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), glucagon elicited a stable desensitized state where resensitization failed to occur even 20 min after exposure of hepatocytes to glucagon. Treatment with IBMX alone did not elicit desensitization. The action of IBMX in stabilizing the glucagon-mediated desensitized state was mimicked by the non-methylxanthine cyclic AMP phosphodiesterase inhibitor Ro-20-1724 [4-(3-butoxy-4-methoxylbenzyl)-2-imidazolidinone]. IBMX inhibited the resensitization process in a dose-dependent fashion with an EC50 (concn. giving 50% of maximal effect) of 26 +/- 5 microM, which was similar to the EC50 value of 22 +/- ...
Background:Dexamethasone may improve multimodal pain management following painful orthopedic day surgery procedures, and decrease the need for post-operative opioids. We hypothesized that dexamethasone would reduce the need for oxycodone after surgical correction of hallux valgus.Methods:Sixty patie
Aim: To explore the association of plasma copeptin, the C-terminal portion of provasopressin and a stable surrogate marker for arginine vasopressin secretion, with plasma glucagon in obese men and men of normal weight. Methods: We measured fasting blood concentrations of copeptin and glucagon in 102 healthy obese men (mean ± sd age 49.4 ± 10.2 years) and a control group 27 healthy men of normal weight (mean ± sd age 51.5 ± 8.4 years). Differences between groups were evaluated using t-tests, and multiple linear regression analysis, adjusting for age and weight status (normal weight vs obese), was used to calculate unstandardized regression coefficients (β) with 95% CIs between copeptin and glucagon. Copeptin was (natural) log-transformed. Results: The obese men had higher [median (interquartile range)] plasma copeptin concentrations [6.6 (4.6-9.5) vs 4.9 (3.5-6.8) pmol/l; P = 0.040] and higher mean ± sd plasma glucagon concentrations (8.5 ± 3.8 vs 5.3 ± 1.4 pmol/l; P , 0.001) than the ...
BioAssay record AID 293012 submitted by ChEMBL: Displacement of [125]glucagon from human glucagon receptor expressed in CHO cells.
Results We found 11 papers comparing dexamethasone to prednisolone of which 8 were controlled trials, one was a retrospective cohort study and two were meta-analyses. There was significant heterogeneity of dosage and method of administration of dexamethasone, including intramuscular, nebulised and oral routes. We analysed four controlled studies of oral dexamethasone, as this was our preferred route. Details of the four studies can be found in Table 1. All of the studies found that dexamethasone was non-inferior to prednisolone. One study compared a single 0.6mg/kg dose of dexamethasone with 5 days of prednisolone, two studies compared two daily 0.6mg/kg doses of dexamethasone with 5 days of prednisolone and the most recent study compared a single 0.3mg/kg dose of dexamethasone with 3 days of prednisolone. Most of the studies have some limitations which may affect the validity of the results. ...
Assays for the pancreatic hormone glucagon have typically been carried out using RIAs, but specificity has always been a problem, as the same amino acid sequence is present in other endogenous peptides in addition to glucagon, as discussed in the Introduction. Sensitivity (i.e. the smallest concentration of a substance that can be reliably measured) is also a prominent issue, as circulating concentrations are likely to be low, around 10 pmol/l or less (22). The relevant changes in glucagon secretion, resulting from changes in plasma glucose concentrations, are also modest with increases in response to hypoglycaemia ranging from 20 to 30 pmol/l, but even more challenging are decreases in response to hyperglycaemia, which may lower the concentrations to 1-2 pmol/l (24). Clearly, assays with sensitivities ,5 pmol/l are, therefore, unsuitable for the complete characterisation of glucagon secretion. The present study demonstrates that it is important to test a commercial assay carefully before being ...
The potential advantages of using ultrasound for drug, gene, and protein delivery, using parameters that cause cavitation and streaming effects, have been confirmed in different experimental studies [24, 28, 32]. Cavitation is known as the creation, oscillation, and collapse of gas bubbles due to acoustic waves [33-35]. It is stated to be the main mechanism responsible for promoting drug delivery through the skin [32, 36]. There are two types of cavitation: stable and inertial. Stable cavitation is defined as the uniform pulsation of bubbles over long time intervals [33], and the oscillation of these bubbles can produce mechanical stresses that may cause cell membrane rupture [37]. In the case of inertial cavitation, collapse of the bubbles causes shock waves and microjets to be generated near the cells, thus producing pits in the cell membranes [38, 39]. The effect of inertial cavitation is greater at lower frequencies because bubbles have more time to grow, which results in a more violent ...
TY - JOUR. T1 - Hydrogen peroxide signaling is required for glucocorticoid-induced apoptosis in lymphoma cells. AU - Tome, Margaret E.. AU - Jaramillo, Melba C.. AU - Briehl, Margaret M.. PY - 2011/12/1. Y1 - 2011/12/1. N2 - Glucocorticoid-induced apoptosis is exploited clinically for the treatment of hematologic malignancies. Determining the required molecular events for glucocorticoid-induced apoptosis will identify resistance mechanisms and suggest strategies for overcoming resistance. In this study, we found that glucocorticoid treatment of WEHI7.2 murine thymic lymphoma cells increased the steady-state [H 2O 2] and oxidized the intracellular redox environment before cytochrome c release. Removal of glucocorticoids after the H 2O 2 increase resulted in a 30% clonogenicity; treatment with PEG-CAT increased clonogenicity to 65%. Human leukemia cell lines also showed increased H 2O 2 in response to glucocorticoids and attenuated apoptosis after PEG-CAT treatment. WEHI7.2 cells that overexpress ...
We examined the direct effects of glucocorticoid treatment on neutrophil survival and function in vitro. Four different glucocorticoids caused a dose-dependent inhibition of apoptosis leading to increased survival of neutrophils. Maximal effects were found with dexamethasone at 10(-6) M, 16.6 +/- 6.2 vs 54.6 +/- 6.9, at 24 h (p , 0.05). Nonglucocorticoid steroids did not modulate apoptosis in neutrophils. Furthermore, the effect was inhibited in a dose-dependent manner by the glucocorticoid antagonist RU 486. Glucocorticoid-treated neutrophils produced significantly more superoxide in response to FMLP than untreated controls (p , 0.05). However, both basal and stimulated superoxide production were less than that found with freshly isolated cells. Such lack of priming or activation by glucocorticoids is in contrast to previous experience when increased survival was accompanied by cell activation. When compared with other stimuli, the effect of glucocorticoids at 24 h was similar to that of LPS ...
OUTLINE: This is a dose-escalation study of calcitriol.. In the first stage of the study, cohorts of 3-6 patients receive escalating doses of oral calcitriol on days 1-3. Dose escalation continues until the maximum tolerated dose (MTD) is determined.. In the second stage, patients receive escalating doses of oral calcitriol on days 1-3 and a fixed dose of oral dexamethasone on days 0-4. Treatment continues weekly in the absence of disease progression or unacceptable toxicity. Dose escalation continues until the MTD is determined.. Six additional patients may receive calcitriol and dexamethasone at one dose level below the MTD determined in the second stage, to confirm the MTD.. The MTD is defined as the dose preceding that at which 2 of 3 or 2 of 6 patients experience dose-limiting toxicity.. PROJECTED ACCRUAL: Approximately 40 patients will be accrued for this study. ...
TY - JOUR. T1 - A role for protein kinase C-mediated phosphorylation in eliciting glucagon desensitization in rat hepatocytes. AU - Savage, A.. AU - Zeng, L.. AU - Houslay, M. D.. PY - 1995/4/1. Y1 - 1995/4/1. N2 - An immobilized hepatocyte preparation was used to show that both vasopressin and glucagon could desensitize the ability of glucagon to increase intracellular cyclic AMP concentrations. This process was not dependent on any influx of extracellular Ca2+ and was not mediated by any rise in the intracellular level of Ca2+. The protein kinase C-selective inhibitors chelerythrine, staurosporine and calphostin C acted as potent inhibitors of the desensitization process but with various degrees of selectivity regarding their ability to inhibit the desensitizing actions of glucagon and vasopressin. The protein phosphatase inhibitor okadaic acid was just as potent as vasopressin and glucagon in causing desensitization. Treatment of hepatocyte membranes with alkaline phosphatase restored to near ...
We investigated the mechanisms by which peripheral or portal insulin can independently alter liver glucose production. Isotopic ([3-3H]glucose) and arteriovenous difference methods were used in conscious overnight-fasted dogs. A pancreatic clamp (somatostatin plus basal insulin and basal glucagon infusions) was used to control the endocrine pancreas. After a 40-min basal period, a 180-min experimental period followed in which selective increases in peripheral (PERI group, n = 5) or portal-vein (PORT group, n = 5) insulin were induced. In control dogs (CONT group, n = 10), insulin was not increased. Glucagon levels were fixed in all studies, and basal euglycemia was maintained by peripheral glucose infusion in the two experimental groups. In the PERI group, arterial insulin rose from 36 ± 12 to 120 ± 12 pmol/l, while portal insulin was unaltered. In the PORT group, portal insulin rose from 108 ± 42 to 192 ± 42 pmol/l, while arterial insulin was unaltered. Neither arterial nor portal insulin ...
OBJECTIVE-Leptin released from adipocytes plays a key role in the control of food intake, energy balance, and glucose homeostasis. In addition to its central action, leptin directly affects pancreatic beta-cells, inhibiting insulin secretion, and, thus, modulating glucose homeostasis. However, despite the importance of glucagon secretion in glucose homeostasis, the role of leptin in a-cell function has not been studied in detail. In the present study, we have investigated this functional interaction. RESEARCH DESIGN AND METHODS-The presence of leptin receptors (ObR) was demonstrated by RT-PCR analysis, Western blot, and immunocytochemistry. Electrical activity was analyzed by patch-clamp and Ca(2+) signals by confocal microscopy. Exocytosis and glucagon secretion were assessed using fluorescence methods and radioimmunoassay, respectively. RESULTS-The expression of several ObR isoforms (a-e) was detected in glucagon-secreting alpha TC1-9 cells. ObRb, the main isoform involved in leptin signaling, ...
Description: A modestly active, nonselective triarylimidazole lead was optimized for binding affinity with the human glucagon receptor. This led to the identification of a 2- and/or 4-alkyl or alkyloxy substituent on the imidazole C4-aryl group as a structural determinant for significant enhancement in binding with the glucagon receptor (e.g., 41, IC(50)=0.053 microM) and selectivity (>1000x) over p38MAP kinase in this class of compounds. ...
The effect of glucagon on the rate of muscle protein synthesis was examined in vivo and in the isolated perfused rat hemicorpus. An inhibition of protein synthesis in skeletal muscles from overnight-fasted rats at various plasma concentrations of glucagon was demonstrated in vivo. The plantaris muscle (Type II, fibre-rich) was more sensitive than the soleus (Type I, fibre-rich). Myofibrillar and sarcoplasmic proteins were equally sensitive in vivo. However, protein synthesis in mixed protein and in sarcoplasmic and myofibrillar fractions of the heart was unresponsive to glucagon in vivo. In isolated perfused muscle preparations from fed animals, the addition of glucagon also decreased the synthesis of mixed muscle proteins in gastrocnemius (Type I and II fibres) and plantaris, but not in the soleus. The sarcoplasmic and myofibrillar fractions of the plantaris were also equally affected in vitro. Similar results were observed in vitro with 1-day-starved rats, but the changes were less marked. ...
A B ST R A CT The effect of equal (1.1±0.1 g/kg body wt) amounts of glucose administered orally, or by peripheral intravenous or intraportal infusion on hepatic glucose uptake and fractional hepatic extraction of insulin and glucagon was studied in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery and catheters in the portal vein, hepatic vein, carotid artery, and superior mesenteric vein. Portal vein and hepatic vein plasma flow increased only after oral glucose administration. Arterial plasma glucose increased equally to 150-160 mg/100 ml after all three routes of glucose administration. Portal vein glucose was similar after oral (195±15 mg/100 ml) and intraportal glucose infusion (215±11 mg/100 ml) and significantly higher than after peripheral intravenous glucose. Hepatic glucose uptake after oral (68±4%) and intraportal glucose administration (65±7%) significantly exceeded that after peripheral intravenous glucose infusion (23±5%). The amount
article{1ab52f88-4d01-45dd-a399-2e230c289278, abstract = {High-resolution capacitance measurements were used to explore the effects of the gut hormones GLP-I(7-36) amide [glucagon-like peptide I(7-36) amide] and GIP (glucose-dependent insulinotropic polypeptide) on Ca2+-dependent exocytosis in glucagon-secreting rat pancreatic alpha-cells. Both peptides produced a greater than threefold potentiation of secretion evoked by voltage-clamp depolarizations, an effect that was associated with an approximately 35% increase of the Ca2+ current. The stimulatory actions of GLP-I(7-36) amide and GIP were mimicked by forskolin and antagonized by the protein kinase A (PKA)-inhibitor Rp-8-Br-cAMPS. The islet hormone somatostatin inhibited the stimulatory action of GLP-I(7-36) amide and GIP via a cyclic AMP-independent mechanism, whereas insulin had no effect on exocytosis. These data suggest that the alpha-cells are equipped with receptors for GLP-I and GIP and that these peptides, in addition to their ...
We have monitored electrical activity, voltage-gated Ca2+ currents, and exocytosis in single rat glucagon-secreting pancreatic A-cells. The A-cells were electrically excitable and generated spontaneous Na+- and Ca2+-dependent action potentials. Under basal conditions, exocytosis was tightly linked to Ca2+ influx through omega-conotoxin-GVIA-sensitive (N-type) Ca2+ channels. Stimulation of the A-cells with adrenaline (via beta-adrenergic receptors) or forskolin produced a greater than fourfold PKA-dependent potentiation of depolarization-evoked exocytosis. This enhancement of exocytosis was due to a 50% enhancement of Ca2+ influx through L-type Ca2+ channels, an effect that accounted for |30% of the total stimulatory action. The remaining 70% of the stimulation was attributable to an acceleration of granule mobilization resulting in a fivefold increase in the number of readily releasable granules near the L-type Ca2+ channels.
Adomeglivant. CAS No:1488363-78-5 Catalog No.:HY-19904 Brief Description: Adomeglivant is a potent and selective glucagon receptor antagonist that is used in clinical trial for type 2 diabetes mellitus.. Price and Availability: 10 mM * 1 mL €134 ( In-stock ); 5mg €109 ( In-stock ); 10mg €164 ( In-stock ); 25mg €262 ( In-stock ); 50mg €481 ( In-stock ); 100mg €711 ( In-stock ); Inquiry Online More Info > ...
Hypothesis:. Pegvisomant combined with the glucagon stimulation test (GST) can improve the accuracy of this test when used to diagnose adult GH and cortisol (steroid hormone)insufficiency.. Study aims:. Diagnosing GH and cortisol deficiency in adults requires a special test. At present, the insulin tolerance test (ITT) is considered the test of choice. However, this test is difficult to perform as it involves giving insulin through the veins to decrease blood sugars to very low levels, and this can be unpleasant, and cannot be performed in elderly adults and in those with a history of heart disease, seizure disorders or stroke. For this reason there is an urgent need for an alternative reliable test. At present, the GST is considered the alternative test to the ITT but its accuracy in obese patients and in those with diabetes remains unclear. Pegvisomant is a medication that can increase GH production in the body. The purpose of this study is to find out if combining pegvisomant with the GST can ...
Peptides , Glucagon-Like Peptides , Glucagon-Like Peptide 1, GLP-1 amide, human, FAM-labeled; This is fluorescent GLP-1 labeled at the peptide C-terminus with FAM, Abs/Em=494/521 nm. In response to Glucose ingestion, proglucagon in the intestinal L cells is cleaved into GLP-1 (1-36). Prior to secretion into the circulation, GLP-1 (1-36) is further processed into amidated GLP-1 (7-36)-cat# AS-22462-and small amounts of glycine-extended GLP-1 (7-37)-cat# AS-20761. Both GLP-1 (7-36) and GLP-1 (7-37), causes glucose dependent release of insulin by pancreatic beta-cells. They also play a role in gastric motility (gastric emptying), on the suppression of plasma glucagon levels (glucose production) and possibly on the promotion of satiety and stimulation of glucose disposal in peripheral tissues independent of the actions of insulin. GLP-1 peptides such as GLP-1 (1-36) have been used to investigate restoration of pancreatic beta cell function. GLP-1 is also produced in the central nervous system. ; FAM
Olfactory receptors (ORs) are extensively expressed in olfactory as well as non-olfactory tissues. Although many OR transcripts are expressed in non-olfactory tissues, only a few studies demonstrate the functional role of ORs. Here, we verified that mouse pancreatic α-cells express potential OR-mediated downstream effectors. Moreover, high levels of mRNA for the olfactory receptors Olfr543, Olfr544, Olfr545, and Olfr1349 were expressed in α-cells as assessed using RNA-sequencing, microarray, and quantitative real-time RT-PCR analyses. Treatment with dicarboxylic acids (azelaic acid and sebacic acid) increased intracellular Ca2+ mobilization in pancreatic α-cells. The azelaic acid-induced Ca2+ response as well as glucagon secretion was concentration- and time-dependent manner. Olfr544 was expressed in α-cells, and the EC50 value of azelaic acid to Olfr544 was 19.97 μM, whereas Olfr545 did not respond to azelaic acid. Our findings demonstrate that Olfr544 responds to azelaic acid to regulate ...
OBJECTIVE: Beta-cell secretory capacity is often evaluated with a glucagon test or a meal test. However, glucagon-like peptide 1 (GLP-1) is the most insulinotropic hormone known, and the effect is preserved in type 2 diabetic patients. RESEARCH DESIGN AND METHODS: We first compared the effects of intravenous bolus injections of 2.5, 5, 15, and 25 nmol GLP-1 with glucagon (1 mg intravenous) and a standard meal (566 kcal) in 6 type 2 diabetic patients and 6 matched control subjects. Next, we studied another 6 patients and 6 control subjects and, in addition to the above procedure, performed a combined glucose plus GLP-1 stimulation, where plasma glucose was increased to 15 mmol/l before injection of 2.5 nmol GLP-1. Finally, we compared the insulin response to glucose plus GLP-1 stimulation with that observed during a hyperglycemic arginine clamp (30 mmol/l) in 8 patients and 8 control subjects. RESULTS: Peak insulin and C-peptide concentrations were similar after the meal, after 2.5 nmol GLP-1, ...
U.S., Dec. 8 -- ClinicalTrials.gov registry received information related to the study (NCT02984644) titled Paradoxical Stimulation of Hepatic Glucose Production With Dapagliflozin on Nov. 30. Brief Summary: To determine the role of plasma glucagon and insulin in the rise of endogenous glucose production (EGP) following the SGLT2 inhibition. Study Start Date: January 2017 Study Type: Interventional Condition: Type II; Diabetes Intervention: Drug: Dapagliflozin Three 5-hour measurements (after dapagliflozin 10mg administration) of endogenous glucose production (EGP) will be performed on separate days. Other Name: Farxiga Drug: Placebo Three 5-hour measurements (after placebo administration) of endogenous glucose production (EGP) will be performed on separate days. Other Name: Placebo for Dapagliflozin Recruitment Status: Not yet recruiting Sponsor: The University of Texas Health Science Center at San Antonio Information provided by (Responsible Party): Eugenio Cersosimo, The University of Texas ...
The glucagon-like peptide 1 receptor (GLP1R) is a receptor protein found on beta cells of the pancreas. It is involved in the control of blood sugar level by enhancing insulin secretion. In humans it is synthesised by the gene GLP1R, which is present on chromosome 6. It is a member of the glucagon receptor family of G protein-coupled receptors. GLP1R is composed of two domains, one extracellular (ECD) that binds the C-terminal helix of GLP-1, and one transmembrane (TMD) domain that binds the N-terminal region of GLP-1. In the TMD domain there is fulcrum of polar residues that regulates the biased signaling of the receptor while the transmembrane helical boundaries and extracellular surface are a trigger for biased agonism. GLP1R binds glucagon-like peptide-1 (GLP1) and glucagon as its natural endogenous agonists. Receptor agonists: GLP-1 - endogenous in humans glucagon - endogenous in humans liraglutide exendin-4, lixisenatide Receptor antagonists: "T-0632" Receptor positive allosteric ...
TY - JOUR. T1 - Glucocorticoid and thyroid hormone regulation of angiotensinogen gene expression in a pancreatic islet cell line.. AU - Brasier, A. R.. AU - Philippe, J.. AU - Campbell, D. J.. AU - Habener, J. F.. PY - 1986/12/1. Y1 - 1986/12/1. N2 - The renin-angiotensin system is an important regulator of blood pressure and volume homeostasis in mammals. Angiotensinogen, a precursor of the octapeptide angiotensin II and an effector of the renin-angiotensin system, is synthesized in numerous rat tissues. Angiotensinogen is expressed in an islet cell line (RIN 1056A) derived from a rat pancreatic tumor. Angiotensinogen mRNA detected by Northern analysis is abundant in the cell line and is approximately 200 bases longer than the mRNA isolated from rat liver, due to both a longer poly(A) tract and the use of a second polyadenylation site. Dexamethasone is a potent inducer of angiotensinogen mRNA, producing a progressive accumulation from 3 to 96 hr in culture (9-fold above control levels). The ...
Inhibitors of dipeptidyl peptidase 4, also DPP-4 inhibitors or gliptins, are a class of oral hypoglycemics that block DPP-4 (DPP-IV). They can be used to treat diabetes mellitus type 2. The first agent of the class - sitagliptin - was approved by the FDA in 2006. Glucagon increases blood glucose levels, and DPP-4 inhibitors reduce glucagon and blood glucose levels. The mechanism of DPP-4 inhibitors is to increase incretin levels (GLP-1 and GIP), which inhibit glucagon release, which in turn increases insulin secretion, decreases gastric emptying, and decreases blood glucose levels. A 2014 meta analysis found no favorable or harmful effect of DPP-4 inhibitors on all-cause mortality, cardiovascular mortality, or stroke, but a marginally statistically significant increase in heart failure. Drugs belonging to this class are: Sitagliptin (FDA approved 2006, marketed by Merck & Co. as Januvia) Vildagliptin (EU approved 2007, marketed in the EU by Novartis as Galvus) Saxagliptin (FDA approved in 2009, ...
Looking for Receptors, pancreatic hormone? Find out information about Receptors, pancreatic hormone. glandular organ that secretes digestive enzymes and hormones. In humans, the pancreas is a yellowish organ about 7 in. long and 1.5 in. wide. Explanation of Receptors, pancreatic hormone
1. The metabolism of glutamine and alanine in the lung was studied in rats made septic by a caecal ligation and puncture technique.. 2. The blood glucose concentration was not significantly different in septic rats, but blood pyruvate, lactate, glutamine and alanine concentrations were markedly increased as compared with sham-operated rats. Conversely, blood ketone body and plasma cholesterol concentrations were significantly decreased in septic rats. Both plasma insulin and plasma glucagon concentrations were markedly elevated in response to sepsis. Sepsis resulted in a negative nitrogen balance.. 3. Sepsis increased the rates of production of glutamine (52.5%, P ,0.001), alanine (38.9%, P ,0.001) and glutamate (48.6%, P ,0.001) by lung slices incubated in vitro.. 4. Sepsis increased lung blood flow by 27.6% (P ,0.05). Blood flow and arteriovenous concentration difference measurement across the lung of septic rats showed an increase in the net exchange ...
Largest Candy Store In Canada p,Pancreas location back also well im all better for now ive decided to cut back on also pancreas anatomy diagram anatomy of the human pancreas together with Leg or foot amputation is the removal of a leg If you have diabetes follow your diet and take your medicines as usual until the day of surgery. An analysis "suggest that the use of diuretics statins and LABAs promotes muscle cramping in older adults." Plasma glucagon concentrations are increased Insulin resistance The Best Foods for Insulin Resistance. Largest Candy Store In Canada undiagnosed Gestational Diabetes ::The 3 Step Trick that Reverses Diabetes Permanently in As Little UNDIAGNOSED GESTATIONAL DIABETES ] The REAL cause of Diabetes (and the solution).. It is an update to the CONTOUR LINK meter visit the Bayer Diabetes Care website to find out how to get a CONTOUR NEXT LINK blood glucose meter FMS fiomyalgia syndrome is sometimes associated with diabetes. Whereas some patients may have extremely ...
Background: Glucagon-like peptide-1 (GLP-1) possesses insulinotropic and glucagonostatic properties, and, therefore, GLP-based antidiabetic therapies have been developed. Even though the insulinotropic potency of GLP-1 has been shown to be reduced in patients with type 2 diabetes mellitus (T2DM), a small dose of GLP-1 is capable of normalizing the beta-cell responsiveness to glucose in these patients. The glucagonostatic potency of GLP-1 in patients with T2DM is not known, and, furthermore, the capability of GLP-1 to reestablish normal glucagon secretion in these patients remains to be elucidated.. Objective: To investigate the alpha-cell sensitivity to GLP-1 in patients with T2DM and to establish if GLP-1 is able to reestablish normal glucagon secretion in such patients.. Method: Ten patients with T2DM and ten healthy control subjects are clamped at their fasting blood glucose levels during GLP-1 infusions at increasing doses (0.25, 0.5, 1.0 and 2.0 pmol/kg/min) and placebo, respectively. ...
Scientists have found the factor which puts type 2 diabetes into remission following bariatric surgery, according to new research. Researchers have identified the gut hormone PYY plays a key role in restoring normal blood glucose levels in people with the condition bariatric surgery.. The team, from the University of Oxford, found that bariatric surgery reverts islets back into working order.. The surgery brought the function of both alpha and beta cells within the islets back to normal: beta cells secrete the hormone insulin and alpha cells secrete the hormone glucagon.. Dr Reshma Ramracheya, lead Diabetes UK researcher based at the University of Oxford, said: "Research has mostly focused on the importance of beta cells and insulin secretion in type 2 diabetes, but thats just part of the story.. "The fact that alpha cells - and glucagon secretion - are also affected goes some way to completing the equation.". The team initially considered that a gut hormone called GLP-1 was the driving factor ...
Cyclic AMP is an adenine nucleotide containing one phosphate group which is esterified to both the 3- and 5-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH. cAMP is synthesized from ATP by adenylate cyclase. Adenylate cyclase is located at the cell membranes. Adenylate cyclase is activated by the hormones glucagon and adrenaline and by G protein. Liver adenylate cyclase responds more strongly to glucagon, and muscle adenylate cyclase responds more strongly to adrenaline. cAMP decomposition into AMP is catalyzed by the enzyme phosphodiesterase ...
This study demonstrates that when lactate, a by-product of anaerobic glucose metabolism, is delivered selectively into the VMH, the catecholamine and glucagon responses are reduced in the face of peripheral hypoglycemia. The delivery of lactate to the VMH also increased the requirement for exogenous glucose to maintain the hypoglycemic plateau, in keeping with its suppressive effect on counterregulatory hormone responses.. The role of energy-yielding fuels other than glucose in brain metabolism during hypoglycemia is poorly understood. Yet, it has been reported that while the glucose metabolic rate in brain falls during hypoglycemia, there is little change in the rate of oxygen consumption (24), implying the utilization of other fuels. Glycogen stores appear to be insufficient to sustain brain metabolism (24) and blood ketones decline during insulin-induced hypoglycemia, making them unlikely candidates. Recent studies suggest that lactate may serve as an important source of fuel. Specifically, ...
Diabetes mellitus is a chronic disease that affects 18.2 million people in the United States.1 Type 2 diabetes is the most commonly diagnosed type; it is frequently caused by peripheral insulin resistance or impaired insulin secretion.2 Combination therapy is often necessary when a single drug fails to control plasma glucose. The FDA has approved Byetta (exenatide), manufactured by Amylin Pharmaceuticals Inc, as an adjunctive therapy for the treatment of type 2 diabetes in patients who cannot achieve blood sugar control on metformin and/or sulfonylurea.3 Pharmacology Byetta is an incretin mimetic agent that is composed of a 39-amino acid peptide. Incretins improve glucose-dependent insulin secretion and inhibit glucagon release. Byetta leads to an increase in insulin secretion, a decrease in glucagon release, a decrease in food intake, delayed gastric emptying, and an elevated beta-cell production.3,4 Clinical Trials A triple-blind, placebo-controlled study evaluated the effectiveness of ...
TY - JOUR. T1 - SAD-A Potentiates Glucose-Stimulated Insulin Secretion as a Mediator of Glucagon-Like Peptide 1 Response in Pancreatic β Cells. AU - Nie, Jia. AU - Lilley, Brendan N.. AU - Pan, Y. Albert. AU - Faruque, Omar. AU - Liu, Xiaolei. AU - Zhang, Weiping. AU - Sanes, Joshua R.. AU - Han, Xiao. PY - 2013/7/1. Y1 - 2013/7/1. N2 - Type 2 diabetes is characterized by defective glucose-stimulated insulin secretion (GSIS) from pancreatic cells, which can be restored by glucagon-like peptide 1 (GLP-1), an incretin hormone commonly used for the treatment of type 2 diabetes. However, molecular mechanisms by which GLP-1 affects glucose responsiveness in islet β cells remain poorly understood. Here we investigated a role of SAD-A, an AMP-activated protein kinase (AMPK)-related kinase, in regulating GSIS in mice with conditional SAD-A deletion. We show that selective deletion of SAD-A in pancreas impaired incretins effect on GSIS, leading to glucose intolerance. Conversely, overexpression of ...
17129PRTArtificialSynthetic peptide sequence 1His Ser Gln Gly Thr Phe Thr Ser Asp Tyr Ser Lys Tyr Leu Asp Ser 1 5 10 15 Arg Arg Ala Gln Asp Phe Val Gln Trp Leu Met Asn Thr 20 25 28PRTArtificialSynthetic peptide sequence 2Lys Arg Asn Arg Asn Asn Ile Ala 1 5 337PRTArtificialSynthetic peptide sequence 3His Ser Gln Gly Thr Phe Thr Ser Asp Tyr Ser Lys Tyr Leu Asp Ser 1 5 10 15 Arg Arg Ala Gln Asp Phe Val Gln Trp Leu Met Asn Thr Lys Arg Asn 20 25 30 Arg Asn Asn Ile Ala 35 429PRTArtificialSynthetic peptide sequence 4His Ser Gln Gly Thr Phe Thr Ser Asp Tyr Ser Lys Tyr Leu Asp Glu 1 5 10 15 Arg Arg Ala Lys Asp Phe Ile Glu Trp Leu Leu Ser Ala 20 25 529PRTArtificialSynthetic peptide sequence 5His Ser Gln Gly Thr Phe Thr Ser Asp Tyr Ser Lys Tyr Leu Asp Glu 1 5 10 15 Arg Arg Ala Lys Asp Phe Ile Glu Trp Leu Xaa Ser Ala 20 25 629PRTArtificialSynthetic peptide sequence 6His Ser Gln Gly Thr Phe Thr Ser Asp Tyr Ser Lys Tyr Leu Asp Glu 1 5 10 15 Arg Arg Ala Xaa Asp Phe Ile Glu Trp Leu Leu Ser Ala 20 25 ...
CONTEXT: Proglucagon-derived hormones are important for glucose metabolism, but little is known about them in pediatric obesity and type 2 diabetes mellitus (T2DM).. OBJECTIVE: Fasting and postprandial levels of proglucagon-derived peptides glucagon, GLP-1, and glicentin in adolescents with obesity across the glucose tolerance spectrum were investigated.. DESIGN: This was a cross-sectional study with plasma hormone levels quantified at fasting and during an oral glucose tolerance test (OGTT).. SETTING: This study took place in a pediatric obesity clinic at Uppsala University Hospital, Sweden.. PATIENTS AND PARTICIPANTS: Adolescents with obesity, age 10-18 years, with normal glucose tolerance (NGT, n = 23), impaired glucose tolerance (IGT, n = 19), or T2DM (n = 4) and age-matched lean adolescents (n = 19) were included.. MAIN OUTCOME MEASURES: Outcome measures were fasting and OGTT plasma levels of insulin, glucagon, active GLP-1, and glicentin.. RESULTS: Adolescents with obesity and IGT had ...
Postprandial gut hormone responses change after Roux-en-Y gastric bypass (RYGB), and we investigated the impact of glucose, protein, and fat (with and without pancreas lipase inhibition) on plasma responses of gut and pancreas hormones, bile acids, and fibroblast growth factor 21 (FGF-21) after RYGB and in nonoperated control subjects. In a randomized, crossover study 10 RYGB operated and 8 healthy weight-matched control subjects were administered 4 different 4-h isocaloric (200 kcal) liquid meal tests containing ,90 energy (E)% of either glucose, protein (whey protein), or fat (butter with and without orlistat). The primary outcome was glucagon-like peptide-1 (GLP-1) secretion (area under the curve above baseline). Secondary outcomes included responses of peptide YY (PYY), glucose-dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), glicentin, neurotensin, ghrelin, insulin, glucagon, bile acids, and FGF-21. In the RYGB group the responses of GLP-1, GIP, glicentin, FGF-21, and ...
After monolayer cultures of rat islets were exposed to [125I]insulin,[125I]glucagon, and [125I]tyrosinyl somatostatin, specific autoradiographic grains associated with each radioactively labeled ligand were found on B, A, and D cells.The density of labeling of the B, A, and D cells with each labeled ligand correlated well with the known actions of the three hormones on each of the islet cells. ...
TY - JOUR. T1 - Dual role of the coactivator TORC2 in modulating hepatic glucose output and insulin signaling. AU - Canettieri, Gianluca. AU - Koo, Seung-Hoi. AU - Berdeaux, Rebecca. AU - Heredia, Jose. AU - Hedrick, Susan. AU - Zhang, Xinmin. AU - Montminy, Marc. PY - 2005/11/1. Y1 - 2005/11/1. N2 - Under fasting conditions, the cAMP-responsive CREB coactivator TORC2 promotes glucose homeostasis by stimulating the gluconeogenic program in liver. Following its nuclear translocation in response to elevations in circulating glucagon, TORC2 regulates hepatic gene expression via an association with CREB on relevant promoters. Here, we show that, in parallel with their effects on glucose output, CREB and TORC2 also enhance insulin signaling in liver by stimulating expression of the insulin receptor substrate 2 (IRS2) gene. The induction of hepatic IRS2 during fasting appears critical for glucose homeostasis; knockdown of hepatic IRS2 expression leads to glucose intolerance, whereas hepatic IRS2 ...
The Ghrelin (ε) Cell Type Represents the Majority of Cells Within the Nkx2.2-/- Islet. To characterize the expanded ghrelin population in the Nkx2.2 mutant islet with respect to glucagon and the other islet hormones, we performed immunohistochemical analysis of the mutant islets. Similar to the wild-type islet, ghrelin-producing cells in the Nkx2.2 mutant islet do not coexpress insulin, somatostatin, or PP (Fig. 2 f, h, and i ). However, unlike its expression in wild-type islets, none of the ghrelin-producing cells in the Nkx2.2 mutant coexpress glucagon (Fig. 2g ). This would suggest that the ghrelin (ε) cell type is expanded, whereas the glucagon/ghrelin double-positive cells are absent from the Nkx2.2 mutant islet. Therefore, we conclude that, in normal islets, a population of glucagon-expressing α cells coexpress ghrelin, but approximately two-thirds of ghrelin-expressing cells define a new endocrine islet ε cell population. Moreover, in the Nkx2.2 mutant islet, the ghrelin-producing ε ...
A new link between obesity and type 2 diabetes found in mice could open the door to exploring new potential drug treatments for diabetes, University of Michigan Health System research has found.. Drugs for type 2 diabetes commonly target insulin, which lowers blood glucose levels. But the U-M study suggests that glucagon - a pancreas-produced hormone that has the opposite effect of insulin by raising blood glucose levels - may also provide a powerful pathway to preventing and treating the increasingly prevalent disease.. Findings of the study were published this week ahead of print in Nature Medicine.. "Reducing sugar levels is the biggest goal for people with type 2 diabetes," says senior author Liangyou Rui, Ph.D., associate professor in the Department of Molecular and Integrative Physiology at the U-M Medical School. "Weve mostly focused on controlling insulin production and action to treat diabetes but there has been very little study on the opposite hormone glucagon.. "Our study shows for ...
Middle East & Africa (United Arab Emirates, Saudi Arabia, South Africa, etc). Glucagon like peptide-1 (GLP-1) agonists Product/Service Development. Knowing how the product/services fit the needs of clients and what changes would require to make the product more attractive is the need of an hour. Useful approaches to focus group by utilizing User Testing and User Experience Research. Demand-side analysis always helps to correlate consumer preferences with innovation.. Marketing Communication and Sales Channel. Understanding "marketing effectiveness" on a continual basis help determine the potential of advertising and marketing communications and allow us to use best practices to utilize an untapped audience. In order to make marketers make effective strategies and identify why the target market is not giving attention, we ensure the Study is Segmented with appropriate marketing & sales channels to identify potential market size by Revenue and Volume* (if Applicable).. Pricing and ...
Glucagon Like Peptide-1 (GLP-1) Agonists Report by Material, Application, and Geography - Global Forecast to 2021 is a professional and in-depth research report on the worlds major regional market conditions, focusing on the main regions (North America, Europe and Asia-Pacific) and the main countries (United States, Germany, united Kingdom, Japan, South Korea and China).
Ketoacidosis is a serious condition that can occur in people with Type 1 diabetes. You may meet the diabetes listing and be eligible for social security disability benefits if you have episodes of ketoacidosis one every two months on average. See Meeting Listing 9.08B for Diabetes.. It results when insulin levels approach zero. It is called ketoacidosis because compounds called ketones are released into the blood and secreted in the urine and breath and the ph of the blood becomes lower than normal making it acidic. Symptoms of ketoacidosis include dehydration, weight loss, mental confusion, nausea and vomiting, rapid and deep breathing, and, if untreated, unconsciousness, coma, and death.. Ketoacidosis develops in the following way. When insulin levels are very low, the cells are starved for glucose, even though glucose is in the blood stream. In an attempt to compensate for the apparent lack of glucose, the pancreas releases the hormone glucagon. Glucagon causes the liver to convert sugar it ...
As part of the endocrine system the pancreas produces several different hormones. The four hormones it produces are called insulin, glucagon somatostatin and pancreatic polypeptide. Insulin is the hormone responsible for decreasing the glucose level (sugars) in your blood. It does this by increasing the rate at which your cells can absorb glucose. When too much glucose is present insulin causes the body to store the excess amount as glycogen in the liver. Glucagon is the hormone the body secretes to increase the level of glucose (sugars) in the blood. The pancreas will release this hormone when the level of glucose (sugars) in the blood falls too low. This triggers the body to convert some of the glycogen stored in the liver back into glucose of the body to use. Without sufficient amounts of glucose the body cannot function correctly as the absorption of glucose releases energy. Somatostatin regulates the production of both hormones insulin and glucagon within the pancreas. The function of ...
pancreatic hormones peptide hormones secreted into the blood by cells in the islets of langerhans of the pancreas. The alpha cells secrete glucagon; the beta cells secrete insulin; the delta cells secrete somatostatin; and the pp cells secrete pancreatic polypeptide. ...
TY - JOUR. T1 - Glucagon in the cerebrospinal fluid. AU - Graner, J. L.. AU - Abraira, C.. PY - 1985/1/1. Y1 - 1985/1/1. UR - http://www.scopus.com/inward/record.url?scp=0021914718&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0021914718&partnerID=8YFLogxK. M3 - Article. C2 - 3974692. AN - SCOPUS:0021914718. VL - 312. SP - 994. EP - 995. JO - New England Journal of Medicine. JF - New England Journal of Medicine. SN - 0028-4793. IS - 15. ER - ...
Over the past century, considerable progress has been made in understanding the role of enteroendocrine signals in regulating glucose. One substantial advance was the delineation of the "the incretin effect," which refers to the ability of orally administered glucose to stimulate pancreatic insulin secretion to a greater extent than glucose administered intravenously.1 Glucagon-like peptide-1 (GLP-1) and glucose dependent insulinotropic polypeptide are the two key enteroendocrine factors responsible for the incretin effect.2 GLP-1, secreted from the lower gastrointestinal tract L-cells after nutrient ingestion, stimulates endogenous insulin secretion in a glucose dependent manner, inhibits postprandial glucagon release, delays gastric emptying, and increases satiety.3 However, GLP-1 is of limited therapeutic use because it is rapidly degraded by dipeptidyl peptidase 4, an enzyme produced at epithelial and endothelial membranes. In the linked systematic review and meta-analysis ...
Blocking hormone lowers sensitivity to sugar, opening door for food additives or drugs. A hormone that helps to regulate blood sugar levels may also influence a persons sensitivity to sweet-tasting foods, according to a new study from researchers at the University of Maryland School of Medicine. They found that blocking the tongues ability to respond to the hormone known as glucagon decreases the taste systems sensitivity to sweetness. That is, changing the actions of the hormone glucagon could control how foods taste, according to the study published online June 14 in the Federation for American Societies for Experimental Biology (FASEB) Journal.. "An interesting possibility resulting from our research is that the development of new food additives could change the way you perceive your food, making it taste more or less sweet," said senior author Steven D. Munger, Ph.D., associate professor of anatomy and neurobiology at the University of Maryland School of Medicine. "From a food industry ...
Glucose tolerance and pancreatic alpha and beta cell functions were evaluated in eight thalassemic patients, from 5 to 31 years old, receiving chronic transfusion therapy. Two patients had insulin-dependent diabetes, and two had a diabetic glucose tolerance test; one patient had a blood glucose response compatible with reactive hypoglycemia. All but two patients had a delayed or diminished insulin response, or both, to glucose infusion. In seven of eight patients the glucagon response to infusion of alanine was significantly reduced. Abnormalities of carbohydrate homeostasis are frequently seen in regularly transfused thalassemic patients. In such patients iron overload often results in diminished alpha and beta cell function. ...
The convergence of newly developed instrumentation and optical probes allows us to examine quantitatively dynamic processes within ever more complicated biological systems. These new tools are revolutionizing almost all fields of biomedical research, and we continue to optimize such methods and expand the scope of their applicability. In our lab, research questions are focused on a model multicellular system, the islet of Langerhans, which is the functional unit responsible for glucose-stimulated insulin secretion and glucose inhibition of glucagon secretion. The islet contains glucagon secreting Alpha-cells, insulin-secreting Beta-cells, and somatostatin-secreting Delta-cells, among others. The long-term goal of our work is to understand at a quantitative molecular level the subcellular, cellular, and multicellular mechanisms of islet function, and its role in the regulation of blood glucose under normal and pathological conditions. Rotation projects are available in all the labs research ...
Ussher, J. R., Campbell, J. E., Mulvihill, E. E., . Baggio, L. L., Bates, H. E., McLean, B. A., Gopal, K., Capozzi, M., Yusta, B., Cao, X., Ali, S., Kim, M., Kabir, M. G., Seino, Y., Suzuki, J., Drucker, D. J. Inactivation of the Glucose-Dependent Insulinotropic Polypeptide Receptor Improves Outcomes Following Experimental Myocardial Infarction Cell Metabolism 2017 27: https://doi.org/10.1016/j.cmet.2017.11.003 Drucker, D. J., Habener, J.F., Holst J.J. Discovery, characterization and clinical development of the glucagon-like peptides J Clin Invest 2017 127(12):4217-4227. Lebrun, L.J., Kaatje Lenaerts, J., Kiers, D., Pais de Barros, J.-P., Le Guern,N., Plesnik, J., Thomas, C., Bourgeois, T., Dejong, C.H.C., Kox, M., Hundscheid, I.H.R., Khan, N.A., Mandard, S., Deckert, V., Pickkers, P., Drucker, D. J., Lagrost, L., Grober, J. Enteroendocrine cells sense LPS after gut barrier injury to enhance GLP-1 secretion Cell Reports Oct 31 2017: 21(5) 1160-1168 Baggio, L.L., Ussher, J.E., McLean, B.A., Cao, ...
0074] The hGcgR-HEK293 cells are harvested from sub-confluent tissue culture dishes with Enzyme-Free Cell Dissociation Solution, (Specialty Media 5-004-B). The cells are pelleted at low speed and washed 3 times with assay buffer [25 mM HEPES in Hanks buffered salt solution (HBSS)--with Mg and Ca (GIBCO, 14025-092) with 0.1% Fatty Acid Free BSA] then diluted to a final concentration of 125,000 cells per ml. Biotinylated cAMP from the Alpha Screen kit is added to the diluted cells at a final concentration of 1 unit/0.04 ml. A phosphodiesterase inhibitor, IBMX (250 mM in dimethyl sulfoxide (DMSO)), is also added to the diluted cells to a final concentration of 500 uM. Glucagon is initially dissolved in 0.01 N HCl at 1 mg/ml and immediately frozen at -80° C. Upon thawing, the glucagon should be used within 1 hr. The glucagon, cAMP standard, and OXM peptide analogue are serially diluted into Assay buffer to a 6× final concentration. The functional assay is performed in 96 well, low-volume, white, ...
Islet amyloid polypeptide (IAPP, or amylin) is one of the major secretory products of beta-cells of the pancreatic islets of Langerhans. It is a regulatory peptide with putative function both locally in the islets, where it inhibits insulin and glucagon secretion, and at distant targets. It has binding sites in the brain, possibly contributing also to satiety regulation and inhibits gastric emptying. Effects on several other organs have also been described. IAPP was discovered through its ability to aggregate into pancreatic islet amyloid deposits, which are seen particularly in association with type 2 diabetes in humans and with diabetes in a few other mammalian species, especially monkeys and cats. Aggregated IAPP has cytotoxic properties and is believed to be of critical importance for the loss of beta-cells in type 2 diabetes and also in pancreatic islets transplanted into individuals with type 1 diabetes. This review deals both with physiological aspects of IAPP and with the ...
Exenatide is a GLP-1 (glucagon-like peptide-1) agonist that has been approved in the UK for use in the management of Type 2 Diabetes Mellitus (T2DM) since 2006. It acts by increasing glucose-induced insulin release and by reducing glucagon secretion postprandially. It therefore increases insulin secretion and reduces glucose levels, especially postprandially. It also reduces gastric emptying and acts centrally to promote satiety. In clinical practice it reduces HbA1c (range; -0.4% to -1.3%), fasting and postprandial blood glucose levels and is the only antidiabetic agent (together with liraglutide; a human GLP-1 analogue) to promote weight loss (range; -1.5 kg to -5.5 kg). It can be used as monotherapy or in combination with metformin and/or sulphonylureas (SU) and/or thiazolinediones (TZD). When compared with insulin it causes similar reductions in HbA1c and glucose levels, but unlike insulin it has the advantage of inducing weight loss. Its main side effect is gastrointestinal (GI) disturbances;
Glycerol uptake and glycerol kinase activity were studied in primary cultures of rat hepatocytes in the presence of either 1 nM insulin, 1 nM glucagon, or 100 nM dexamethasone, alone or in combination in
Regulation of hepatic gluconeogenesis by hormones insulin and glucagon is central to glucose homeostasis. Recent work has proposed that amongst the salt inducible kinase isoforms (SIK1, 2 and 3), members of the AMPK-related kinase family, the SIK2 isoform may play a role as signalling mediator in the control of insulin- and glucagon-regulated hepatic gluconeogenesis. However, the mechanisms of the hormonal-regulation of SIK2 in liver remain controversial, with much of the data based on the studies in non-hepatic tissues/cells. Therefore, the exact molecular regulation of SIK2 by these hormones in the liver required robust and intensive molecular/biochemical research coupled to physiological readout (e.g. gluconeogenesis). My studies with phosphopeptide mapping by mass spectrometry followed by verification with well-characterised phospho-specific antibodies revealed that SIK2 was phosphorylated on Ser343, Ser358, Thr484 and Ser587 in response to glucagon and fasting but not following insulin ...
The effect of xylazine and xylazine followed 20 minutes later by insulin upon glucose metabolism and plasma insulin concentrations was examined in three cows. After doses of 0.18 mg per kg xylazine given intramuscularly (IM) or 0.15 mg per kg given intravenously (IV) hepatic glucose production increased, plasma insulin concentrations decreased to 25 to 33 per cent of control values, and there was a prolonged hyperglycaemia. When 200 units of soluble insulin were given 20 minutes after similar doses of xylazine there was a rapid fall in blood glucose and a reduction in the rate of glucose production by the liver. Xylazine-induced hyperglycaemia arose from a combination of increased hepatic glucose production and reduced plasma insulin concentrations. Peripheral tissues were still responsive to insulin and when adequate insulin was available blood glucose concentrations rapidly decreased.. ...
Antagonism of the glucagon receptor (GCGR) is associated with increased circulating levels of glucagon-like peptide-1 (GLP-1). To investigate the contribution of GLP-1 to the antidiabetic actions of GCGR antagonism, we administered an anti-GCGR monoclonal antibody (mAb B) to wild-type mice and GLP-1 receptor knockout (GLP-1R KO) mice. Treatment of wild-type mice with mAb B lowered fasting blood glucose, improved glucose tolerance, and enhanced glucose-stimulated insulin secretion during an intraperitoneal glucose tolerance test (ipGTT). In contrast, treatment of GLP-1R KO mice with mAb B had little efficacy during an ipGTT. Furthermore, pretreatment with the GLP-1R antagonist exendin-(9-39) diminished the antihyperglycemic effects of mAb B in wild-type mice. To determine the mechanism whereby mAb B improves glucose tolerance, we generated a monoclonal antibody that specifically antagonizes the human GLP-1R. Using a human islet transplanted mouse model, we demonstrated that pancreatic islet ...
TY - JOUR. T1 - Polymorphism and ligand dependent changes in human glucagon-like peptide-1 receptor (GLP-1R) function: allosteric rescue of loss of function mutation. AU - Koole, Cassandra. AU - Wootten, Denise. AU - Simms, John. AU - Valant, Celine. AU - Miller, Laurence J. AU - Christopoulos, Arthur. AU - Sexton, Patrick. PY - 2011. Y1 - 2011. N2 - The glucagon-like peptide-1 receptor (GLP-1R) is a key physiological regulator of insulin secretion and a major therapeutic target for the treatment of diabetes. However, regulation of GLP-1R function is complex with multiple endogenous peptides that interact with the receptor, including full length (1-37) and truncated (7-37) forms of GLP-1 that can exist in an amidated form (GLP-1(1-36)NH(2) and GLP-1(7-36)NH(2)), and the related peptide oxyntomodulin. In addition, the GLP-1R possesses exogenous agonists, including exendin-4, and the allosteric modulator, compound 2 (6,7-dichloro2-methylsulfonyl-3-tert-butylaminoquinoxaline). The complexity of ...
Science & Technology, Life Sciences & Biomedicine, Endocrinology & Metabolism, ENDOCRINOLOGY & METABOLISM, glycation, gastric inhibitory polypeptide, obese mice, hyperglycemia, GLUCAGON-LIKE PEPTIDE-1(7-36)AMIDE, DEPENDENT INSULINOTROPIC POLYPEPTIDE, PANCREATIC B-CELLS, RAT ADIPOSE-TISSUE, NONENZYMATIC GLYCOSYLATION, TERMINAL GLYCATION, HUMAN-SERUM, IN-VITRO, GLUCOSE, GIP ...
Because of the low absorption and high excretion rates of chromium toxicity is not common. Diabetes affects how your body uses insulin to handle glucose. Making Potato Pancakes Ahead if you didnt have gestational diabetes when you were pregnant before you might have it with this What does gestational diabetes mean for my baby? During and Right After Birth. Oral surgery is any procedure that involves cutting into or removing tissue from your mouth.. Unfortunately I did not find an easy recipe for this pie. N explain the causes of some pancreatic liver and gall bladder disorders; secrete the peptide hormones glucagon and insulin that regulate the concen- Developing gestational diabetes at week 24 or after ings on the possibility of other risks for both the mother and the baby. Diabetic Eye Diseases Include Diabetic retinopathy (the most common eye disease in people with diabetes) Cataract Diabetic retinopathy is a leading cause of blindness in American adults.. Genetics of Diabetes Mellitus (Type ...
The pancreas is a glandular organ in the upper abdomen that serves as both a hormone-producing endocrine gland and a digestive exocrine gland. The endocrine cells are located in the islets of Langerhans, which are irregularly shaped patches of tissue that release hormones directly into the bloodstream (Islets of Langerhans). There are five known types of hormone-producing cells in the pancreas: alpha cells producing glucagon, beta cells producing insulin, delta cells producing somatostatin, PP cells producing pancreatic polypeptide, and epsilon cells producing ghrelin.. All of these hormones work together to maintain a balance in the body. Insulins main function is lowering glucose concentration in the bloodstream, and glucose works to raises sugar levels when they are too low. Somatostatin inhibits glucagon and insulin secretion, PP regulates pancreatic secretion activities and ghrelin regulates appetite, while also playing a role in regulating energy use. Endocrine features of PWS include low ...
The gut-derived incretin hormone, glucagon-like peptide 1 (GLP-1) lowers postprandial blood glucose levels by stimulating insulin and inhibiting glucagon secretion. Two novel antihyperglycaemic drug classes augment these effects; GLP-1 receptor agonists and inhibitors of the GLP-1 degrading enzyme dipeptidyl peptidase 4. These so called GLP-1 based or incretin based drugs are increasingly used to treat type 2 diabetes, because of a low risk of hypoglycaemia and favourable effect on body weight, blood pressure and lipid profiles. Besides glucose control, GLP-1 functions as an enterogastrone, causing a wide range of GI responses. Studies have shown that endogenous GLP-1 and its derived therapies slow down digestion by affecting the stomach, intestines, exocrine pancreas, gallbladder and liver. Understanding the GI actions of GLP-1 based therapies is clinically relevant; because GI side effects are common and need to be recognised, and because these drugs may be used to treat GI disease. ...
Latent autoimmune diabetes in adults (LADA) is a disorder in which, despite the presence of islet antibodies at diagnosis of diabetes, the progression of autoimmune ß-cell failure is slow. LADA patients are therefore not insulin requiring, at least during the first 6 months after diagnosis of diabetes. Among patients with phenotypic type 2 diabetes, LADA occurs in 10% of individuals older than 35 years and in 25% below that age. Prospective studies of ß-cell function show that LADA patients with multiple islet antibodies develop ß-cell failure within 5 years, whereas those with only GAD antibodies (GADAs) or only islet cell antibodies (ICAs) mostly develop ß-cell failure after 5 years. Even though it may take up to 12 years until ß-cell failure occurs in some patients, impairments in the ß-cell response to intravenous glucose and glucagon can be detected at diagnosis of diabetes. Consequently, LADA is not a latent disease; therefore, autoimmune diabetes in adults with slowly progressive ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
INTRODUCTION: Lixisenatide is a once-daily short-acting glucagon-like peptide-1 (GLP-1) receptor agonist (GLP-1RA) used in the treatment of type 2 diabetes mellitus (T2DM). It is used in combination with oral antidiabetics and/or basal insulin in patients inadequately controlled on these medications and who are undergoing diet and lifestyle modification. GLP-1RAs glucose-dependently increase insulin secretion, decrease glucagon secretion, and slow gastric emptying, thereby improving glycemic control. GLP-1RAs are associated with body weight benefits and low rates of hypoglycemia which are welcome in patients with T2DM. AREAS COVERED: The authors describe the identification of GLP-1RAs as suitable targets for modification with structure-inducing probe technology to improve stability and resistance to proteolytic degradation. Clinical studies have assessed lixisenatide across , 5000 patients as a monotherapy or add-on to a variety of commonly used antidiabetic medications. These studies ...
Glucagon-like peptide 2 (GLP-2) is a recently identified intestinal epithelium-specific growth factor that has been shown to reduce the severity of inflammatory disorders of the intestine in rodent models. Currently Glucagon-Like Peptide 2 is used as a potential therapeutic agent for the human s...
Find Glucagon-Like Peptide 1 Receptor research area related information and Glucagon-Like Peptide 1 Receptor research products from R&D Systems. Learn more.
TY - JOUR. T1 - Dose-response characteristics for effects of insulin on production and utilization of glucose in man.. AU - Rizza, R. A.. AU - Mandarino, L. J.. AU - Gerich, J. E.. PY - 1981/6/1. Y1 - 1981/6/1. N2 - To determine the dose-response characteristics for the effects of insulin on glucose production, glucose utilization, and overall glucose metabolism in normal man, 15 healthy subjects were infused with insulin for 8 h at sequential rates ranging from 0.2 to 5.0 mU.kg-1.min-1; each rate was used for 2 h. Glucose production and utilization were measured isotopically ([3-3H]glucose). Tissue insulin receptor occupancy was estimated from erythrocyte insulin binding. Glucose production was completely suppressed at plasma insulin concentrations of approximately 60 microunits/ml. Maximal glucose utilization (10-11 mg.kg-1.min-1) occurred at insulin concentrations of 200-700 microunits/ml. The concentration of insulin causing half-maximal glucose utilization (55 + 7 microunits/ml) was ...
Glucagon-like peptide-1 (GLP-1) elevates the intracellular free calcium concentration ([Ca2+]i) and insulin secretion in a Na+-dependent manner. To investigate a possible role of Na ion in the action of GLP-1 on pancreatic islet cells, we measured th
TY - JOUR. T1 - Vagally mediated effects of glucagon-like peptide 1. T2 - In vitro and in vivo gastric actions. AU - Holmes, Gregory M.. AU - Browning, Kirsteen N.. AU - Tong, Melissa. AU - Qualls-Creekmore, Emily. AU - Travagli, R. Alberto. PY - 2009/10/1. Y1 - 2009/10/1. N2 - Glucagon-like peptide-1 (GLP-1) is a neuropeptide released following meal ingestion that, among other effects, decreases gastric tone and motility. The central targets and mechanism of action of GLP-1 on gastric neurocircuits have not, however, been fully investigated. A high density of GLP-1 containing neurones and receptors are present in brainstem vagal circuits, suggesting that the gastroinhibition may be vagally mediated. We aimed to investigate: (1) the response of identified gastric-projecting neurones of the dorsal motor nucleus of the vagus (DMV) to GLP-1 and its analogues; (2) the effects of brainstem application of GLP-1 on gastric tone; and (3) the vagal pathway utilized by GLP-1 to induce gastroinhibition. We ...

carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity | SGDcarbamoyl-phosphate synthase (glutamine-hydrolyzing) activity | SGD

carbamoyl phosphate synthase (glutamine-hydrolyzing) activity, carbamoyl phosphate synthetase activity, carbamoyl-phosphate ... carbamoyl-phosphate synthetase (glutamine-hydrolysing) activity, carbamoyl-phosphate synthetase (glutamine-hydrolyzing) ... Gene Ontology Term: carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity. GO ID. GO:0004088 Aspect. Molecular Function ... glutamine-dependent carbamoyl-phosphate synthase activity, glutamine-dependent carbamyl phosphate synthetase activity, hydrogen ...
more infohttps://www.yeastgenome.org/go/GO:0004088

carB - Carbamoyl-phosphate synthase large chain - Pseudomonas aeruginosa (strain ATCC 15692 / DSM 22644 / CIP 104116 / JCM...carB - Carbamoyl-phosphate synthase large chain - Pseudomonas aeruginosa (strain ATCC 15692 / DSM 22644 / CIP 104116 / JCM...

... glutamine-hydrolyzing) activity, cellular response to amino acid stimulus, glutamate metabolic process, glutamine metabolic ... Carbamoyl-phosphate synthase large chain (carB), Carbamoyl-phosphate synthase small chain (carA) ... Carbamoyl-phosphate synthase large chain (carB), Carbamoyl-phosphate synthase small chain (carA) ... carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity Source: PseudoCAP ,p>Inferred from Direct Assay,/p> ,p>Used to ...
more infohttps://www.uniprot.org/uniprot/P38100

Dexamethasone and glucagon cause synergistic increases of urea cycle enzyme activities in livers of normal but not...Dexamethasone and glucagon cause synergistic increases of urea cycle enzyme activities in livers of normal but not...

Argininosuccinate Synthase / analysis. Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) / analysis. Dexamethasone / ... EC 6.3.4.5/Argininosuccinate Synthase; EC 6.3.5.5/Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) ...
more infohttp://www.biomedsearch.com/nih/Dexamethasone-glucagon-cause-synergistic-increases/1806364.html

Browse ORF cDNA clones by species Saccharomyces cerevisiae S288C, page 25Browse ORF cDNA clones by species Saccharomyces cerevisiae S288C, page 25

carbamoyl-phosphate synthase (glutamine-hydrolyzing) CPA1. protein-coding. AHP1. thioredoxin peroxidase AHP1. protein-coding. ...
more infohttps://www.genscript.com/gene/559292/saccharomyces-cerevisiae-s288c?page=25

pyrAA - Carbamoyl-phosphate synthase pyrimidine-specific small chain - Lactobacillus plantarum (strain ATCC BAA-793 / NCIMB...pyrAA - Carbamoyl-phosphate synthase pyrimidine-specific small chain - Lactobacillus plantarum (strain ATCC BAA-793 / NCIMB...

Carbamoyl-phosphate synthase pyrimidine-specific large chain (pyrAB), Carbamoyl-phosphate synthase (glutamine-hydrolyzing) ( ... carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity Source: UniProtKB-EC. View the complete GO annotation on QuickGO ... 2 ATP + L-glutamine + HCO3- + H2O = 2 ADP + phosphate + L-glutamate + carbamoyl phosphate. ... Carbamoyl-phosphate synthase pyrimidine-specific small chain (EC:6.3.5.5). Alternative name(s): ...
more infohttps://www.uniprot.org/uniprot/P77885

Lawrence T Drzal - Publications
     - MSU ScholarsLawrence T Drzal - Publications - MSU Scholars

Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) 8 Citations Non-linear numerical study of the single-fiber fragmentation ...
more infohttps://scholars.opb.msu.edu/en/persons/lawrence-t-drzal-2/publications/?page=6

pyrF protein (Pelagibaca bermudensis) - STRING interaction networkpyrF protein (Pelagibaca bermudensis) - STRING interaction network

Carbamoyl-phosphate synthase (glutamine-hydrolyzing) 0.960. R2601_11831. carA. R2601_11831. R2601_19422. Dihydropyrimidine ... Orotate phosphoribosyltransferase ; Catalyzes the transfer of a ribosyl phosphate group from 5-phosphoribose 1-diphosphate to ... Orotate phosphoribosyltransferase ; Catalyzes the transfer of a ribosyl phosphate group from 5-phosphoribose 1-diphosphate to ... Orotate phosphoribosyltransferase ; Catalyzes the transfer of a ribosyl phosphate group from 5-phosphoribose 1-diphosphate to ...
more infohttps://string-db.org/network/314265.R2601_13524

RSAG 03171 protein (Ruminococcus sp. 5139BFAA) - STRING interaction networkRSAG 03171 protein (Ruminococcus sp. 5139BFAA) - STRING interaction network

Carbamoyl-phosphate synthase (glutamine-hydrolyzing) Transcript cleavage factor GreA ; Necessary for efficient RNA polymerase ... tRNA-dihydrouridine synthase ; Catalyzes the synthesis of 5,6-dihydrouridine (D), a modified base found in the D-loop of most ... tRNA-dihydrouridine synthase ; Catalyzes the synthesis of 5,6-dihydrouridine (D), a modified base found in the D-loop of most ... tRNA-dihydrouridine synthase ; Catalyzes the synthesis of 5,6-dihydrouridine (D), a modified base found in the D-loop of most ...
more infohttps://string-db.org/network/457412.RSAG_03171

Panoply™ Human CAD Knockdown Stable Cell Line - Creative BiogenePanoply™ Human CAD Knockdown Stable Cell Line - Creative Biogene

... carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity; carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity; ...
more infohttps://www.creative-biogene.com/Panoply-Human-CAD-Knockdown-Stable-Cell-Line-CSC-DC002281-1255300-14.html

Faculty | Programs in Biomedical and Biological ScienceFaculty | Programs in Biomedical and Biological Science

Heat sensitivity and Sp1 activation of complex formation at the Syrian hamster carbamoyl-phosphate synthase (glutamine- ... hydrolyzing)/aspartate carbamoyltransferase/dihydroorotase promoter in vitro J Biol Chem. 1992 Jan 05; 267(1):385-91. . View in ...
more infohttps://keck.usc.edu/pibbs/faculty/Peggy-Farnham/

Carbamoyl phosphate synthase II - WikipediaCarbamoyl phosphate synthase II - Wikipedia

Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) at the US National Library of Medicine Medical Subject Headings (MeSH) ... glutamine) glutamine-dependent carbamyl phosphate synthetase carbamoyl phosphate synthetase CPS carbon-dioxide:L-glutamine ... Carbamoyl-phosphate synthetase (glutamine-hydrolysing) is also known as: hydrogen-carbonate:L-glutamine amido-ligase (ADP- ... Carbamoyl phosphate synthetase II (EC 6.3.5.5) is an enzyme that catalyzes the reactions that produce carbamoyl phosphate in ...
more infohttps://en.wikipedia.org/wiki/Carbamoyl_phosphate_synthase_II

Gentaur antibody-antibodies.com The Marketplace for AntibodiessGentaur antibody-antibodies.com The Marketplace for Antibodiess

GO; GO:0004088; F:carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity; IDA:BHF-UCL.. GO; GO:0004151; F:dihydroorotase ... CPS1 Gene carbamoyl-phosphate synthase 1, mitochondrial. CPSM_RAT. Rat ELISA Kit FOR Carbamoyl-phosphate synthase [ammonia], ... Rat Carbamoyl-phosphate synthase [ammonia], mitochondrial(CPS1) ELISA kit. 96T. CSB-EL005913HU. Human Carbamoyl-phosphate ... Carbamoyl-phosphate synthase [ammonia], mitochondrial,Carbamoyl-phosphate synthetase I,Cps1,CPSase I,Rat,Rattus norvegicus. ...
more infohttps://www.antibody-antibodies.com/gene.php?title_uniprot=CAD+protein+%5BIncludes%3A+Glutamine-dependent+carbamoyl-phosphate+synthase+%28EC+6.3.5.5%29%3B+Aspartate+carbamoyltransferase+%28EC+2.1.3.2%29%3B+Dihydroorotase+%28EC+3.5.2.3%29%5D&uniprot_id=P08955

NWMN 1114 - AureoWikiNWMN 1114 - AureoWiki

Carbamoyl-phosphate synthase (glutamine-hydrolyzing)2 ATP + L-glutamine + HCO3(-) + H2O = 2 ADP + phosphate + L-glutamate + ... Nucleosides and NucleotidesPyrimidinesDe Novo Pyrimidine Synthesis Carbamoyl-phosphate synthase large chain (EC 6.3.5.5) ... ATP-grasp (CL0179) CPSase_L_D2; Carbamoyl-phosphate synthase L chain, ATP binding domain (PF02786; HMM-score: 404.7) ... MetabolismPurines, pyrimidines, nucleosides, and nucleotidesPyrimidine ribonucleotide biosynthesiscarbamoyl-phosphate synthase ...
more infohttp://aureowiki.med.uni-greifswald.de/NWMN_1114

SAUSA300 1095 - AureoWikiSAUSA300 1095 - AureoWiki

Carbamoyl-phosphate synthase (glutamine-hydrolyzing)2 ATP + L-glutamine + HCO3(-) + H2O = 2 ADP + phosphate + L-glutamate + ... Carbamoyl-phosphate synthase small chain, CPSase domain (PF00988; HMM-score: 167.7) Glutaminase_I (CL0014) GATase; Glutamine ... product: carbamoyl phosphate synthase small subunit. ⊟Genome View[edit source , edit]. Meta Function Gene Functional Class ( ... Nucleosides and NucleotidesPyrimidinesDe Novo Pyrimidine Synthesis Carbamoyl-phosphate synthase small chain (EC 6.3.5.5) ...
more infohttp://aureowiki.med.uni-greifswald.de/SAUSA300_1095

List of MeSH codes (D08) - WikipediaList of MeSH codes (D08) - Wikipedia

... carbamoyl-phosphate synthase (glutamine-hydrolyzing) MeSH D08.811.464.259.550 --- formate-tetrahydrofolate ligase MeSH D08.811. ... carbamoyl-phosphate synthase (ammonia) MeSH D08.811.464.259.400 --- carbon-nitrogen ligases with glutamine as amide-n-donor ... glutamate synthase MeSH D08.811.913.477.700.500 --- glutamine-fructose-6-phosphate transaminase (isomerizing) MeSH D08.811. ... riboflavin synthase MeSH D08.811.913.225.825 --- spermidine synthase MeSH D08.811.913.225.912 --- spermine synthase MeSH ...
more infohttps://en.wikipedia.org/wiki/List_of_MeSH_codes_(D08)

1994 McArdle Publications | McArdle Laboratory for Cancer Research1994 McArdle Publications | McArdle Laboratory for Cancer Research

Start Site Selection at the TATA-less Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/Aspartate Carbamoyltransferase/ ...
more infohttps://mcardle.wisc.edu/what-we-do/research/publications/1994-mcardle-publications

Carbamoyl phosphate synthetase, large subunit connection domain superfamilyCarbamoyl phosphate synthetase, large subunit connection domain superfamily

The SCOP classification for the Carbamoyl phosphate synthetase, large subunit connection domain superfamily including the ... Carbamoyl-phosphate synthase (ammonia). Enzyme Commission (EC). Carbamoyl-phosphate synthase (glutamine-hydrolyzing). 0. 2.049 ... Carbamoyl-phosphate synthase (glutamine-hydrolyzing). 0. Highly Informative. Direct. Enzyme Commission (EC). Dihydroorotase. ... Carbamoyl-phosphate synthase (CPSase) catalyzes the ATP-dependent synthesis of carbamyl-phosphate from glutamine or ammonia and ...
more infohttp://supfam.org/SUPERFAMILY/cgi-bin/scop.cgi?sunid=48108

Carbamoyl phosphate synthetase, small subunit N-terminal domain superfamilyCarbamoyl phosphate synthetase, small subunit N-terminal domain superfamily

The SCOP classification for the Carbamoyl phosphate synthetase, small subunit N-terminal domain superfamily including the ... Carbamoyl-phosphate synthase (ammonia). Enzyme Commission (EC). Carbamoyl-phosphate synthase (glutamine-hydrolyzing). 0. 2.05. ... Carbamoyl-phosphate synthase catalyses the ATP-dependent synthesis of carbamoyl-phosphate from glutamine or ammonia and ... Carbamoyl-phosphate synthase (glutamine-hydrolyzing). 0. Highly Informative. Direct. Enzyme Commission (EC). Dihydroorotase. ...
more infohttp://supfam.org/SUPERFAMILY/cgi-bin/scop.cgi?ipid=SSF52021

Methylglyoxal synthase-like superfamilyMethylglyoxal synthase-like superfamily

The SCOP classification for the Methylglyoxal synthase-like superfamily including the families contained in it. Additional ... Carbamoyl-phosphate synthase (ammonia). Enzyme Commission (EC). Carbamoyl-phosphate synthase (glutamine-hydrolyzing). 0. 2.154 ... Carbamoyl-phosphate synthase (glutamine-hydrolyzing). 0. Highly Informative. Direct. Enzyme Commission (EC). Carbamoyl- ... carbamoyl-phosphate synthase (glutamine-hydrolyzing) activity. Molecular Function (MF). ion binding. 0.005302. 0.7738. --. ...
more infohttp://supfam.cs.bris.ac.uk/SUPERFAMILY/cgi-bin/scop.cgi?ipid=SSF52335

Welcome to LibAge, the ageing reference resourceWelcome to LibAge, the ageing reference resource

Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/genetics *Cell Aging/genetics *Cell Division *Cells, Cultured ...
more infohttp://libage.ageing-map.org/entries/tags/249/

Search Articles | University of Toronto LibrariesSearch Articles | University of Toronto Libraries

Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) - genetics , Spasms, Infantile - diagnostic imaging , Spasms, Infantile - ... MITOCHONDRIAL ATP-SYNTHASE , OXIDATIVE-PHOSPHORYLATION , HYPERTROPHIC CARDIOMYOPATHY , LEUCINE METABOLISM , PEARSON SYNDROME , ...
more infohttps://query.library.utoronto.ca/index.php/search/q?kw=Author:Wortmann,%20Saskia%20B

Regulation of carbamoylphosphate synthesis in Escherichia coli: an amazing metabolite at the crossroad of arginine and...Regulation of carbamoylphosphate synthesis in Escherichia coli: an amazing metabolite at the crossroad of arginine and...

... carbamoylphosphate (CP) is a precursor common to the synthesis of arginine and pyrimidines. In Escherichia coliand most other ... Glutamine hydrolyzing site of Escherichia coli carbamyl phosphate synthetase. J Biol Chem 261:11320-11327PubMedGoogle Scholar ... coli carbamoylphosphate synthase (pdb-1JDB) [133]. The small, carA encoded, glutamine amidotransferase subunit (magenta), and ... carbamoyl phosphate is synthesized by two carbamoyl-phosphate synthetases (CPS): carbon dioxide differentiates the arginine- ...
more infohttps://rd.springer.com/article/10.1007/s00726-018-2654-z

Genome-scale metabolic analysis of Clostridium thermocellum for bioethanol production | BMC Systems Biology | Full TextGenome-scale metabolic analysis of Clostridium thermocellum for bioethanol production | BMC Systems Biology | Full Text

... a small glutamine-hydrolyzing chain and a large chain that synthesizes carbamoyl phosphate. We found two C. thermocellum genes ... "carbamoyl-phosphate synthase, small subunit" (Cthe_1867, Cthe_0950) and two genes annotated as "carbamoyl-phosphate synthase, ... As a specific example of this process, consider the reaction corresponding to carbamoyl-phosphate synthase (R_CBPS), EC 6.3. ... For the purpose of this study, it was assumed that one ATP molecule must be hydrolyzed to ADP and inorganic phosphate to build ...
more infohttps://bmcsystbiol.biomedcentral.com/articles/10.1186/1752-0509-4-31