The aim of the study was to assess if mechanisms of glucose trafficking by red blood cells (RBCs) relates to species specific extracellular glucose levels. Atlantic cod (Gadus morhua), Atlantic salmon (Salmo salar), cunner (Tautogolabrus adspersus), and short-horned sculpin (Myoxocephalus scorpius) had plasma glucose levels of 4 mmol l-1, 4.1 mmol l-1, 1.95 mmol l-1, and 0.73 mmol l-1, respectively. Glucose uptake by isolated RBCs was measured by the initial incorporation of [6-14C]-glucose and steady state glucose metabolism was determined by the production of 3H2O from [2-3H]-glucose. Saturation kinetics of glucose uptake and inhibition of both glucose uptake and metabolism by cytochalasin B and phloretin revealed that Atlantic cod, cunner, and sculpin RBCs all had a facilitated transport component to glucose trafficking. RBCs from Atlantic salmon showed a linear relationship between glucose uptake and extracellular glucose level but exhibited clear inhibition of glucose metabolism by ...
Author: Gylfe, E. et al.; Genre: Journal Article; Published in Print: 1993-08; Title: Triphasic changes of cytoplasmic CA2+ associated with early glucose effects on beta-cell membrane potential.
Glucose is not detectable in airways secretions of normoglycaemic volunteers, but is present at 1-9 mmol·l-1 in airways secretions from people with hyperglycaemia. These observations suggest the existence of a blood glucose threshold at which glucose appears in airways secretions, similar to that seen in renal and salivary epithelia. In the present study we determined the blood glucose threshold at which glucose appears in nasal secretions. Blood glucose concentrations were raised in healthy human volunteers by 20% dextrose intravenous infusion or 75 g oral glucose load. Nasal glucose concentrations were measured using modified glucose oxidase sticks as blood glucose concentrations were raised. Glucose appeared rapidly in nasal secretions once blood glucose was clamped at approx. 12 mmol·l-1 (n=6). On removal of the clamp, nasal glucose fell to baseline levels in parallel with blood glucose concentrations. An airway glucose threshold of 6.7-9.7 mmol·l-1 was identified (n=12). In six subjects ...
1. The effects of glucose on insulin secretion and Rb-86 efflux from isolated rat islets were studied at six different times during a 24-h period (00.00, 04.00, 08.00, 12.00, 16.00 and 20.00 h), 2. In the absence of glucose and in the presence of substimulatory concentrations (2.8 mmol/L) of the sugar, insulin secretion did not vary with the time of day. At a glucose concentration of 5.6 mmol/L the stimulated insulin secretion was greater than basal levels only at 20.00 h, 3. At a higher sugar concentration (8.3 mmol/L) the increase in insulin secretion and the reduction in Rb-86 efflux rate were more marked during the dark period. No effect of the time of day on insulin secretion was observed at glucose concentrations above 8.3 mmol/L (except in 27.7 mmol/L), 4. The time of day appears to affect insulin secretion mainly at glucose concentrations close to physiological values (5.6-8.3 mmol/L), 5. This result agrees with the ability of physiological amounts of glucose to alter the ...
Our previous studies demonstrated that high glucose-induced apoptosis in human umbilical vein endothelial cells (HUVECs) is mediated by sequential activation of c-Jun N-terminal kinase (JNK) and caspase, and prevented by exogenous nitric oxide (NO). In this study we further elucidated the roles of t …
Insulin secretion from pancreatic beta cells is stimulated by glucose metabolism. However, the relative importance of metabolizing glucose via mitochondrial oxidative phosphorylation versus glycolysis for insulin secretion remains unclear. von Hippel-Lindau (VHL) tumor suppressor protein, pVHL, negatively regulates hypoxia-inducible factor HIF1alpha, a transcription factor implicated in promoting a glycolytic form of metabolism. Here we report a central role for the pVHL-HIF1alpha pathway in the control of beta-cell glucose utilization, insulin secretion, and glucose homeostasis. Conditional inactivation of Vhlh in beta cells promoted a diversion of glucose away from mitochondria into lactate production, causing cells to produce high levels of glycolytically derived ATP and to secrete elevated levels of insulin at low glucose concentrations. Vhlh-deficient mice exhibited diminished glucose-stimulated changes in cytoplasmic Ca(2+) concentration, electrical activity, and insulin secretion, which culminate
Transcription of the yeast HXT2 and HXT4 genes, which encode glucose transporters, is induced only by low levels of glucose. This low-glucose-induced expression is mediated by two independent repression mechanisms: in the absence of glucose, transcription of both genes is prevented by Rgt1p, a C6 zinc cluster protein; at high levels of glucose, expression of HXT2 and HXT4 is repressed by Mig1p. Only at low glucose concentrations are both repressors inactive, leading to a 10- to 20-fold induction of gene expression. Mig1p and Rgt1p act directly on HXT2 and HXT4 by binding to their promoters. This transcriptional regulation is physiologically very important to the yeast cell because it causes these glucose transporters to be expressed only in low-glucose media, in which they are required for growth. ...
Effect of glucose treatment on basal and FSH- or IGF-1-stimulated progesterone and oestradiol secretions by rat granulosa cells. Granulosa cells from immature r
In diabetic patients, glucose does not enter the cells sufficiently, thus staying in the blood and creating high blood sugar levels. All rights reserved. Insulin is a hormone made by the pancreas, an organ near the stomach. Glucose comes from most foods, and the body uses other chemicals to create glucose in the liver and muscles. The danger of continuously high blood glucose or hyperglycemia is that sugar coats the high glucose level in blood red blood cells, causing them to become stiff and sticky. You should know Answers to your question are meant to provide general health information but should not replace medical advice you receive from how to treat a fatty liver naturally a doctor. You probably want to keep a close eye on your diet and excercise regimen and test your blood sugar often high glucose level in blood just to be sure. Hyperglycemia, or high blood glucose levels, may be due to diabetes, medications, stress, illness, hyperthyroidism, Cushing syndrome, pancreatitis or ...
In this study we studied two aspects of enterochromaffin cell function; the nature of both the acute and chronic response to increased glucose availability. We demonstrate using intact tissue preparations and single cell approaches that acute increases in glucose, at levels found in the gut lumen rather than in plasma, trigger Ca2+ entry and 5-HT secretion in EC cells. Furthermore, this increased 5-HT release occurs through an increase in the amount of 5-HT released from vesicles in each exocytosis event. The effects of a more chronic exposure to high glucose, this time at levels akin to those observed in plasma post-prandially, cause a reduction in the synthesis and release of EC cell 5-HT. Thus EC cells respond in a diverse manner to different glucose concentrations over different periods of time to either increase or suppress 5-HT output.. Our data in intact colon tissue is the first ex vivo demonstration that EC cells are glucose-sensing cells. This is in agreement with earlier findings in ...
TY - JOUR. T1 - High-density lipoprotein delivered after myocardial infarction increases cardiac glucose uptake and function in mice. AU - Heywood, Sarah E.. AU - Richart, Adele L.. AU - Henstridge, Darren C.. AU - Alt, Karen. AU - Kiriazis, Helen. AU - Zammit, Claire. AU - Carey, Andrew L.. AU - Kammoun, Helene L.. AU - Delbridge, Lea M.. AU - Reddy, Medini. AU - Chen, Yi Ching. AU - Du, Xiao Jun. AU - Hagemeyer, Christoph E.. AU - Febbraio, Mark A.. AU - Siebel, Andrew L.. AU - Kingwell, Bronwyn A.. PY - 2017/10/11. Y1 - 2017/10/11. N2 - Protecting the heart after an acute coronary syndrome is a key therapeutic goal to support cardiac recovery and prevent progression to heart failure. A potential strategy is to target cardiac glucose metabolism at the early stages after ischemia when glycolysis is critical for myocyte survival. Building on our discovery that high-density lipoprotein (HDL) modulates skeletal muscle glucose metabolism, we now demonstrate that a single dose of reconstituted HDL ...
The addition of glucose to tps1Δ cells of the yeast S. cerevisiae causes hyperaccumulation of all glycolytic metabolites upstream and depletion of all metabolites downstream of GAPDH, suggesting that the deletion of Tps1 in some way creates a bottleneck in glycolysis at the level of GAPDH (27). Measurements of the specific activity of the glycolytic enzymes in cell extracts as well as determination of initial glucose uptake rates did not reveal significant differences between the wild-type and tps1 strains that could explain the glycolytic bottleneck in tps1Δ cells (1, 11). More detailed measurements of the glucose uptake rate and the pH dependency of GAPDH in the present work have underscored the conclusion that there is no difference in the inherent activity of these two crucial components in the tps1Δ strain. Hence, the bottleneck appears to be due to a metabolic or regulatory problem at the level of GAPDH that is not maintained in cell extracts and is not apparent from the Vmax or Km of ...
To examine the mechanism by which free fatty acids (FFA) induce insulin resistance in human skeletal muscle, glycogen, glucose-6-phosphate, and intracellular glucose concentrations were measured using carbon-13 and phosphorous-31 nuclear magnetic resonance spectroscopy in seven healthy subjects before and after a hyperinsulinemic-euglycemic clamp following a five-hour infusion of either lipid/heparin or glycerol/heparin. IRS-1-associated phosphatidylinositol 3-kinase (PI 3-kinase) activity was also measured in muscle biopsy samples obtained from seven additional subjects before and after an identical protocol. Rates of insulin stimulated whole-body glucose uptake. Glucose oxidation and muscle glycogen synthesis were 50%-60% lower following the lipid infusion compared with the glycerol infusion and were associated with a ∼90% decrease in the increment in intramuscular glucose-6-phosphate concentration, implying diminished glucose transport or phosphorylation activity. To distinguish between ...
We studied regional cerebral glucose metabolism in 15 patients with a clinical diagnosis of corticobasal degeneration (CBD), 15 patients with probable Alzheimers disease (AD), and 15 healthy controls
Cancer cells increase glucose metabolism to support aerobic glycolysis. However, only some cancer cells are acutely sensitive to glucose withdrawal, and the underlying mechanism of this selective sensitivity is unclear. We showed that glucose deprivation initiates a cell death pathway in cancer cells that is dependent on the kinase RIPK1. Glucose withdrawal triggered rapid plasma membrane depolarization and an influx of extracellular calcium into the cell through the L-type calcium channel Cav1.3 (CACNA1D), followed by activation of the kinase CAMK1. CAMK1 and the demethylase PPME1 were required for the subsequent demethylation and inactivation of the catalytic subunit of the phosphatase PP2A (PP2Ac) and the phosphorylation of RIPK1. Plasma membrane depolarization, PP2Ac demethylation, and cell death were prevented by glucose and, unexpectedly, by its nonmetabolizable analog 2-deoxy-d-glucose (2-DG), a glycolytic inhibitor. These findings reveal a previously unknown function of glucose as a ...
The role of splanchnic glucose uptake (SGU) after oral glucose administration as a potential factor contributing to postprandial hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM) has not been established conclusively. Therefore, we investigated SGU in six patients with NIDDM and six w …
Liver glucose metabolism plays a central role in glucose homeostasis and may also regulate feeding and energy expenditure. Here we assessed the impact of glucose transporter 2 (Glut2) gene inactivation in adult mouse liver (LG2KO mice). Loss of Glut2 suppressed hepatic glucose uptake but not glucose output. In the fasted state, expression of carbohydrate-responsive element-binding protein (ChREBP) and its glycolytic and lipogenic target genes was abnormally elevated. Feeding, energy expenditure, and insulin sensitivity were identical in LG2KO and control mice. Glucose tolerance was initially normal after Glut2 inactivation, but LG2KO mice exhibited progressive impairment of glucose-stimulated insulin secretion even though β cell mass and insulin content remained normal. Liver transcript profiling revealed a coordinated downregulation of cholesterol biosynthesis genes in LG2KO mice that was associated with reduced hepatic cholesterol in fasted mice and reduced bile acids (BAs) in feces, with a similar
Objective: To investigate the effect and mechanism of CTRP13 on hepatic sinusoidal capillarization induced by high glucose in rat liver sinusoidal endothelial cells (rLSECs).Results: CTRP13 was reduced in high glucose-treated rLSECs. High glucose increased LN and CAV-1 expression and inhibited CaMKKβ and AMPK phosphorylation. CTRP13 overexpression protected rLSECs against high glucose-induced increase of LN and CAV-1 expression. Moreover, CTRP13 overexpression increased high glucose-induced inhibition of CaMKKβ and AMPK activation in CTRP13-overexpressing rLSECs. Inhibition of CaMKKβ and AMPK disturbed the protective effects of CTRP13 in high glucose-induced increase of LN and CAV-1. Hepatic steatosis was enhanced and basement membrane was thickened in liver of diabetic fatty liver rats.Conclusions: Our data identified the protective role of CTRP13 in hepatic sinusoidal capillarization induced by high glucose via activating CAMKKβ/AMPK pathway. CTRP13 may be a potential target
Any approach to management needs to account for the overall metabolic and physiologic status of the infant and should not unnecessarily disrupt the mother-infant relationship and breastfeeding. The definition of a plasma glucose concentration at which intervention is indicated needs to be tailored to the clinical situation and the particular characteristics of a given infant. For example, further investigation and immediate intravenous glucose treatment might be instituted for an infant with clinical signs and a plasma glucose concentration of less than 40 mg/dL, whereas an at-risk but asymptomatic term formula-fed infant may only require an increased frequency of feeding and would receive intravenous glucose only if the glucose values decreased to less than 25 mg/dL (birth to 4 hours of age) or 35 mg/dL (4-24 hours of age).32 Follow-up glucose concentrations and clinical evaluation must always be obtained to ensure that postnatal glucose homeostasis is achieved and maintained.. Because severe, ...
In the present study, we have confirmed the findings of previous investigations demonstrating that, in the insulin-resistant, hyperinsulinemic, and dyslipidemic obese Zucker rat, exercise training by treadmill running (2, 3, 6, 9, 13, 19, 37) or chronic administration of the ACE inhibitor trandolapril (20) results in significant improvements in whole body insulin action on peripheral disposal of a glucose load and in insulin action on skeletal muscle glucose transport activity. Moreover, we have shown that these increases in insulin action on skeletal muscle glucose transport were associated with upregulation of the GLUT-4 glucose transporter isoform (2, 6, 13, 20) and in total hexokinase (19, 20, 32). More importantly, we have demonstrated for the first time that greater improvements in whole body glucose tolerance and insulin-stimulated muscle glucose transport activity in the obese Zucker rat could be achieved through the combination of exercise training and trandolapril treatment than with ...
TY - JOUR. T1 - Effect of alcohol and glucose infusion on pituitary-gonadal hormones in normal females. AU - Becker, Ulrik. AU - Gluud, Christian. AU - Bennett, Paul. AU - Micic, Snezana. AU - Svenstrup, Birgit. AU - Winkler, Kjeld. AU - Christensen, Niels Juel. AU - Hardt, Finn. PY - 1988/1/1. Y1 - 1988/1/1. N2 - During 1 h, median 976 mmol ethanol in 5.5% glucose was administered i.v. to six healthy female volunteers (aged 26-37 years) in the luteal phase of the menstrual cycle. The median maximal blood ethanol concentration was median 33.5 mmol/1 and serum ethanol concentrations of 2 mmol/1 were reached after 8 h. Four of the women participated in a control experiment with infusion of an equal volume of glucose 5.5%. Venous blood samples were drawn 5 times during the 24-h follow up period. Serum concentrations of sex steroids and pituitary hormones decreased in both ethanol and control experiments and the results did not differ significantly. The lowest hormone concentrations were observed ...
Figure: High levels of glucose alter VEGF and miR-200b expression in HRMECs. A: HRMECs exposed to various concentrations of D-glucose for 24 hours exhibited differential mRNA levels of VEGF. Compared to 5mM D-glucose, VEGF expression was significantly increased at 15mM and 25mM D-glucose concentrations, with no change at 20mM L-glucose. B: Measured by WST-1 assay, HRMECs exposed to increasing concentrations of D-glucose for 24 hours exhibited decreased cell viability at 25mM, 50mM and 100mM compared to 5mM. C: HRMECs exposed to 25mM (high glucose; HG) glucose for 24 and 48 hours demonstrated significantly increased VEGF mRNA compared to 5mM (normal glucose; NG). These differences were not observed at time points earlier than 24 hours. D,E: HRMECs exposed to 5mM D-glucose (NG) 25mM D-glucose (HG) and 20mM L-glucose+5mM D-glucose (osmotic control; OSM). HRMECs cultured for 24 hours and 48 hours in HG showed significantly decreased levels of miR-200b with parallel increased levels of VEGF ...
Anticoagulant Citrate Dextrose Solution Formula B information about active ingredients, pharmaceutical forms and doses by Baxter, Anticoagulant Citrate Dextrose Solution Formula B indications, usages and related health products lists
Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia and disturbed metabolism of carbohydrates, fats and proteins that occurs due damaged insulin secretion or disorder in insulin signal pathways. Liver has the essential role in maintenance adequate glucose concentration in blood. Glucose metabolism in liver is regulated by hormones which effect enzyme activity or enzyme synthesis. Depending on the metabolic needs, glycolysis and gluconeogenesis are exchanged. Regulating the essential enzymes of these processes is important to maintain glucose concentration within reference range. In diabetes mellitus, gluconeogenesis and glycogenolysis in liver cells are increased. On the other hand, activity of glycolytic and glycogenesis enzymes is decreased. The aim of this study was to examine the rate of glycolysis in tumor HepG2 cells in hyperglycemic conditions. HepG2 cells were treated with four different glucose concentrations (5 mM, 20 mM, 30 mM and 50 mM) and such treated ...
This study presents a novel finding that rosiglitazone therapy enhances myocardial glucose uptake in ischemic and nonischemic regions in addition to its positive effects on whole-body insulin sensitivity and on glycemic control in type 2 diabetic patients with CAD. Moreover, myocardial glucose uptake is associated with whole-body insulin sensitivity, suggesting a direct relationship between myocardial insulin sensitivity and the capacity of whole-body glucose disposal in these patients.. Although glucose is considered to be important for metabolism in ischemic myocardium, most human studies until now have evaluated myocardial glucose uptake in regions of normal perfusion and wall motion (5,7,10). In a study with intracoronary insulin infusions and the measurement of arterial-coronary sinus glucose balance, cardiac glucose uptake was similar in type 2 diabetic patients with and without CAD (8). This is in agreement with our previous studies with PET and FDG (5,6). Some other studies have ...
The Buoyancy module is key to both the Degradation and the Aggregation systems. Buoyancy is required to position our bacteria in the water column, and also to enable them to buoy the plastic aggregates. This module requires driving the expression of a gas vesicle gene cluster. Gas vesicles are formed within the cell, and are hollow spaces surrounded by a wall of hydrophobic protein. These gas vesicles are permeable to gases, which diffuse into the gas vesicles, increasing its partial pressure, thereby increasing buoyancy. The Buoyancy system is subject to the control of a glucose-repressible promoter, cstA (BBa_K118011). During carbon starvation, ATP is transformed into cAMP and then it binds the cAMP receptor protein, this complex activates the cstA promoter. Studies suggest that cstA promoter can be used to induce the expression of reporter genes in cultures with different glucose concentrations (Schultz and Matin, 1990). Free glucose concentration varies in the upper 300 m of the seawater ...
The Buoyancy module is key to both the Degradation and the Aggregation systems. Buoyancy is required to position our bacteria in the water column, and also to enable them to buoy the plastic aggregates. This module requires driving the expression of a gas vesicle gene cluster. Gas vesicles are formed within the cell, and are hollow spaces surrounded by a wall of hydrophobic protein. These gas vesicles are permeable to gases, which diffuse into the gas vesicles, increasing its partial pressure, thereby increasing buoyancy. The Buoyancy system is subject to the control of a glucose-repressible promoter, cstA (BBa_K118011). During carbon starvation, ATP is transformed into cAMP and then it binds the cAMP receptor protein, this complex activates the cstA promoter. Studies suggest that cstA promoter can be used to induce the expression of reporter genes in cultures with different glucose concentrations (Schultz and Matin, 1990). Free glucose concentration varies in the upper 300 m of the seawater ...
Under the severe glucose limitation at the low dilution rate used here, substantial fluxes through the PEP-glyoxylate cycle were expected (12, 25, 35). The precise regulation mechanism that effectively controlled this major flux rerouting from the TCA cycle to the PEP-glyoxylate cycle, however, was unclear. Based on in vivo flux and in vitro enzyme data on global regulator mutants, we demonstrate that PEP-glyoxylate cycle activity is strongly controlled by induction through the cAMP-CRP complex under the conditions applied. This finding is consistent with the reported increased mRNA and protein levels of PEP carboxykinase and glyoxylate shunt enzymes at a dilution rate of 0.1 h−1, relative to higher growth rates (25). Thus, growth rate-dependent PEP-glyoxylate cycle fluxes under glucose limitation (35) are apparently controlled by the intracellular cAMP level, which is elevated at dilution rates below 0.1 h−1 (32, 37). Strain-dependent differences in fluxes through the PEP-glyoxylate cycle ...
An increase in circulating levels of specific NEFAs (non-esterified fatty acids) has been implicated in the pathogenesis of insulin resistance and impaired glucose disposal in skeletal muscle. In particular, elevation of SFAs (saturated fatty acids), such as palmitate, has been correlated with reduced insulin sensitivity, whereas an increase in certain MUFAs and PUFAs (mono- and poly-unsaturated fatty acids respectively) has been suggested to improve glycaemic control, although the underlying mechanisms remain unclear. In the present study, we compare the effects of palmitoleate (a MUFA) and palmitate (a SFA) on insulin action and glucose utilization in rat L6 skeletal muscle cells. Basal glucose uptake was enhanced approx. 2-fold following treatment of cells with palmitoleate. The MUFA-induced increase in glucose transport led to an associated rise in glucose oxidation and glycogen synthesis, which could not be attributed to activation of signalling proteins normally modulated by stimuli such ...
Accu Chek Active Glucose Monitor Accu-Chek Active Glucose Monitor for your routine blood sugar testing device. A handy glucose monitoring device for at home or anywhere else. Pre-meal and post-meal flagging of glucose levels make it easy to differentiate from other results at Elawoman.com
In skeletal muscle, separate and distinct signaling pathways can activate glucose transport. Insulin increases glucose transport via activation of PI 3-kinase (13,14) and possibly via activation of the CAP/TC10 pathway (32,33). However, the latter pathway has not been validated in skeletal muscle. Exercise (34), muscle contraction (35,36), and hypoxia (28,37) increase glucose transport via insulin-independent pathways (13-15), presumably via activation of AMPK (17,18). In type 2 diabetic patients, defects in insulin-mediated whole-body glucose uptake are coupled to impairments in glucose transport in skeletal muscle (4,10), which arise from aberrant signal transduction at the level of insulin receptor substrate-1, PI 3-kinase (6,8,9), and GLUT4 translocation (10,38). Since muscle contraction and hypoxia increase glucose transport via an alternative mechanism that bypasses defective insulin signaling (37,39,40), strategies to identify and characterize components of this insulin-independent ...
antibody-antibodies.com is the marketplace for research antibodies. Find the right antibody for your research needs. Lysosomal Ca2+ Signaling Regulates High Glucose-Mediated Interleukin-1β Secretion via Transcription Factor EB in Human Monocytic Cells.
The development of novel small molecule inhibitors of the cancer-associated tropomyosin 3.1 (Tpm3.1) provides the ability to examine the metabolic function of specific actin filament populations. We have determined the ability of these anti-Tpm (ATM) compounds to regulate glucose metabolism in mice. Acute treatment (1 h) of wild-type (WT) mice with the compounds (TR100 and ATM1001) led to a decrease in glucose clearance due mainly to suppression of glucose-stimulated insulin secretion (GSIS) from the pancreatic islets. The impact of the drugs on GSIS was significantly less in Tpm3.1 knock out (KO) mice indicating that the drug action is on-target. Experiments in MIN6 beta-cells indicated that the inhibition of GSIS by the drugs was due to disruption to the cortical actin cytoskeleton. The impact of the drugs on insulin-stimulated glucose uptake (ISGU) was also examined in skeletal muscle ex vivo. In the absence of drug, ISGU was decreased in KO compared to WT muscle, confirming a role of Tpm3.1 in
Glucose transporters are a wide group of membrane proteins that facilitate the transport of glucose over a plasma membrane. Because glucose is a vital source of energy for all life, these transporters are present in all phyla. The GLUT or SLC2A family are a protein family that is found in most mammalian cells. 14 GLUTS are encoded by human genome. GLUT is a type of uniporter transporter protein. Most non-autotrophic cells are unable to produce free glucose because they lack expression of glucose-6-phosphatase and, thus, are involved only in glucose uptake and catabolism. Usually produced only in hepatocytes, in fasting conditions other tissues such as the intestines, muscles, brain, and kidneys are able to produce glucose following activation of gluconeogenesis. In Saccharomyces cerevisiae glucose transport takes place through facilitated diffusion. The transport proteins are mainly from the Hxt family, but many other transporters have been identified. GLUTs are integral membrane proteins that ...
Catabolite repression was extensively studied in Escherichia coli. E. coli grows faster on glucose than on any other carbon source. For example, if E. coli is placed on an agar plate containing only glucose and lactose, the bacteria will use glucose first and lactose second. When glucose is available in the environment, the synthesis of β-galactosidase is under repression due to the effect of catabolite repression caused by glucose. The catabolite repression in this case is achieved through the utilization of phosphotransferase system. An important enzyme from the phosphotransferase system called Enzyme II A (EIIA) plays a central role in this mechanism. There are different catabolite-specific EIIA in a single cell, even though different bacterial groups have specificities to different sets of catabolites. In enteric bacteria one of the EIIA enzymes in their set is specific for glucose transport only. When glucose levels are high inside the bacteria, EIIA mostly exists in its unphosphorylated ...
S. cerevisiae has membrane proteins that act as glucose receptors. Glucose binds to these receptors and generates an intracellular signal. In the Rgt2/Snf3 pathway, these two proteins act as glucose receptors. The Rgt2 and Snf3 proteins resemble hexose transporters in structure but have long cytoplasmic tails that are required for signal transduction [7]. Glucose binding to these transmembrane proteins initiates signals that activate a pathway that allows hexose transporter gene expression by repressing Rgt1 function [8].. An additional pathway that involves transcriptional changes in response to glucose is the stimulation of adenylyl cyclase and the increase in intracellular cyclic AMP. This pathway includes a G-protein coupled receptor (Gpr1) and two G proteins Gpa1 and 2, necessary for the glucose-specific increase in cAMP [9,10]. Finally, glucose activation of adenylyl cyclase leads to activation of the cAMP-dependent protein kinase A (PKA). Upon activation of PKA by cAMP the Rap1 ...
Type 2 diabetes is characterized by hyperglycemia due to insulin resistance in the target tissue and insufficient insulin secretion from the beta cells. Finding new mechanisms and pathways involved in the regulation of insulin secretion from the pancreatic beta cells is of great importance. Our group has earlier found, miRNA-212 and miRNA-132 to be upregulated in the non-obese type 2 diabetic GK rat. We hypothesize that the upregulation of these miRNAs is caused by a misregulation of the presumptive promoter of this miRNA-212/132 cluster. In this thesis I have therefore investigated mechanisms involved in transcriptional regulation of the miRNA-212/132-cluster and their regulation of insulin secre-tion in the pancreatic beta cell through their target proteins.. The studies were performed in INS1 832/13 cells and primary rat and human pancreatic islets. Cells were incubatedat different glucose concentrations in the absence or prescence of cAMP-stimulation using GLP-1 or a combinationof forskolin ...
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 ...
Cerebral metabolic rate for glucose (CMRG) was measured using the 14C-deoxyglucose technique in a stroke model of the gerbil produced by bilateral common carotid artery occlusion. During 30 minutes of ischemia, 14C-deoxyglucose uptake in the brain was increased along the border zone between the ischemic and nonischemic area and decreased in the ischemic areas. During the early stage of reperfusion (2 or 3 to 30 minutes), CMRG increased 50 to 150% in the cerebral cortex, caudoputamen and thalamus and 270 to 320% in the hippocampus, globus pallidus and amygdala. During the late stage of reperfusion (15 to 45 minutes), heterogeneity of CMRG appeared in the cerebral cortex, caudoputamen and thalamus. CMRG decreased to less than 50% of the control value in the cerebral cortex but remained at 200 to 300% of control in the hippocampus, globus pallidus and amygdala. The latter structures exhibited a larger and more protracted increase in glucose metabolism than the other structures most probably due to ...
TY - JOUR. T1 - Radiopharmaceuticals based on the glucose derivatives for tumor diagnosis. AU - Zeltchan, R. V.. AU - Medvedeva, A. A.. AU - Sinilkin, I. G.. AU - Bragina, O. V.. AU - Chernov, V. J.. PY - 2018. Y1 - 2018. N2 - The purpose of the study was to review available literature on the effcacy of radiopharmaceuticals based on glucose derivatives labeled with radioactive isotopes for detection of various cancers. material and methods. A systematic literature review was performed using the Scopus, Web of Science, MedLine, Cochrane Library, EMBASE, and Global Health databases from 2000 to 2016. Out of 900 papers in the feld of nuclear medicine, 58 were included into the review. results. 18F-fluoro-2-deoxy-D-glucose (18F-FDG) has been approved to be a powerful imaging tool for the detection of various cancers as well as for the assessment of tumor extent and therapy response. There is a continuous search for new more specifc and effective radiopharmaceuticals for visualization of tumor ...
TY - JOUR. T1 - Serum glucose. T2 - Effects on tumor and normal tissue accumulation of 2-[F-18]-fluoro-2-deoxy-D-glucose in rodents with mammary carcinoma. AU - Wahl, Richard L.. AU - Henry, Christine A.. AU - Ethier, Stephen P.. PY - 1992/6. Y1 - 1992/6. N2 - The positron-emitter-labeled glucose analogue 2-[fluorine-18]-fluoro-2-deoxy-D-glucose (FDG) accumulates into many cancers after intravenous injection, but the effect of serum glucose levels on FDG uptake in the tumor has not been extensively studied. In vitro, elevated media glucose levels markedly diminished FDG and FDG 6-phosphate uptake and retention in human adenocarcinoma cells, while insulin had no effect. Mammary cancers were established subcutaneously in 12 rats. Six control rats with mammary tumors were fasted overnight. Hyperglycemia was established in six rats by means of continuous glucose infusion (glucose clamp). All animals were then intravenously administered 50 μCi of FDG. Serum glucose levels were 87 mg/dL (4.83 mmol/L) ...
In their 2011 paper, Cunnane and colleagues review the literature on brain glucose metabolism studies in Alzheimers Type Dementia. One of the key concepts in understanding brain glucose metabolism is the cerebral metabolic rate of glucose. This was calculated by comparing the glucose content of cerebral arterial and cerebral venous blood. When this difference is…
The EU funded project CLINICIP (Closed Loop Insulin Infusion for Critically Ill Patients) aims to develop a low-risk monitoring and control device which allows maintaining metabolic control in intensive care units. A system will be developed comprising three subsystems: a body interface for the delivery of biofluids, biosensors for the determination of glucose concentration in these biofluids and an adaptive control algorithm that generates advice and thus represents a decision support system with respect to insulin infusion rate to establish glycaemic control in critically ill patients. Within a closed loop system, intensified insulin treatment will make use of the calculations leading to external regulation of glucose.. It is the aim of this study to evaluate the correlation between arterial blood glucose concentrations and interstitial fluid glucose concentrations in post surgery patients in the Intensive Care Unit (ICU). Interstitial fluid glucose concentrations are based on microdialysis in ...
Livers role in glucose production. The liver plays an important role in gluconeogenesis the production of glucose (from non-sugar source) in response to need, as when you fast. It keeps glucose levels in balance increasing the levels when needed and turning off that spigot when you eat and the levels of glucose increase.. Ninety percent of endogenous (within the body) glucose production is in the liver, said Louet. He and his colleagues showed that mice that lack SRC-1 have hypoglycemia (too little sugar in their blood) when they have just eaten and when they are fasting.. Without SRC-1, glucose production is impaired in the animals, he said. When he and his colleagues restored the SRC-1 to the liver tissues in the animal, glucose levels in the blood became normal.. In collaboration with members of the laboratory of Dr. Christopher B. Newgard (another senior author of the report) at Duke, the team used metabolomics to see what was happening in the tissue and blood from the mice that ...
Several previous studies have examined the role of muscle glucose transport in whole body glucose homeostasis using genetically engineered mice with whole body GLUT4 disruption and have shown conflicting results (19-22). Katz and colleagues (19) have shown that mice with homozygous disruption of whole body GLUT4 have normal fasting plasma glucose and insulin concentrations (at 2-4 months of age). Similarly, Rossetti and colleagues (20) have shown that mice with heterozygous disruption of whole body GLUT4 (at 4-5 months of age) have normal plasma glucose concentration despite a significant decrease in insulin-stimulated muscle glucose transport. In contrast, Stenbit and colleagues (21) found that mice with heterozygous disruption of whole body GLUT4 develop a diabetes phenotype (e.g., hyperglycemia) associated with decreases in insulin-stimulated glucose transport in skeletal muscle. The reason for this discrepancy is unclear but may be due to a difference in the age of mice. In this regard, ...
Background Elevated glucose transporter 1 (GLUT1) expression and glucose utilization that come with pressure overload\induced hypertrophy (POH) are thought to be cardioprotective. mRNA appearance of oxidative phosphorylation (OXPHOS) genes had been low in Cont mice, but had been maintained in collaboration with elevated glucose usage in G1HA pursuing TAC. Despite attenuated undesirable redecorating in G1HA in accordance with control TAC mice, cardiac hypertrophy was exacerbated in these mice, and positive dP/dt (in vivo) and cardiac power (ex girlfriend or boyfriend vivo) had been equivalently reduced in Cont and G1HA TAC mice in comparison to shams, in keeping with still left ventricular dysfunction. O\GlcNAcylation of Ca2+ bicycling proteins was elevated in G1HA TAC hearts. Conclusions Brief\term cardiac particular induction of GLUT1 on the starting point of POH preserves mitochondrial function and attenuates pathological redecorating, but exacerbates the hypertrophic phenotype and it is ...
Yeast cells cultivated in glucose-rich medium showed Golgi-specific localization of the PtdIns(4)P-specific probe FAPP1-PH-GFP (Fig. 4 F). In glucose-deprived cells, FAPP1-PH-GFP staining at Golgi structures was decreased, and this probe showed mainly diffuse cytosolic distribution with some accumulation at perinuclear ER regions (Fig. 4 F and Fig. S2 D). Similar localization of FAPP1-PH-GFP was observed in late log cells (Fig. S2 D). A sac1Δ strain showed accumulation of PtdIns(4)P at the ER, but also at other cellular membranes (Roy and Levine, 2004; Tahirovic et al., 2005). Golgi-localized PtdIns(4)P persisted in glucose-deprived sac1Δ cells (Fig. S2 D), which suggests that Sac1p contributes to the controlling of Golgi PtdIns(4)P in response to growth conditions. Because the total cellular levels of PtdIns(4)P decreased significantly in late log phase (Fig. 4 G), the increase in ER-localized PtdIns(4)P probably occurred at the expense of the Golgi pool of this lipid. This difference in ...
Im glad you asked. There are so many people, blogs, sites and books out there now with a sugar-free label. Despite that label, you may often find the following sugars in the recipes: Agave nectar, honey, brown rice syrup, glucose syrup, dextrose powder. Read about agave nectar here (to be honest, I fail to see this product as being healthy for anyone) and read about honey here (depends if you are overweight, diabetic or neither, but generally avoid it).. When it comes to brown rice syrup (also known as rice malt syrup or rice syrup), glucose syrup (also know as liquid glucose) and dextrose powder, these are all broken down to 100% glucose in our bodies. Glucose can processed by every cell in our body and is the brains main source of energy. So, not all sugar is evil, we do need some (our brains main source of energy is glucose). You just need to withdraw from your fructose addiction first before starting to swap to glucose. And even then, everything in moderation! Glucose does raise your ...
Im glad you asked. There are so many people, blogs, sites and books out there now with a sugar-free label. Despite that label, you may often find the following sugars in the recipes: Agave nectar, honey, brown rice syrup, glucose syrup, dextrose powder. Read about agave nectar here (to be honest, I fail to see this product as being healthy for anyone) and read about honey here (depends if you are overweight, diabetic or neither, but generally avoid it).. When it comes to brown rice syrup (also known as rice malt syrup or rice syrup), glucose syrup (also know as liquid glucose) and dextrose powder, these are all broken down to 100% glucose in our bodies. Glucose can processed by every cell in our body and is the brains main source of energy. So, not all sugar is evil, we do need some (our brains main source of energy is glucose). You just need to withdraw from your fructose addiction first before starting to swap to glucose. And even then, everything in moderation! Glucose does raise your ...
TY - JOUR. T1 - Glucose phosphorylation as a barrier to muscle glucose uptake. AU - Fueger, Patrick T.. PY - 2005/4. Y1 - 2005/4. N2 - 1. Glucose phosphorylation is the first irreversible step of the muscle glucose uptake pathway and is catalysed by a hexokinase isozyme. 2. While glucose transport is the primary barrier to muscle glucose uptake during basal conditions, glucose phosphorylation becomes an important barrier to muscle glucose uptake during stimulated conditions such as hyperinsulinaemia or exercise. 3. High fat feeding markedly impairs insulin- and exercise-stimulated muscle glucose uptake. As hexokinase II overexpression corrects this dietary-induced deficit during exercise, glucose phosphorylation is a site of impairment following high fat feeding. 4. Exercise is an important tool for diagnosing deficits in glucose phosphorylation.. AB - 1. Glucose phosphorylation is the first irreversible step of the muscle glucose uptake pathway and is catalysed by a hexokinase isozyme. 2. While ...
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
1. Rat pancreatic islets were isolated and then maintained in culture for 2-4 days before being incubated in groups of 100 in the presence of different glucose (0-20 mM) or CaCl2 (1.2-4.2 mM) concentrations, or with uncoupler. 2. Increases in extracellular glucose concentration resulted in increases in the amount of active, non-phosphorylated, pyruvate dehydrogenase in the islets, with half-maximal effects around 5-6 mM-glucose. Increasing extracellular glucose from 3 to 20 mM resulted in a 4-6-fold activation of pyruvate dehydrogenase within 2 min. 3. The total enzyme activity was unchanged, and averaged 0.4 m-unit/100 islets at 37 degrees C. 4. These changes in active pyruvate dehydrogenase were broadly similar to changes in insulin secretion by the islets. 5. Increasing extracellular Ca2+ or adding uncoupler also activated pyruvate dehydrogenase to a similar degree, but only the former was associated with increased insulin secretion. ...
In this study, echocardiography was used to monitor the progression of LV hypertrophy and to determine the timing for the study of glucose uptake and glucose transporter protein content. The observations derived from this investigation reveal that a decrease in glucose uptake rate is evident early in the transition from compensated to decompensated pressure-overload hypertrophy, as determined by an index of LV M/V ratio. The defect in insulin-stimulated glucose uptake precedes the downregulation of sarcoplasmic reticulum Ca-ATPase (SERCA-2) and glucose transporter expression (GLUT-4 and GLUT-1).15 26 Under pathophysiological conditions such as hypertrophy or during ischemia and early reperfusion, a high rate of cardiac glucose metabolism may be crucial.27 28 29 Glucose transport is thought to be rate-limiting for glucose use. In the heart, 2 distinctive glucose transporters are responsible for glucose uptake across the plasma membrane. The GLUT-1 transporter, which is present in low levels in ...
article{d63a054c-dfe7-4d78-994c-6543142f8a11, abstract = {Hormone-sensitive lipase (HSL) is expressed and enzymatically active in beta-cells and has been proposed to be involved in the generation of the lipid-derived signal that seems to be necessary for glucose-stimulated insulin secretion. In this study, we investigated whether the expression of HSL in INS-1 cells and in rat islets is affected by exposure to high glucose concentrations. Incubation of INS-1 cells in 25 mmol/l glucose for 16 and 32 h induced HSL protein expression twofold, whereas no effect was observed after 4 and 8 h of incubation. The HSL activity, defined as the diglyceride lipase activity inhibited by anti-rat HSL antibodies, constituted approximately 25% of total diglyceride lipase activity and was induced to a similar extent as HSL protein levels. The glucose effect at 16 h on HSL protein expression level was confirmed in freshly isolated rat islets. Exposure of INS-1 cells to different glucose concentrations for 16 h ...
The aim of the present thesis was to further increase our understanding of mechanisms contributing to and maintaining cellular insulin resistance in type 2 diabetes (T2D). For this reason, the effects of high glucose and insulin levels on glucose transport capacity and insulin signaling, with emphasis on insulin receptor substrate 1 (IRS-1) were assessed in fat cells. Altered levels of IRS-1 have previously been observed in adipose tissue from insulin-resistant and T2D subjects.. A high glucose level (≥15 mM) for 24 h exerted only a minor impairment on glucose transport capacity in human adipocytes, as opposed to rat adipocytes. However, when combined with a high insulin level (104 µU/ml), basal and insulin-stimulated glucose transport was significantly impaired in both human and rat adipocytes. This was associated with a depletion of IRS-1 and IRS-2 protein levels in rat adipocytes, as a result of post-translational changes and altered gene transcription, respectively. In human adipocytes ...
Neuronal Cell Protective Effect of Dendropanax morbifera Extract against High Glucose-Induced Oxidative Stress - Dendropanax morbifera;antioxidant;oxidative stress;high glucose;neuroprotective effect;
TY - JOUR. T1 - Clonal insulinoma cell line that stably maintains correct glucose responsiveness. AU - Knaack, D.. AU - Fiore, D. M.. AU - Surana, M.. AU - Leiser, M.. AU - Laurance, M.. AU - Fusco-DeMane, D.. AU - Hegre, O. D.. AU - Fleischer, N.. AU - Efrat, S.. PY - 1994/12/1. Y1 - 1994/12/1. N2 - A number of pancreatic β-tumor cell (βTC) lines have been derived from insulinomas arising in transgenic mice expressing the SV40 T antigen gene under control of the insulin promoter. Some of these lines secrete insulin in response to physiological glucose concentrations. However, this phenotype is unstable. After propagation in culture, these nonclonal lines become responsive to subphysiological glucose levels and/or manifest reduced insulin release. Here we report the use of soft-agar cloning to isolate single-cell clones from a βTC line, which give rise to sublines that maintain correct glucose responsiveness and high insulin production and secretion for ,55 passages (over a year) in culture. ...
TY - JOUR. T1 - Longevity is associated with increased vascular resistance to high glucose-induced oxidative stress and inflammatory gene expression in Peromyscus leucopus. AU - Labinskyy, Nazar. AU - Mukhopadhyay, Partha. AU - Toth, Janos. AU - Szalai, Gabor. AU - Veres, Monika. AU - Losonczy, Gyorgy. AU - Pinto, John T.. AU - Pacher, Pal. AU - Ballabh, Praveen. AU - Podlutsky, Andrej. AU - Austad, Steven N.. AU - Csiszar, Anna. AU - Ungvari, Zoltan. PY - 2009/4/1. Y1 - 2009/4/1. N2 - Vascular aging is characterized by increased oxidative stress and proinflammatory pheno- typic alterations. Metabolic stress, such as hyperglycemia in diabetes, is known to increase the production of ROS and promote inflammatory gene expression, accelerating vascular aging. The oxidative stress hypothesis of aging predicts that vascular cells of long-lived species exhibit lower steady-state production of ROS and/or superior resistance to the prooxidant effects of metabolic stress. We tested this hypothesis using ...
Methods HUVECs were incubated for 8 days in media containing different glucose concentrations: 5.56 mmol/l (normal glucose), 25 mmol/l (constant high glucose), or a daily alternating 5.56 or 25 mmol/l glucose (intermittent high glucose). Meanwhile, drug intervention was performed in different glucose conditions with TMP at concentrations of 500 μmol/L, 100 μmol/L and 20 μmol/L. Then cell viability was measured by MTT method, cell membrane damage was determined by lactate dehydrogenase (LDH) leakage, and Nitric oxide (NO), endothelin-1 (ET-1), soluble intercellular adhesion molecule-1 (sICAM-1) and tumour necrosis factor-α (TNF-α) concentrations in the cell culture supernatant were measured. The activities of superoxide dismutase (SOD), nitric oxide synthetase (NOS) and the contents of malondialdehyde (MDA) in the cell lysate were examined by enzyme method or spectrophotometry.. ...
1977).. To determine whether Acebutolol stimulates the glucose uptake, one of the most important phenotype in diabetes, we performed glucose analog, 2-NBDG, uptake assay in both TNFα-induced diabetic model cells and non-induced normal cells (Fig. 3). Without TNFα pretreatment, insulin increased glucose uptake about 30% (1.28 ± 0.13). BI-78D3 increased glucose uptake about 90% (1.97 ± 0.11) and Acebutolol increase glucose uptake about 50% (1.48 ± 0.17) comparing with control respectively. With TNFα treatment, insulin increased glucose uptake about 20% (1.18 ± 0.12). BI-78D3 increased glucose uptake about 50% (1.54 ± 0.16) and Acebutolol increase glucose uptake about 45% (1.46 ± 0.02) comparing with control respectively. Because relatively short time incubation of TNFα (6 h) in our experimental condition, glucose uptake by insulin treatment was slightly decreased (Fig. 3A). The effect of BI-78D3 on glucose uptake is higher in normal cells than TNFα treated cells. Interestingly, in both ...
Insulin stimulates the uptake of glucose in several target tissues, including skeletal muscle and adipose tissue, thereby contributing to the decline in the blood glucose level. In this book, the authors present current research in the study of the regulation, signaling pathways and health implications of glucose uptake.. Topics include glucose uptake and transport regulation; the mechanisms that contribute to glucose homeostasis; expression and regulation of neuronal glucose transporters in health and disease; role for the microvasculature in glucose uptake in skeletal muscle; implications of diabetes on sperm glucose uptake and metabolism; the beneficial role of estrogen signaling in glucose homeostasis and energy expenditure; glucose uptake and androgen responsiveness of prostate cancer cells; regulation of intestinal glucose uptake by leptin; and the Ras superfamily of small GTP-binding proteins in glucose transporter type 4-mediated glucose uptake in insulin-responsive tissues. (Imprint: ...
AbstractIn the present work we set out to investigate the neuroprotective effects of noscapine (0.5-2 µM) in presence of D-glucose on primary murine foetal cortical neurons after oxygen-glucose deprivation/24 hrs recovery. Cell viability, nitric oxide production and intracellular calcium ([ca2+]i) levels were evaluated by MTT assay, the modified Griess method and Fura-2 respectively. 25 and 100 mM D-glucose could, in a concentration dependent manner, improve cell viability and decrease NO production and [ca2+]i level in neuronal cells after ischemic insult. Moreover, pre-incubation of cells with noscapine, noticeably enhanced protective effects of 25 and 100 mM D-glucose compared to similar conditions without noscapine pre-treatment. In fact, noscapine attenuated NO production in a dose-dependent fashion, after 30 minutes (min) OGD, during high-glucose (HG) condition in cortical neurons. Pretreatment with 2 μM noscapine and 25 or 100 mM D-glucose, was shown to decrease the rise in [ca2+]i induced by
5-AMP-activated protein kinase (AMPK) has been suggested to be a metabolic master switch regulating various aspects of muscle glucose and fat metabolism. In isolated rat skeletal muscle, glucose suppresses the activity of AMPK and in human muscle glycogen loading decreases exercise-induced AMPK activation. We hypothesized that oral glucose ingestion during exercise would attenuate muscle AMPK activation. Nine male subjects performed two bouts of one-legged knee-extensor exercise at 60% of maximal workload. The subjects were randomly assigned to either consume a glucose containing drink or a placebo drink during the two trials. Muscle biopsies were taken from the vastus lateralis before and after 2 h of exercise. Plasma glucose was higher (6.0 +/- 0.2 vs. 4.9 +/- 0.1 mmol L-1, P , 0.001), whereas glycerol (44.8 +/- 7.8 vs. 165.7 +/- 22.3 micromol L-1), and free fatty acid (169.3 +/- 9.5 vs. 1161 +/- 144.9 micromol L-1) concentrations were lower during the glucose compared to the placebo trial ...
HIV protease inhibitors (PIs) have been associated with type 2 diabetes. To design future HIV drugs that have have the least adverse metabolic effects, it is necessary to identify the disorders of glucose metabolism with PI therapy. Previously PIs have been shown to acutely induce insulin resistance in the periphery. Preliminary data show that PIs also impair insulin secretion and increase hepatic glucose production in humans. These lesions are key contributors to the development of type 2 diabetes. Due to the difficulty in separating out factors related to HIV infection from the direct effect of PIs, an effective design is to study HIV-negative subjects to define the direct effects of PIs on the liver and pancreas on glucose metabolism:. Specific Aim 1: To determine which PIs acutely inhibit insulin secretion in humans; randomized, double-blind, placebo-controlled trials will be performed on healthy normal volunteers given either a single dose of PI or placebo using the hyperglycemic clamp to ...
Overconsumption of high-fat diet (HFD) and sugar-sweetened beverages are risk factors for developing obesity, insulin resistance, and fatty liver disease. Here we have dissected mechanisms underlying this association using mice fed either chow or HFD with or without fructose- or glucose-supplemented water. In chow-fed mice, there was no major physiological difference between fructose and glucose supplementation. On the other hand, mice on HFD supplemented with fructose developed more pronounced obesity, glucose intolerance, and hepatomegaly as compared to glucose-supplemented HFD mice, despite similar caloric intake. Fructose and glucose supplementation also had distinct effects on expression of the lipogenic transcription factors ChREBP and SREBP1c. While both sugars increased ChREBP-β, fructose supplementation uniquely increased SREBP1c and downstream fatty acid synthesis genes, resulting in reduced liver insulin signaling. In contrast, glucose enhanced total ChREBP expression and ...
The pathogenesis of ischemic diseases remains unclear. Here we demonstrate the induction of microRNA-668 (miR-668) in ischemic acute kidney injury (AKI) in human patients, mice, and renal tubular cells. The induction was HIF-1 dependent, as HIF-1 deficiency in cells and kidney proximal tubules attenuated miR-668 expression. We further identified a functional HIF-1 binding site in the miR-668 gene promoter. Anti-miR-668 increased apoptosis in renal tubular cells and enhanced ischemic AKI in mice, whereas miR-668 mimic was protective. Mechanistically, anti-miR-668 induced mitochondrial fragmentation, whereas miR-668 blocked mitochondrial fragmentation during hypoxia. We analyzed miR-668 target genes through immunoprecipitation of microRNA-induced silencing complexes followed by RNA deep sequencing and identified 124 protein-coding genes as likely targets of miR-668. Among these genes, only mitochondrial protein 18 kDa (MTP18) has been implicated in mitochondrial dynamics. In renal cells and mouse ...
Overconsumption of high-fat diet (HFD) and sugar-sweetened beverages are risk factors for developing obesity, insulin resistance, and fatty liver disease. Here we have dissected mechanisms underlying this association using mice fed either chow or HFD with or without fructose- or glucose-supplemented water. In chow-fed mice, there was no major physiological difference between fructose and glucose supplementation. On the other hand, mice on HFD supplemented with fructose developed more pronounced obesity, glucose intolerance, and hepatomegaly as compared to glucose-supplemented HFD mice, despite similar caloric intake. Fructose and glucose supplementation also had distinct effects on expression of the lipogenic transcription factors ChREBP and SREBP1c. While both sugars increased ChREBP-β, fructose supplementation uniquely increased SREBP1c and downstream fatty acid synthesis genes, resulting in reduced liver insulin signaling. In contrast, glucose enhanced total ChREBP expression and ...
Overconsumption of high-fat diet (HFD) and sugar-sweetened beverages are risk factors for developing obesity, insulin resistance, and fatty liver disease. Here we have dissected mechanisms underlying this association using mice fed either chow or HFD with or without fructose- or glucose-supplemented water. In chow-fed mice, there was no major physiological difference between fructose and glucose supplementation. On the other hand, mice on HFD supplemented with fructose developed more pronounced obesity, glucose intolerance, and hepatomegaly as compared to glucose-supplemented HFD mice, despite similar caloric intake. Fructose and glucose supplementation also had distinct effects on expression of the lipogenic transcription factors ChREBP and SREBP1c. While both sugars increased ChREBP-β, fructose supplementation uniquely increased SREBP1c and downstream fatty acid synthesis genes, resulting in reduced liver insulin signaling. In contrast, glucose enhanced total ChREBP expression and ...
Abstract Prolonged fasting (for days or weeks) decreases glucose production and oxidation. The effects of short-term starvation (ie, < 24 hours) on glucose metabolism are not known. To evaluate this issue, glucose oxidation and glucose turnover were measured after 16-hour and subsequently after 22-hour fasting. Glucose oxidation was calculated by indirect calorimetry in 12 healthy men (age 22 to 44 years); glucose turnover was measured by primed, continuous infusion of 3-3H-glucose in eight of these 12 volunteers. After 16-hour fasting net glucose oxidation was 0.59 ± 0.17 mg · kg−1 · min−1 and glucose tissue uptake 2.34 ± 0.12 mg · kg−1 · min−1. No correlation was found between net glucose oxidation and glucose tissue uptake. Prolonging fasting with an addtional 6 hours resulted in decreases of respiratory quotient (0.77 ± 0.01 v 0.72 ± 0.01) (P < .005), plasma glucose concentration (4.7 ± 0.1 v 4.6 ± 0.1 mmol/L) (P < .05), glucose tissue uptake (2.10 ± 0.12 mg · kg−1 · ...
TY - JOUR. T1 - Acute Enterocyte Adaptation to Luminal Glucose. T2 - A Posttranslational Mechanism for Rapid Apical Recruitment of the Transporter GLUT2. AU - Chaudhry, Rizwan M.. AU - Scow, Jeffrey. AU - Madhavan, Srivats. AU - Duenes, Judith A.. AU - Sarr, Michael G.. PY - 2012/2/1. Y1 - 2012/2/1. N2 - Background: Glucose absorption postprandially increases markedly to levels far greater than possible by the classic glucose transporter sodium-glucose cotransporter 1 (SGLT1). Hypothesis: Luminal concentrations of glucose ,50 mM lead to rapid, phenotypic, non-genomic adaptations by the enterocyte to recruit another transporter, glucose transporter 2 (GLUT2), to the apical membrane to increase glucose absorption. Methods: Isolated segments of jejunum were perfused in vivo with glucose-containing solutions in anesthetized rats. Carrier-mediated glucose uptake was measured in 10 and 100 mM glucose solutions (n = 6 rats each) with and without selective inhibitors of SGLT1 and GLUT2. Results: The ...
DIABETIC EMERGENCY HYPOGLYCAEMIA GLUCOSE REPLACEMENT THERAPY KIT. The HypoWallet is an attractive robust, portable wallet which contains effective remedies for any patient suffering from an occurrence of hypoglycaemia (low blood sugar level), allowing the patient to replenish their glucose levels and avoid potentially detrimental consequences.. Each kit contains:. 2 x 25g tubes of GlucoGel. 1 x 10 pack of chewable Orange GlucoTabs. 1 x 60ml of GlucoJuice. Protective portable case. Dimensions: 14cm x 9.5cm x 5cm. The treatments are measured, established glucose treatments and the case in easily identified as glucose treatment with HypoWallet in distinctive Red and White writing on a black background which is easily identifiable as a treatment kit.. ...
The second messenger cAMP mediates potentiation of glucose-stimulated insulin release. Use of inhibitors of cAMP-hydrolyzing phosphodiesterase (PDE) 3 and overexpression of PDE3B in vitro have demonstrated a regulatory role for this enzyme in insulin secretion. In this work, the physiological significance of PDE3B-mediated degradation of cAMP for the regulation of insulin secretion in vivo and glucose homeostasis was investigated in transgenic mice overexpressing PDE3B in pancreatic beta-cells. A 2-fold overexpression of PDE3B protein and activity blunted the insulin response to intravenous glucose, resulting in reduced glucose disposal. The effects were dose-dependent because mice overexpressing PDE3B 7-fold failed to increase insulin in response to glucose and hence exhibited pronounced glucose intolerance. Also, the insulin secretory response to intravenous glucagon-like peptide 1 was reduced in vivo. Similarly, islets stimulated in vitro exhibited reduced insulin secretory capacity in ...
In this study, the presence of mild hypertension did not significantly exacerbate the marked defect of insulin-mediated glucose disposal present in abdominally obese subjects. In fact, multiple measurements were not significantly different in the two obese groups, including fasting insulin and, more importantly, glucose metabolized over the prevailing insulin concentration during both levels of euglycemic hyperinsulinemia.24 The abdominally obese hypertensive group included four female subjects who may have had less severe insulin resistance than the obese normotensive men. However, the results were unchanged when these four women were excluded from the analysis.. Glucose metabolism was diminished in both the obese hypertensive and normotensive groups. To further evaluate the mechanism of insulin resistance in the abdominally obese subjects, we performed indirect calorimetry to provide measures of both glycogenesis and glycolysis. Oxidative and nonoxidative glucose metabolisms were comparably ...
Multiple proteins have been implicated as mediators of hyperglycemia and cancer cell proliferation (Fig. 1). Recent in vitro studies suggest that the expression of glucose transporters, such as the GLUT1 and GLUT3 isoforms, is regulated under hyperglycemic conditions in JAR cells, a choriocarcinoma cell line [20]. Hyperglycemic conditions in vitro (such as 25 mM D-glucose) trigger increased glucose uptake in JAR cells due to a transcriptional increase and enhanced protein levels for GLUT1 and GLUT3 [20]. Growth factors, such as epidermal growth factor (EGF) levels are augmented by high glucose treatment in pancreatic cancer cell lines, such as BxPC-3 and Panc-1, and subsequently activate its receptor, the epidermal growth factor receptor (EGFR), a well-known oncogenic pathway [21]. In addition, the levels of protein kinase C (PKC) and peroxisome proliferator-activated receptors (PPARs) are stimulated under hyperglycemic conditions in MCF-7 human breast cancer cells [22]. Overexpression of PKC-α ...
Modelling ischaemia in vitro: Effects of temperature and glucose concentration on dopamine release evoked by oxygen and glucose depletion in a mouse brain ...
When cells were subjected to glucose at 30 mM for 24 hr, it was observed early apoptotic changes. MTT assays showed that treatment with a high concentration of glucose (30 mM) significantly increased apoptosis among cultured GECs as compared with that observed for a normal glucose concentration (5 mM). Pretreatment with EGCG (1-100 μM) significantly increased cell viability under the high glucose condition in a dose-dependent manner. DNA fragments was induced by glucose at 30 mM for 24 hr, whereas pretreatment for 2 hr with EGCG (1-100 μM) conferred significant protection against this glucose-induced DNA fragmentation. Moreover, DAPI staining assays showed that treatment with a high concentration of glucose (30 mM) increased DNA fragmentation / condensation in GECs as compared with that observed for a normal glucose concentration (5 mM). Pretreatment of GECs with EGCG (1-100 μM) significantly increased cell viability under the high glucose condition in a dose-dependent manner. Mechanism of ...
Insulin controls glucose homeostasis by regulating glucose use in peripheral tissues, and its own production and secretion in pancreatic beta cells. These responses are largely mediated downstream of the insulin receptor substrates, IRS-1 and IRS-2 (refs 4-8), through distinct signalling pathways. Although a number of effectors of these pathways have been identified, their roles in mediating glucose homeostasis are poorly defined. Here we show that mice deficient for S6 kinase 1, an effector of the phosphatidylinositide-3-OH kinase signalling pathway, are hypoinsulinaemic and glucose intolerant. Whereas insulin resistance is not observed in isolated muscle, such mice exhibit a sharp reduction in glucose-induced insulin secretion and in pancreatic insulin content. This is not due to a lesion in glucose sensing or insulin production, but to a reduction in pancreatic endocrine mass, which is accounted for by a selective decrease in beta-cell size. The observed phenotype closely parallels
BACKGROUND: Glucose homeostasis is distorted by defects of the PI3K/AKT and AMPK pathways in insulin-sensitive tissues, allowing the accumulation of glucose in the blood. The purpose of this study was to assess the effects and mechanisms by which ethanol extract of Caulerpa lentillifera (CLE) regulates glucose metabolism in C57BL/KsJ-db/db (db/db) mice. METHODS: Mice were administered CLE (250 or 500 mg/kg BW) or rosiglitazone (RSG, 10 mg/kg BW) for 6 weeks. Then, oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) were performed, and blood glucose was measured in db/db mice. Levels of insulin and insulin resistance factors in plasma, glycogen content in the liver, and IRS, PI3K, AKT, and GLUT4 expressions in skeletal muscles were measured in db/db mice. Glucose uptake and insulin signaling molecules were measured in L6 myocytes, using fluorometry and Western blotting. RESULTS: CLE significantly decreased fasting blood glucose, glucose level in OGTT and IPITT, ...
Our results from the 1-week culture at various glucose concentrations revealed that increasing glucose concentrations lead to an increased proinsulin secretion to the culture medium. We believe that the increase in proinsulin secretion could be explained by a sustained state of cellular activation.. The half-time of conversion of newly synthesized proinsulin from the intracellular pool was determined using three time points. In all experiments, except those in which islets were treated with IL-1β, the T1/2 was found to be 40-50 min when 15 min after the start of radioactive labelling was set as time 0. This agrees well with previously published studies (Steiner et al. 1972, Rhodes & Halban 1987 Nagamatsu et al. 1987) indicating an intracellular T1/2 of proinsulin of about 60 min in freshly isolated islets. In the present study, this rate of conversion was maintained after culture in glucose concentrations in the range 5.6-28 mM, whereas a decreased rate was measured only in islets which had ...
Circulating apelin is well recognised as a factor involved in the control of glucose homeostasis by modulating glucose utilisation acting directly on tissues (adipose tissue, muscle, intestine). In the brain, apelin exerts a dual effect depending on the nutritional state and its levels present in the hypothalamus. We have previously demonstrated that low dose of apelin administrated intracerebroventricularly improves glycaemia in fed mice.9 This effect could be linked to the slight and continuous increase in plasma apelin observed during the dark period (corresponding to the fed state). All these data suggest that a physiological rise of apelin in the whole body exerts beneficial effect on glucose metabolism as previously observed after an acute intravenous injection.10 Here, we show that apelin has a dual effect on ENS neurons similar to that observed in the CNS. In particular, we show that apelin induces modulations of duodenal contractility and subsequently modifies hypothalamic activity via ...
Fifty normal people and 50 diabetic patients were studied by means of an enzymatic method for the glucose content in the blood, tears, and urine before and after the peroral glucose load. In normal subjects the fasting glucose levels in the tears averaged 3.6 mg/100 ml (0.2 mmol/l) and in the diabetic patients it averaged 16.6 mg/100 ml (0.92 mmol/l). As in blood and urine, tear glucose levels are significantly higher in diabetic patients than normal persons both at fasting and after the peroral glucose load test. The fasting tear glucose level did not appear to be a satisfactory index for classifying a person as a diabetic or normal. It was found that after the peroral glucose load test a tear glucose level at 11 mg/100 ml (0.61 mmol/l) resulted in only 4.6% of the diabetics being missed, while 5.8% of the normal persons were misclassified as diabetics. ...
Ginkgo biloba, an herbal medication, is capable of lowering glucose, fat, and lipid peroxide in diabetic patients. In the current study, we tested the hypothesis that Ginkgo biloba extract (GBE) prevented hyperinsulinism-induced glucose intolerance in hepatocytes. We investigated the effects of GBE on glucose consumption, glucokinase activity, and mRNA levels of key genes in glucose metabolism and the insulin signaling pathway. To better show its efficacy, we included a control group that was treated with rosiglitazone, a type of thiazolidinedione (TZD). The data indicated that GBE repressed glucose uptake under normal conditions, while it dramatically improved glucose tolerance under insulin-resistant conditions. Furthermore, after analyzing gene expression, we suggest that GBE chiefly exerts its effects by stimulating IRS-2 transcription. It should be noted that, unlike rosiglitazone, GBE did not stimulate excessive glucose uptake as it improved glucose tolerance. It is said that GBE treatment ...
Why would blood glucose levels fluctuate when on LCHF?. Dramatic improvements in blood glucose can be expected within the first days of adopting an LCHF diet. However, its very normal for diabetics not to achieve perfect fasting (morning) blood glucose early on or sometimes ever. Morning fasting blood glucose levels usually continue to remain high, even after adopting a ketogenic LCHF diet and even when blood glucose over the rest of the day is well controlled. This is due to the dawn phenomenon - high morning blood glucose caused by raised concentrations of growth hormone, cortisol, adrenaline and glucagon in the morning.. Achieving good blood glucose control over the rest of the day is what is really important. It takes time and trial and error, with close post-meal blood glucose monitoring to determine exactly which foods affect blood glucose levels and to what extent. This will help find the foods and amounts that help keep blood glucose stable so that the patient can try to eat those as ...
Obesity is considered a state of low-grade inflammation, and this inflammation is strongly related to development of systematic insulin resistance. Hyperglycemia develops during insulin resistance as insulin-stimulated glucose uptake in peripheral insulin sensitive tissues is reduced. Hepatic insulin resistance is often accompanied with increased gluconeogenesis and increased hepatic glucose output, which further increase blood glucose. To cope with the hyperglycemia, the pancreatic -cells compensate by increasing insulin secretion. However, after a certain amount of time, the -cells are no longer able to compensate, and insulin production stops. This may be accompanied with apoptosis in the -cells. Indomethacin is an NSAID and a non-selective inhibitor of cyclooxygenase 1 (COX-1) and 2 (COX-2). In this study we have demonstrated that COX-inhibition using indomethacin, attenuated high fat/high sucrose-induced obesity in C57BL/6J mice. Obesity and glucose intolerance ...
The current goal of diabetes therapy is to reduce time-averaged mean levels of glycemia, measured as HbA1c, to prevent diabetic complications. However, HbA1c only explains ,25% of the variation in risk of developing complications. Because HbA1c does not correlate with glycemic variability when adjusted for mean blood glucose, we hypothesized that transient spikes of hyperglycemia may be an HbA1c-independent risk factor for diabetic complications. We show that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells both in vitro and in nondiabetic mice, which cause increased p65 gene expression. Both the epigenetic changes and the gene expression changes persist for at least 6 d of subsequent normal glycemia, as do NF-κB-induced increases in monocyte chemoattractant protein 1 and vascular cell adhesion molecule 1 expression. Hyperglycemia-induced epigenetic changes and increased p65 ...
Review. 1826 (2), 370-84. Dec 2012. Dysregulation of Glucose Transport, Glycolysis, TCA Cycle and Glutaminolysis by Oncogenes and Tumor Suppressors in Cancer Cells. Jin-Qiang Chen 1, Jose Russo. PMID: 22750268. DOI: 10.1016/j.bbcan.2012.06.004. Abstract. A common set of functional characteristics of cancer cells is that cancer cells consume a large amount of glucose, maintain high rate of glycolysis and convert a majority of glucose into lactic acid even in the presence of oxygen compared to that of normal cells (Warburgs Effects). In addition, cancer cells exhibit substantial alterations in several energy metabolism pathways including glucose transport, tricarboxylic acid (TCA) cycle, glutaminolysis, mitochondrial respiratory chain oxidative phosphorylation and pentose phosphate pathway (PPP). In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis, TCA cycle and ...