Monosaccharide transport proteins that function as active symporters. They utilize SODIUM or HYDROGEN IONS to transport GLUCOSE across CELL MEMBRANES.
The founding member of the sodium glucose transport proteins. It is predominately expressed in the INTESTINAL MUCOSA of the SMALL INTESTINE.
A sodium-glucose transporter that is expressed in the luminal membrane of the PROXIMAL KIDNEY TUBULES.
A ubiquitously expressed glucose transporter that is important for constitutive, basal GLUCOSE transport. It is predominately expressed in ENDOTHELIAL CELLS and ERYTHROCYTES at the BLOOD-BRAIN BARRIER and is responsible for GLUCOSE entry into the BRAIN.
A large group of membrane transport proteins that shuttle MONOSACCHARIDES across CELL MEMBRANES.
Glucosides are glycosides that contain glucose as the sugar component, often forming part of the plant's defense mechanism and can have various pharmacological effects when extracted and used medically.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
Phlorhizin is a non-transportable glucose analog that inhibits the sodium-glucose cotransporter 1 (SGLT1) and aldohexose transporter (GLUT2), leading to reduced intestinal absorption and increased renal excretion of glucose, which is used in research to study glucose transport and diabetes-related processes.
A glucose transport protein found in mature MUSCLE CELLS and ADIPOCYTES. It promotes transport of glucose from the BLOOD into target TISSUES. The inactive form of the protein is localized in CYTOPLASMIC VESICLES. In response to INSULIN, it is translocated to the PLASMA MEMBRANE where it facilitates glucose uptake.
A major glucose transporter found in NEURONS.
The appearance of an abnormally large amount of GLUCOSE in the urine, such as more than 500 mg/day in adults. It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA).
Methylglucosides are a type of sugar alcohols, specifically methylated glucose derivatives, which are used as sweetening agents, excipients, and solvents in pharmaceutical and cosmetic products due to their low toxicity and good solubility in water.
A glucose transport facilitator that is expressed primarily in PANCREATIC BETA CELLS; LIVER; and KIDNEYS. It may function as a GLUCOSE sensor to regulate INSULIN release and glucose HOMEOSTASIS.
A family of monosaccharide transport proteins characterized by 12 membrane spanning helices. They facilitate passive diffusion of GLUCOSE across the CELL MEMBRANE.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Substances which lower blood glucose levels.
The middle portion of the SMALL INTESTINE, between DUODENUM and ILEUM. It represents about 2/5 of the remaining portion of the small intestine below duodenum.
2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
A cytotoxic member of the CYTOCHALASINS.
Glucose in blood.

Missense mutations in SGLT1 cause glucose-galactose malabsorption by trafficking defects. (1/325)

Glucose-galactose malabsorption (GGM) is an autosomal recessive disorder caused by defects in the Na+/glucose cotransporter (SGLT1). Neonates present with severe diarrhea while on any diet containing glucose and/or galactose [1]. This study focuses on a patient of Swiss and Dominican descent. All 15 exons of SGLT1 were screened using single stranded conformational polymorphism analyses, and aberrant PCR products were sequenced. Two missense mutations, Gly318Arg and Ala468Val, were identified. SGLT1 mutants were expressed in Xenopus laevis oocytes for radiotracer uptake, electrophysiological experiments, and Western blotting. Uptakes of [14C]alpha-methyl-d-glucoside by the mutants were 5% or less than that of wild-type. Two-electrode voltage-clamp experiments confirmed the transport defects, as no noticeable sugar-induced current could be elicited from either mutant [2]. Western blots of cell protein showed levels of each SGLT1 mutant protein comparable to that of wild-type, and that both were core-glycosylated. Presteady-state current measurements indicated an absence of SGLT1 in the plasma membrane. We suggest that the compound heterozygote missense mutations G318R and A468V lead to GGM in this patient by defective trafficking of mutant proteins from the endoplasmic reticulum to the plasma membrane.  (+info)

Ontogeny of intestinal safety factors: lactase capacities and lactose loads. (2/325)

We measured intestinal safety factors (ratio of a physiological capacity to the load on it) for lactose digestion in developing rat pups. Specifically, we assessed the quantitative relationships between lactose load and the series capacities of lactase and the Na+-glucose cotransporter (SGLT-1). Both capacities increased significantly with age in suckling pups as a result of increasing intestinal mass and maintenance of mass-specific activities. The youngest pups examined (5 days) had surprisingly high safety factors of 8-13 for both lactase and SGLT-1, possibly because milk contains lactase substrates other than lactose; it also, however, suggests that their intestinal capacities were being prepared to meet future demands rather than just current ones. By day 10 (and also at day 15), increased lactose loads resulted in lower safety factors of 4-6, values more typical of adult intestines. The safety factor of SGLT-1 in day 30 (weanling) and day 100 (adult) rats was only approximately 1.0. This was initially unexpected, because most adult intestines maintain a modest reserve capacity beyond nutrient load values, but postweaning rats appear to use hindgut fermentation, assessed by gut morphology and hydrogen production assays, as a built-in reserve capacity. The series capacities of lactase and SGLT-1 varied in concert with each other over ontogeny and as lactose load was manipulated by experimental variation in litter size.  (+info)

Acute increase, stimulated by prostaglandin E2, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine. (3/325)

BACKGROUND/AIMS: Acute stimulation by cAMP of the sodium dependent glucose cotransporter SGLT1 has previously been shown. As prostaglandin E2 (PGE2) increases intracellular cAMP concentrations via its receptor subtypes EP2R and EP4R, it was investigated whether PGE2 could enhance intestinal glucose absorption. METHODS: The action of PGE2 on carbohydrate absorption in the ex situ perfused rat small intestine and on 3-O-[14C]methylglucose uptake in isolated villus tip enterocytes was determined. Expression of mRNA for the PGE2 receptor subtypes 1-4 was assayed in enterocytes by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: In the perfused small intestine, PGE2 acutely increased absorption of glucose and galactose, but not fructose (which is not a substrate for SGLT1); in isolated enterocytes it stimulated 3-O-[14C]methylglucose uptake. The 3-O-[14C]methylglucose uptake could be inhibited by the cAMP antagonist RpcAMPS and the specific inhibitor of SGLT1, phlorizin. High levels of EP2R mRNA and EP4R mRNA were detected in villus tip enterocytes. CONCLUSION: PGE2 acutely increased glucose and galactose absorption by the small intestine via the SGLT1, with cAMP serving as the second messenger. PGE2 acted directly on the enterocytes, as the stimulation was still observed in isolated enterocytes and RT-PCR detected mRNA for the cAMP-increasing PGE2 receptors EP2R and EP4R.  (+info)

Cloning and characterization of the transport modifier RS1 from rabbit which was previously assumed to be specific for Na+-D-glucose cotransport. (4/325)

Previously we cloned membrane associated polypeptides from pig and man (pRS1, hRS1) which altered rate and glucose dependence of Na+-d-glucose cotransport expressed by SGLT1 from rabbit and man. This paper describes the cloning of a related cDNA sequence from rabbit intestine (rbRS1) which encodes a gene product with about 65% amino acid identity to pRS1 and hRS1. Hybridization of endonuclease-restricted genomic DNA with cDNA fragments of rbRS1 showed that there is only one gene with similarity to rbRS1 in rabbit, and genomic PCR amplifications revealed that the rbRS1 gene is intronless. Comparing the transcription of rbRS1 and rbSGLT1 in various tissues and cell types, different mRNA patterns were obtained for both genes. In Xenopus oocytes the Vmax of expressed Na+-d-glucose cotransport was increased or decreased when rbRS1 was coexpressed with rbSGLT1 or hSGLT1, respectively. After coexpression with hSGLT1 the glucose dependence of the expressed transport was changed. By coexpression of rbRS1 with the human organic cation transporter hOCT2 the expressed cation uptake was not altered; however, the expressed cation uptake was drastically decreased when hRS1 was coexpressed with hOCT2. The data show that RS1 can modulate the function of transporters with non-homologous primary structures.  (+info)

Sucrase-isomaltase and hexose transporter gene expressions are coordinately enhanced by dietary fructose in rat jejunum. (5/325)

We previously demonstrated that the levels of mRNAs of both sucrase-isomaltase (SI) and sodium/D-glucose transporter (SGLT1) are modulated by dietary sucrose in the rat jejunum. In the present study, we investigated whether the transcription of the gene coding SI is regulated by certain types of monosaccharides. Force-feeding a fructose and sucrose diet, (40% energy as fructose or sucrose) gave rise to parallel increases in the transcripts of SI and intestinal hexose transporters (SGLT1, GLUT5, and GLUT2) within 12 h. Force-feeding a glycerol-containing diet also caused an enhancement of SI, SGLT1, and GLUT2 mRNA levels. However, feeding the diet containing glucose or alpha-methylglucoside generally did not increase the transcript levels of SI or the intestinal hexose transporters. Nuclear run-on assays revealed that fructose as well as sucrose increased the transcription of both SI and GLUT5 genes and that the transcription rates of these genes were unaffected by glucose. These results suggest that fructose (or a metabolite) is capable of increasing the mRNA levels of SI and hexose transporters in the small intestine and that transcriptional regulation might play a pivotal role in the carbohydrate-induced coordinate enhancement of SI and fructose transporter gene expression  (+info)

PKC regulates turnover rate of rabbit intestinal Na+-glucose transporter expressed in COS-7 cells. (6/325)

We have used the recombinant NH2-terminal myc-tagged rabbit Na+-glucose transporter (SGLT1) to study the regulation of this carrier expressed in COS-7 cells. Treatment of cells with a protein kinase C (PKC) agonist, phorbol 12-myristate 13-acetate (PMA), caused a significant decrease (38.03 +/- 0.05%) in methyl alpha-D-glucopyranoside transport activity that could not be emulated by 4alpha-phorbol 12,13-didecanoate. The decrease in sugar uptake stimulated by PMA was reversed by the PKC inhibitor bisindolylmaleimide I. The maximal rate of Na+-glucose cotransport activity (Vmax) was decreased from 1.29 +/- 0.09 to 0.85 +/- 0.04 nmol. min-1. mg protein-1 after PMA exposure. However, measurement of high-affinity Na+-dependent phloridzin binding revealed that there was no difference in the number of cell surface transporters after PMA treatment; maximal binding capacities were 1.54 +/- 0.34 and 1.64 +/- 0.21 pmol/mg protein for untreated and treated cells, respectively. The apparent sugar binding affinity (Michaelis-Menten constant) and phloridzin binding affinity (dissociation constant) were not affected by PMA. Because PKC reduced Vmax without affecting the number of cell surface SGLT1 transporters, we conclude that PKC has a direct effect on the carrier, resulting in a lowering of the transporter turnover rate by a factor of two.  (+info)

Cloning and functional expression of an SGLT-1-like protein from the Xenopus laevis intestine. (7/325)

A cDNA encoding an Na+-glucose cotransporter type 1 (SGLT-1)-like protein was cloned from the Xenopus laevis intestine by the 5'- and 3'-rapid amplification of cDNA ends method. The deduced amino acid sequence was 673 residues long, with a predicted mass of 74.1 kDa and 52-53% identity to mammalian SGLT-1s. This gene was expressed in the small intestine and kidney, reflecting a tissue distribution similar to that of SGLT-1. The function of the protein was studied using the two-microelectrode voltage-clamp technique after injection of cRNA into Xenopus laevis oocytes. Perfusion with myo-inositol elicited about twofold larger inward currents than perfusion with D-glucose. The order of the substrate specificity was myo-inositol > D-glucose > D-galactose >/= alpha-methyl-D-glucoside. The current induced by myo-inositol increased with membrane hyperpolarization and depended on external myo-inositol and Na+: the apparent Michaelis-Menten constant was 0.25 +/- 0.07 (SD) mM with myo-inositol, whereas the apparent concentration for half-maximal activation was 12.5 +/- 1.0 mM and the Hill coefficient was 1.6 +/- 0.1 with Na+. In conclusion, the cloned protein shares features with both SGLT-1 and the Na+-myo-inositol cotransporter.  (+info)

Passive water and ion transport by cotransporters. (8/325)

1. The rabbit Na+-glucose (SGLT1) and the human Na+-Cl--GABA (GAT1) cotransporters were expressed in Xenopus laevis oocytes, and passive Na+ and water transport were studied using electrical and optical techniques. Passive water permeabilities (Lp) of the cotransporters were determined from the changes in oocyte volume in response to osmotic gradients. The specific SGLT1 and GAT1 Lp values were obtained by measuring Lp in the presence and absence of blockers (phlorizin and SKF89976A). In the presence of the blockers, the Lp values of oocytes expressing SGLT1 and GAT1 were indistinguishable from the Lp of control oocytes. Passive Na+ transport (Na+ leak) was obtained from the blocker-sensitive Na+ currents in the absence of substrates (glucose and GABA). 2. Passive Na+ and water transport through SGLT1 were blocked by phlorizin with the same sensitivity (inhibitory constant (Ki), 3-5 microM). When Na+ was replaced with Li+, phlorizin also inhibited Li+ and water transport, but with a lower affinity (Ki, 100 microM). When Na+ was replaced by choline, which is not transported, the SGLT1 Lp was indistinguishable from that in Na+ or Li+, but in this case water transport was less sensitive to phlorizin. 3. The activation energies (Ea) for passive Na+ and water transport through SGLT1 were 21 and 5 kcal mol-1, respectively. The high Ea for Na+ transport is comparable to that of Na+-glucose cotransport and indicates that the process is dependent on conformational changes of the protein, while the low Ea for water transport is similar to that of water channels (aquaporins). 4. GAT1 also behaved as an SKF89976A-sensitive water channel. We did not observe passive Na+ transport through GAT1. 5. We conclude that passive water and Na+ transport through cotransporters depend on different mechanisms: Na+ transport occurs by a saturable uniport mechanism, and water permeation is through a low conductance water channel. In the case of SGLT1, we suggest that both the water channel and water cotransport could contribute to isotonic fluid transport across the intestinal brush border membrane.  (+info)

Sodium-glucose transport proteins (SGLTs) are a group of membrane transporters that facilitate the active transport of glucose across cell membranes in various tissues, including the kidneys and intestines. They function by coupling the movement of glucose molecules with sodium ions, using the energy generated by the sodium gradient across the membrane.

The two main types of SGLTs are:

1. SGLT1: This transporter is primarily found in the intestines and plays a crucial role in glucose absorption from food. It has a high affinity for glucose and transports it along with sodium ions, which helps create an electrochemical gradient that drives the transport process.

2. SGLT2: This transporter is mainly located in the early proximal tubules of the kidneys and is responsible for reabsorbing about 90% of the filtered glucose back into the bloodstream. It has a lower affinity for glucose compared to SGLT1 but operates at a higher transport rate, allowing it to efficiently reabsorb large amounts of glucose.

Inhibitors of SGLT2, known as SGLT2 inhibitors or gliflozins, have been developed for the treatment of type 2 diabetes. By blocking SGLT2-mediated glucose reabsorption in the kidneys, these medications promote urinary glucose excretion and help lower blood glucose levels. Examples of SGLT2 inhibitors include canagliflozin, dapagliflozin, and empagliflozin.

Sodium-Glucose Transporter 1 (SGLT1) is a protein found in the membrane of intestinal and kidney cells. It is responsible for the active transport of glucose and sodium ions from the lumen into the epithelial cells. In the intestine, SGLT1 plays a crucial role in glucose absorption after meals, while in the kidneys, it helps reabsorb glucose back into the bloodstream to prevent wasting through urine. The transport process is driven by the sodium gradient created by Na+/K+ ATPase, which actively pumps sodium ions out of the cell. SGLT1 inhibitors are used in the treatment of type 2 diabetes to reduce glucose reabsorption and enhance urinary glucose excretion, leading to better glycemic control.

Sodium-Glucose Transporter 2 (SGLT2) is a medically recognized term referring to a specific protein that plays a crucial role in the reabsorption of glucose in the kidneys. It is a type of membrane transport protein located in the proximal convoluted tubule of the nephron, where it actively transports glucose and sodium ions from the urine back into the bloodstream.

In healthy individuals, SGLT2 is responsible for reabsorbing about 90% of the filtered glucose, maintaining normal blood glucose levels. However, in certain medical conditions like diabetes, the amount of glucose in the blood can be significantly higher than normal. As a result, SGLT2 inhibitors have been developed as a class of medications to block this transporter's function, thereby increasing glucose excretion through urine and lowering blood glucose levels.

SGLT2 inhibitors are often prescribed in combination with other diabetes medications to help manage type 2 diabetes more effectively. Common SGLT2 inhibitors include canagliflozin, dapagliflozin, and empagliflozin.

Glucose Transporter Type 1 (GLUT1) is a specific type of protein called a glucose transporter, which is responsible for facilitating the transport of glucose across the blood-brain barrier and into the brain cells. It is encoded by the SLC2A1 gene and is primarily found in the endothelial cells of the blood-brain barrier, as well as in other tissues such as the erythrocytes (red blood cells), placenta, and kidney.

GLUT1 plays a critical role in maintaining normal glucose levels in the brain, as it is the main mechanism for glucose uptake into the brain. Disorders of GLUT1 can lead to impaired glucose transport, which can result in neurological symptoms such as seizures, developmental delay, and movement disorders. These disorders are known as GLUT1 deficiency syndromes.

Monosaccharide transport proteins are a type of membrane transport protein that facilitate the passive or active transport of monosaccharides, such as glucose, fructose, and galactose, across cell membranes. These proteins play a crucial role in the absorption, distribution, and metabolism of carbohydrates in the body.

There are two main types of monosaccharide transport proteins: facilitated diffusion transporters and active transporters. Facilitated diffusion transporters, also known as glucose transporters (GLUTs), passively transport monosaccharides down their concentration gradient without the need for energy. In contrast, active transporters, such as the sodium-glucose cotransporter (SGLT), use energy in the form of ATP to actively transport monosaccharides against their concentration gradient.

Monosaccharide transport proteins are found in various tissues throughout the body, including the intestines, kidneys, liver, and brain. They play a critical role in maintaining glucose homeostasis by regulating the uptake and release of glucose into and out of cells. Dysfunction of these transporters has been implicated in several diseases, such as diabetes, cancer, and neurological disorders.

Glucosides are chemical compounds that consist of a glycosidic bond between a sugar molecule (typically glucose) and another non-sugar molecule, which can be an alcohol, phenol, or steroid. They occur naturally in various plants and some microorganisms.

Glucosides are not medical terms per se, but they do have significance in pharmacology and toxicology because some of them may release the sugar portion upon hydrolysis, yielding aglycone, which can have physiological effects when ingested or absorbed into the body. Some glucosides are used as medications or dietary supplements due to their therapeutic properties, while others can be toxic if consumed in large quantities.

Glucose is a simple monosaccharide (or single sugar) that serves as the primary source of energy for living organisms. It's a fundamental molecule in biology, often referred to as "dextrose" or "grape sugar." Glucose has the molecular formula C6H12O6 and is vital to the functioning of cells, especially those in the brain and nervous system.

In the body, glucose is derived from the digestion of carbohydrates in food, and it's transported around the body via the bloodstream to cells where it can be used for energy. Cells convert glucose into a usable form through a process called cellular respiration, which involves a series of metabolic reactions that generate adenosine triphosphate (ATP)—the main currency of energy in cells.

Glucose is also stored in the liver and muscles as glycogen, a polysaccharide (multiple sugar) that can be broken down back into glucose when needed for energy between meals or during physical activity. Maintaining appropriate blood glucose levels is crucial for overall health, and imbalances can lead to conditions such as diabetes mellitus.

Phlorhizin is not a medical condition or term, but rather a chemical compound. It is a glucoside that can be found in the bark of apple trees and other related plants. Phlorhizin has been studied in the field of medicine for its potential effects on various health conditions. Specifically, it has been shown to inhibit the enzyme called glucose transporter 2 (GLUT2), which is involved in the absorption of glucose in the body. As a result, phlorhizin has been investigated as a potential treatment for diabetes, as it may help regulate blood sugar levels. However, more research is needed to fully understand its effects and safety profile before it can be used as a medical treatment.

Glucose Transporter Type 4 (GLUT4) is a type of glucose transporter protein that plays a crucial role in regulating insulin-mediated glucose uptake into cells, particularly in muscle and fat tissues. GLUT4 is primarily located in intracellular vesicles within these cell types and moves to the plasma membrane upon stimulation by insulin or muscle contraction, facilitating the influx of glucose into the cell. Dysfunction in GLUT4 regulation has been implicated in various metabolic disorders, including type 2 diabetes and insulin resistance.

Glucose Transporter Type 3 (GLUT3) is defined in medical terms as a specific type of glucose transporter protein, also known as solute carrier family 2, member 1 (SLC2A1). It is primarily found in the membranes of neurons and plays a crucial role in facilitating the transport of glucose from the extracellular space into the intracellular compartment of these cells. GLUT3 is notable for its high affinity for glucose, allowing it to effectively transport this essential energy source even under conditions of low glucose concentration. Its presence in neurons is particularly important, as these cells have a high demand for glucose to support their metabolic needs and maintain proper function.

Glycosuria is a medical term that refers to the presence of glucose in the urine. Under normal circumstances, the kidneys are able to reabsorb all of the filtered glucose back into the bloodstream. However, when the blood glucose levels become excessively high, such as in uncontrolled diabetes mellitus, the kidneys may not be able to reabsorb all of the glucose, and some of it will spill over into the urine.

Glycosuria can also occur in other conditions that affect glucose metabolism or renal function, such as impaired kidney function, certain medications, pregnancy, and rare genetic disorders. It is important to note that glycosuria alone does not necessarily indicate diabetes, but it may be a sign of an underlying medical condition that requires further evaluation by a healthcare professional.

Methylglucosides are not a medical term, but rather a chemical term referring to a type of compound known as glycosides, where a methanol molecule is linked to a glucose molecule. They do not have a specific medical relevance, but they can be used in various industrial and laboratory applications, including as sweetening agents or intermediates in chemical reactions.

However, if you meant "Methylglucamine," it is a related term that has medical significance. Methylglucamine is an organic compound used as an excipient (an inactive substance that serves as a vehicle or medium for a drug) in some pharmaceutical formulations. It is often used as a solubilizing agent to improve the solubility and absorption of certain drugs, particularly those that are poorly soluble in water. Methylglucamine is generally considered safe and non-toxic, although it can cause gastrointestinal symptoms such as diarrhea or nausea in some individuals if taken in large amounts.

Glucose Transporter Type 2 (GLUT2) is a protein responsible for the facilitated diffusion of glucose across the cell membrane. It is a member of the solute carrier family 2 (SLC2), also known as the facilitative glucose transporter family. GLUT2 is primarily expressed in the liver, kidney, and intestines, where it plays a crucial role in regulating glucose homeostasis.

In the pancreas, GLUT2 is found in the beta cells of the islets of Langerhans, where it facilitates the uptake of glucose from the bloodstream into the cells. Once inside the cell, glucose is metabolized, leading to an increase in ATP levels and the closure of ATP-sensitive potassium channels. This results in the depolarization of the cell membrane and the subsequent opening of voltage-gated calcium channels, allowing for the release of insulin from secretory vesicles into the bloodstream.

In the intestines, GLUT2 is expressed in the enterocytes of the small intestine, where it facilitates the absorption of glucose and other monosaccharides from the lumen into the bloodstream. In the kidneys, GLUT2 is found in the proximal tubules, where it plays a role in reabsorbing glucose from the filtrate back into the bloodstream.

Mutations in the gene that encodes GLUT2 (SLC2A2) can lead to several genetic disorders, including Fanconi-Bickel syndrome, which is characterized by impaired glucose and galactose absorption in the intestines, hepatic glycogen accumulation, and renal tubular dysfunction.

Glucose Transporter Proteins, Facilitative (GLUTs) are a group of membrane proteins that facilitate the passive transport of glucose and other simple sugars across the cell membrane. They are also known as solute carrier family 2 (SLC2A) members. These proteins play a crucial role in maintaining glucose homeostasis within the body by regulating the uptake of glucose into cells. Unlike active transport, facilitative diffusion does not require energy and occurs down its concentration gradient. Different GLUT isoforms have varying tissue distributions and substrate specificities, allowing them to respond to different physiological needs. For example, GLUT1 is widely expressed and is responsible for basal glucose uptake in most tissues, while GLUT4 is primarily found in insulin-sensitive tissues such as muscle and adipose tissue, where it mediates the increased glucose uptake in response to insulin signaling.

Sodium is an essential mineral and electrolyte that is necessary for human health. In a medical context, sodium is often discussed in terms of its concentration in the blood, as measured by serum sodium levels. The normal range for serum sodium is typically between 135 and 145 milliequivalents per liter (mEq/L).

Sodium plays a number of important roles in the body, including:

* Regulating fluid balance: Sodium helps to regulate the amount of water in and around your cells, which is important for maintaining normal blood pressure and preventing dehydration.
* Facilitating nerve impulse transmission: Sodium is involved in the generation and transmission of electrical signals in the nervous system, which is necessary for proper muscle function and coordination.
* Assisting with muscle contraction: Sodium helps to regulate muscle contractions by interacting with other minerals such as calcium and potassium.

Low sodium levels (hyponatremia) can cause symptoms such as confusion, seizures, and coma, while high sodium levels (hypernatremia) can lead to symptoms such as weakness, muscle cramps, and seizures. Both conditions require medical treatment to correct.

Hypoglycemic agents are a class of medications that are used to lower blood glucose levels in the treatment of diabetes mellitus. These medications work by increasing insulin sensitivity, stimulating insulin release from the pancreas, or inhibiting glucose production in the liver. Examples of hypoglycemic agents include sulfonylureas, meglitinides, biguanides, thiazolidinediones, DPP-4 inhibitors, SGLT2 inhibitors, and GLP-1 receptor agonists. It's important to note that the term "hypoglycemic" refers to a condition of abnormally low blood glucose levels, but in this context, the term is used to describe agents that are used to treat high blood glucose levels (hyperglycemia) associated with diabetes.

The jejunum is the middle section of the small intestine, located between the duodenum and the ileum. It is responsible for the majority of nutrient absorption that occurs in the small intestine, particularly carbohydrates, proteins, and some fats. The jejunum is characterized by its smooth muscle structure, which allows it to contract and mix food with digestive enzymes and absorb nutrients through its extensive network of finger-like projections called villi.

The jejunum is also lined with microvilli, which further increase the surface area available for absorption. Additionally, the jejunum contains numerous lymphatic vessels called lacteals, which help to absorb fats and fat-soluble vitamins into the bloodstream. Overall, the jejunum plays a critical role in the digestion and absorption of nutrients from food.

Deoxyglucose is a glucose molecule that has had one oxygen atom removed, resulting in the absence of a hydroxyl group (-OH) at the 2' position of the carbon chain. It is used in research and medical settings as a metabolic tracer to study glucose uptake and metabolism in cells and organisms.

Deoxyglucose can be taken up by cells through glucose transporters, but it cannot be further metabolized by glycolysis or other glucose-utilizing pathways. This leads to the accumulation of deoxyglucose within the cell, which can interfere with normal cellular processes and cause toxicity in high concentrations.

In medical research, deoxyglucose is sometimes labeled with radioactive isotopes such as carbon-14 or fluorine-18 to create radiolabeled deoxyglucose (FDG), which can be used in positron emission tomography (PET) scans to visualize and measure glucose uptake in tissues. This technique is commonly used in cancer imaging, as tumors often have increased glucose metabolism compared to normal tissue.

Biological transport refers to the movement of molecules, ions, or solutes across biological membranes or through cells in living organisms. This process is essential for maintaining homeostasis, regulating cellular functions, and enabling communication between cells. There are two main types of biological transport: passive transport and active transport.

Passive transport does not require the input of energy and includes:

1. Diffusion: The random movement of molecules from an area of high concentration to an area of low concentration until equilibrium is reached.
2. Osmosis: The diffusion of solvent molecules (usually water) across a semi-permeable membrane from an area of lower solute concentration to an area of higher solute concentration.
3. Facilitated diffusion: The assisted passage of polar or charged substances through protein channels or carriers in the cell membrane, which increases the rate of diffusion without consuming energy.

Active transport requires the input of energy (in the form of ATP) and includes:

1. Primary active transport: The direct use of ATP to move molecules against their concentration gradient, often driven by specific transport proteins called pumps.
2. Secondary active transport: The coupling of the movement of one substance down its electrochemical gradient with the uphill transport of another substance, mediated by a shared transport protein. This process is also known as co-transport or counter-transport.

Cytochalasin B is a fungal metabolite that inhibits actin polymerization in cells, which can disrupt the cytoskeleton and affect various cellular processes such as cell division and motility. It is often used in research to study actin dynamics and cell shape.

Blood glucose, also known as blood sugar, is the concentration of glucose in the blood. Glucose is a simple sugar that serves as the main source of energy for the body's cells. It is carried to each cell through the bloodstream and is absorbed into the cells with the help of insulin, a hormone produced by the pancreas.

The normal range for blood glucose levels in humans is typically between 70 and 130 milligrams per deciliter (mg/dL) when fasting, and less than 180 mg/dL after meals. Levels that are consistently higher than this may indicate diabetes or other metabolic disorders.

Blood glucose levels can be measured through a variety of methods, including fingerstick blood tests, continuous glucose monitoring systems, and laboratory tests. Regular monitoring of blood glucose levels is important for people with diabetes to help manage their condition and prevent complications.

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Effects of Sodium Glucose Co-Transporter 2 Inhibitors in Type 1 Diabetes Mellitus on Body Composition and Glucose Variabilities ... Effects of Sodium Glucose Co-Transporter 2 Inhibitors in Type 1 Diabetes Mellitus on Body Composition and Glucose Variabilities ...
Sotaglifozin is a sodium-glucose co-transporter 1 and 2 inhibitor that reduces both postprandial glucose and insulin levels by ... a dual sodium-dependent glucose transporter 1/2 inhibitor". Diabetes & Vascular Disease Research. 12 (2): 101-10. doi:10.1177/ ... Sotagliflozin Decreases Postprandial Glucose and Insulin Concentrations by Delaying Intestinal Glucose Absorption. The Journal ... 18 (1): 20. doi:10.1186/s12933-019-0828-y. PMC 6393994. PMID 30819210. Lapuerta P, Zambrowicz B, Strumph P, Sands A (March 2015 ...
... the sodium-glucose co-transporter 2 (SGLT2) inhibitors, and pioglitazone. Those are the three drugs that I use in combination ... and a new class of drugs that dont lower glucose, but finerenone, which is effective in providing protection against ... Weve also learned from the Diabetes Control and Complications Trial (DCCT) in patients with type 1 diabetes and from the ... From the standpoint of renal disease, we also now have very strong data with the SGLT2 inhibitors, emerging data from the GLP-1 ...
Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature 514, 181-186 (2014). This study ... High-dose saccharin supplementation does not induce gut microbiota changes or glucose intolerance in healthy humans and mice. ... Personalized microbiome-driven effects of non-nutritive sweeteners on human glucose tolerance. Cell 185, 3307-3328 (2022). ... A cluster of physiological conditions - including excess visceral fat, high fasting glucose, high triglycerides, low HDL ...
... a sodium-glucose co-transporter 2 inhibitor developed, has been shown to reduce cardiovascular events in patients with type 2 ... Empagliflozin, a sodium-glucose co-transporter 2 inhibitor developed, has been shown to reduce cardiovascular events in ... Off-target effects of sodium-glucose co-transporter 2 blockers: empagliflozin does not inhibit Na+/H+ exchanger-1 or lower [Na+ ... Lopaschuk, G. D. & Verma, S. Mechanisms of cardiovascular benefits of sodium glucose co-transporter 2 (SGLT2) inhibitors: a ...
Dual inhibitor of selective sodium-glucose transporters 1 and 2 (SGLT1 and SGLT2) ... Inhibiting SGLT2 reduces renal reabsorption of glucose and sodium which may influence several physiological functions, such as ... Inhibiting SGLT1 reduces intestinal absorption of glucose and sodium which likely contributes to diarrhea ... Urine glucose tests are not recommended in patients taking SGLT2 inhibitors, as SGLT2 inhibitors increase urinary glucose ...
... angiotensin receptor-neprilysin inhibitors and sodium-glucose co-transporter 2 inhibitors) [1]. Due to small numbers in patient ... Table 1 Baseline clinical and demographic characteristics of the study population by American College of Cardiology/American ... 1). Even at stages A or B, , 20% of the patients had CKD (Table 1), and prevalence rose with each stage (to , 50% at stages C2/ ... 1. Prevalence of chronic kidney disease (CKD) and/or anaemia by American Heart Association/American College of Cardiology (ACC/ ...
... analogs or sodium-glucose-linked transporter-2 [SGLT-2] inhibitors) are suggested, in addition to the first-line agent for type ... Fasting glucose and HgA1c were also lower at 3 years in the duodenal switch group. [200] ... Ketone bodies tend to be generated when an individuals daily dietary carbohydrate intake is under 50 g, and sodium diuresis is ... Mingrone et al reported regression of diabetes (defined as fasting glucose , 100 mg/dL and hemoglobin A1c [HbA1c] , 6.5% in the ...
Inhibition of the intestinal sodium-coupled glucose transporter 1 (SGLT1) by extracts and polyphenols from apple reduces ... Taking apple polyphenols before a meal might cause blood glucose levels to rise more slowly after a meal. Using insulin before ... Apple polyphenol-rich drinks dose-dependently decrease early-phase postprandial glucose concentrations following a high- ... 2019;11(1). pii: E163. View abstract.. Soriano-Maldonado A, Hidalgo M, Arteaga P, de Pascual-Teresa S, Nova E. Effects of ...
Polyphenols and phenolic acids from strawberry and apple may decrease glucose uptake by blocking transport through human ... By using sodium-containing (to activate both SGLT1 and GLUT2 glucose transporters) and sodium-free (activating GLUT2 only) ... inhibition of sodium-dependent glucose transporter 1 (SGLT1 - an active transport mechanism in which glucose is co-transported ... Glucose regulation​. Repeated high post meal (post-prandial) blood plasma glucose spikes are associated with an increased ...
... nonproliferative diabetic retinopathy to proliferative disease or diabetic macular edema than those who took sodium-glucose ... Patients taking glucagon-like peptide-1 agonists were more likely to progress from ... SEATTLE - A family of blockbuster drugs for managing blood glucose - and now for promoting weight loss - has been linked to ... Whether worsening of retinopathy stems from rapid weight loss and acute reductions in concentrations of blood glucose or is a ...
Specifically, we will quantify population-level use of two classes of glucose-lowering agents: Sodium-glucose co-transporter 2 ... We know both these classes of glucose-lowering agents vastly reduce cardiovascular death and improve heart and kidney outcomes ... inhibitors (SGLT2i) and glucagon-like peptide-1 analogues (GLP-1A). We will map out how these are being used relative to the ...
Carbohydrates, such as glucose, are absorbed into the body via a specific transporter called sodium-glucose cotransporter 1, or ... These transporters act as a conveyor belt for glucose and sodium, moving them across the small intestine without the need for ... For every single glucose molecule (and 2 sodium molecules) that is moved by SGLUT1, 260 water molecules are moved with it (Loo ... As carbohydrate and sodium is moved through the SGLUT1 transporter, it also drags with it large volumes of fluid, significantly ...
... is an oral dual inhibitor of two proteins responsible for glucose regulation known as sodium-dependent glucose co-transporter ... which are responsible for glucose absorption in the gastrointestinal tract, and glucose reabsorption by the kidney, ...
Sodium-dependent glucose transporter 1 and glucose transporter 2 mediate intestinal transport of quercetrin (Li et al. 2020). ... Sodium/glucose cotransporter 2 (Na+/glucose cotransporter 2; SGLT2) of 672 aas and 14 TMSs. It is a low affinity sodium-glucose ... Low affinity sodium-glucose cotransporter (Sodium/glucose cotransporter 3) (Na+/glucose cotransporter 3) (Solute carrier family ... Sodium-coupled monocarboxylate transporter 2 (Electroneutral sodium monocarboxylate cotransporter) (Low-affinity sodium-lactate ...
Epithelial Sodium Channels *Equilibrative Nucleoside Transporters *ER *ErbB *ERK *ERR *Esterases *Estrogen (GPR30) Receptors ... GLP-1 or sodium-glucose co-transporter 2 inhibitors, or pioglitazone found in the treating Bosutinib type 2 diabetes (as ...
... and glucose transporter (GLUT2) in the intestinal mucosa (P < 0.05). Our results suggested a novel function of the ... Moreover, BMGlvA2 significantly down-regulated the expression levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and the ... Sodium-dependent glucose transporter-1; GLUT-2: Glucose transporter-2; Caspase8, cysteinyl aspartate specific proteinase 8; ... and glucose transporter (GLUT2) in the intestinal mucosa (P , 0.05).. Conclusion. Our results suggested a novel function of the ...
... sodium-dependent glucose transporter 1; SI: sucrase-isomaltase; T2DM: type 2 diabetes mellitus; TNFα: tumor necrosis factor-α. ... sodium-dependent glucose transporter 1; SI: sucrase-isomaltase; T2DM: type 2 diabetes mellitus; TNFα: tumor necrosis factor-α. ... 2; CFTR: cystic fibrosis transmembrane conductance regulator; TG: triacylglycerol; FA: fatty acid; GLUT4: glucose transporter ... 2; CFTR: cystic fibrosis transmembrane conductance regulator; TG: triacylglycerol; FA: fatty acid; GLUT4: glucose transporter ...
Sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 agonists (GLP1a) have cardiovascular benefit, ... Cost-effectiveness of Sodium-Glucose Cotransporter-2 Inhibitors for Patients With Heart Failure and Preserved Ejection Fraction ... and sodium-glucose cotransporter 2 inhibitor in the early stage would prevent the progression and morbidity of HF. Concurrently ... Immune thrombocytopenia Hospital Medicine Clinics Ma, I., Sandhu, A. T. 2016; 6 (1): 53-66 View details for DOI 10.1016/j.ehmc. ...
UK Kidney association clinical practice guideline: sodium-glucose co-transporter-2 (SGLT-2) inhibition in adults with kidney ... UK Kidney association clinical practice guideline: sodium-glucose co-transporter-2 (SGLT-2) inhibition in adults with kidney ...
Sodium-glucose co-transporter 2 (SGLT2) inhibitors are agents that reduce the level of blood glucose in these patients. In the ... Sodium-glucose co-transporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) agonists should be included in the ... Of these, sodium-glucose co-transporter-2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) agonists represent novel ... Clinical outcomes of sodium-glucose co-transporter 2 (SGLT2) inhibitors in cardiovascular treatment. Despite the prevalence of ...
Type I, Type II, Artificial Pancreas, Drugs, Glucose & Insulin, Lifestyle & Diet, Medical Research, and Other News. ... Sotagliflozin is an investigational drug that belongs to the class of medications known as sodium-glucose co-transporter 1 and ... A recent study says that the access of people with type 2 diabetes to sodium-glucose cotransporter 2 (SGLT2) inhibitor ... July 22, 2021 Glucose & Insulin GLP-1 RA Medications and the Heart. GLP-1 RAs are a class of diabetes medication that includes ...
A dolgozat eredm nyei szerint 2014-2016 k z tt haz nkban az antidiabetikus ter pia intenzifik l sakor a DPP-4-g tl k 1 s 2 ves ... 1% volt. A dolgozatban az letkori dek dok szerinti perzisz... ... Sodium-Glucose Co-Transporter-2 Inhibitors, and Glucagon-Like ... perzisztenci ja 69,6% s 57,3%, az SGLT-2-g tl k 67,8% s 56,8%, m g a GLP-1-receptoragonist k 66,3% s 52, ... A dolgozat eredm nyei szerint 2014-2016 k z tt haz nkban az antidiabetikus ter pia intenzifik l sakor a DPP-4-g tl k 1 s 2 ves ...
... both active and passive intestinal glucose absorption by upregulating the expression of sodium-dependent glucose transporter ... The sodium-restricted diet group received a regimen aiming a maximum intake of 3 g of sodium per day (equivalent to 7.5 g of ... Its also worth asking whether sodium was the only important dietary change, or if avoiding sodium caused many other dietary ... glucose] and isomaltotriose from the glucoamylase-catalyzed condensation of glucose. If Im understanding this correctly, all I ...
Sodium-glucose cotransporter 1 as a sugar taste sensor in mouse tongue. Yasumatsu, K., Ohkuri, T., Yoshida, R., Iwata, S., ... The sweet taste receptor, glucose transporters, and the ATP-sensitive K+ (KATP) channel: sugar sensing for the regulation of ... Takai, S., Yoshida, R., Yasumatsu, K., Shigemura, N. & Ninomiya, Y., Feb 1 2016, In: journal of oral biosciences. 58, 1, p. 10- ... Niki, M., Jyotaki, M., Yoshida, R., Yasumatsu, K., Shigemura, N., DiPatrizio, N. V., Piomelli, D. & Ninomiya, Y., Jun 1 2015, ...

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