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Glucose Transporters In Diabetes

Type 2 (non-insulin-dependent) Diabetes Mellitus And Glucose Transporter Gene (glut 1 Andglut 4) Polymorphism

Type 2 (non-insulin-dependent) Diabetes Mellitus And Glucose Transporter Gene (glut 1 Andglut 4) Polymorphism

Abstract Glucose transporter genes have been proposed as candidate genes for type 2 (non-insulin-dependent) diabetes mellitus. We chose to study the adult skeletal muscle glucose transporter gene (GLUT 4) andGLUT 1 in consideration of previous conflicting results obtained by different authors. We studied 68 patients with type 2 diabetes, and 66 non-diabetic controls matched for age, sex, and body mass index (BMI). Women and men were considered separately, according to BMI (≤24.0 and >24.0 for women; ≤25.0 and >25.0 for men). Allele and genotype frequencies were not significantly different in controls and in type 2 diabetic patients. ForGLUT 1 allele 1 and genotype x1x1 were more frequent, although not significantly (P=0.064 at χ2,P=0.025 at Fisher exact test) in overweight/obese diabetic women than in overweight/obese non-diabetic women. These data do not support the hypothesis that these genes play a major role in genetic susceptibility to type 2 diabetes mellitus, but suggest a possible association, at least in women, of allele 1 ofGLUT 1 with obese type 2 diabetes mellitus. Preview Unable to display preview. Download preview PDF. Continue reading >>

Glucose Transporter

Glucose Transporter

Glucose 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. Synthesis of free glucose[edit] 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. Glucose transport in yeast[edit] In Saccharomyces cerevisiae glucose transport takes place through facilitated diffusion.[1] The transport proteins are mainly from the Hxt family, but many other transporters have been identified.[2] Name Properties Notes Snf3 low-glucose sensor; repressed by glucose; low expression level; repressor of Hxt6 Rgt2 high-glucose sensor; low expression level Hxt1 Km: 100 mM,[3] 129 - 107 mM[1] low-affinity glucose transporter; induced by high glucose level Hxt2 Km = 1.5[1] - 10 mM[3] high/intermediate-affinityglucose transporter; induced by low glucose level[3] Hxt3 Vm = 18.5, Kd = 0.078, Km = 28.6/34.2[1] - 60 mM[3] low-affinity glucose transporter[3] Hxt4 Vm = 12.0, Kd = 0.049, Km = 6.2[1] intermediate-affinity glucose transporter[3] Hxt5 Km = 10 mM[4] Moderate glucose affinity. Abundant during stationary phase, sporulation and low glucose conditions. Transcription repressed by glucose.[4] Hxt6 Vm = 11.4, Kd = 0.029, Km = 0.9/14,[1] 1.5 mM[3] Continue reading >>

Glucose Transport

Glucose Transport

The oxidation of glucose represents a major source of metabolic energy for mammalian cells. Because the plasma membrane is impermeable to polar molecules such as glucose, the cellular uptake of this important nutrient is accomplished by special carrier proteins called glucose transporters[1][2][3][4][5][6][7]. These are integral membrane proteins located in the plasma membrane that bind glucose and transfer it across the lipid bilayer. The rate of glucose transport is limited by the number of glucose transporters on the cell surface and the affinity of the transporters for glucose. There are two classes of glucose carriers described in mammalian cells: the Na+-glucose cotransporters (SGLTs) and the facilitative glucose transporters (GLUTs)[1-7]. There are two families of glucose transporters The Na+-glucose cotransporter or symporter is expressed by specialized epithelial (brush border) cells of the small intestine and the proximal tubule of the kidney and mediates an active, Na+-linked transport process against an electrochemical gradient[1-3] . It actively transports glucose from the lumen of the intestine or the nephron against its concentration gradient by coupling glucose uptake with that of Na+, which is being transported down its concentration gradient. The Na+ gradient is maintained by the active transport of Na+ across the basolateral (antiluminal) surface of the brush border cells by membrane-bound Na+-K+- ATPase[1-3,7]. The second class of glucose carriers is the facilitative glucose transporters (GLUTs) of which there are 14 genes in the human genome[1,4-7] . These proteins mediate a bidirectional and energy-independent process of glucose transport in most tissues and cells where glucose is transported down its concentration gradient by facilitative diffusio Continue reading >>

Enhancement Of Glucose Transport By Vascular Endothelial Growth Factor In Retinal Endothelial Cells | Iovs | Arvo Journals

Enhancement Of Glucose Transport By Vascular Endothelial Growth Factor In Retinal Endothelial Cells | Iovs | Arvo Journals

Enhancement of Glucose Transport by Vascular Endothelial Growth Factor in Retinal Endothelial Cells From the Department of Internal Medicine and From the Department of Internal Medicine and From the Department of Internal Medicine and Michigan Diabetes Research and Training Center, University of Michigan Medical School, Ann Arbor. Investigative Ophthalmology & Visual Science June 2000, Vol.41, 1876-1884. doi: Enhancement of Glucose Transport by Vascular Endothelial Growth Factor in Retinal Endothelial Cells You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Hirohito Sone, Baljit K. Deo, Arno K. Kumagai; Enhancement of Glucose Transport by Vascular Endothelial Growth Factor in Retinal Endothelial Cells. Invest. Ophthalmol. Vis. Sci. 2000;41(7):1876-1884. ARVO (1962-2015); The Authors (2016-present) purpose. To investigate effects of vascular endothelial growth factor (VEGF) onglucose transport and GLUT1 glucose transporter expression in primarybovine retinal endothelial cell (BREC) cultures. methods. Glucose transport in control and VEGF-treated BREC cultures wasdetermined by measurement of[ 14C]-3-O-methylglucose (3MG) uptake.GLUT1 protein and mRNA was determined by Western and Northern blotanalyses, respectively. Protein kinase C (PKC) activity was measured incontrol and VEGF-treated cultures, and glucose transport was determinedwith and without prior PKC depletion and PKC inhibition. results. Dose-dependent increases in 3MG uptake were seen in the VEGF-treatedcultures, with an increase of 69% after a 24-hour exposure to 50 ng/mlVEGF (P < 0.001). Total cellular GLUT1 mRNA orprotein, however, was unchanged. Western blot analysis of plasmamembrane fractions revealed a Continue reading >>

Pathway To Diabetes Through Attenuation Of Pancreatic Beta Cell Glycosylation And Glucose Transport

Pathway To Diabetes Through Attenuation Of Pancreatic Beta Cell Glycosylation And Glucose Transport

Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport Nature Medicine volume 17, pages 10671075 (2011) A connection between diet, obesity and diabetes exists in multiple species and is the basis of an escalating human health problem. The factors responsible provoke both insulin resistance and pancreatic beta cell dysfunction but remain to be fully identified. We report a combination of molecular events in human and mouse pancreatic beta cells, induced by elevated levels of free fatty acids or by administration of a high-fat diet with associated obesity, that comprise a pathogenic pathway to diabetes. Elevated concentrations of free fatty acids caused nuclear exclusion and reduced expression of the transcription factors FOXA2 and HNF1A in beta cells. This resulted in a deficit of GnT-4a glycosyltransferase expression in beta cells that produced signs of metabolic disease, including hyperglycemia, impaired glucose tolerance, hyperinsulinemia, hepatic steatosis and diminished insulin action in muscle and adipose tissues. Protection from disease was conferred by enforced beta cellspecific GnT-4a protein glycosylation and involved the maintenance of glucose transporter expression and the preservation of glucose transport. We observed that this pathogenic process was active in human islet cells obtained from donors with type 2 diabetes; thus, illuminating a pathway to disease implicated in the diet- and obesity-associated component of type 2 diabetes mellitus. Subscribe to Nature Medicine for full access: Olefsky, J.M. & Courtney, C.H. Type 2 diabetes mellitus: etiology, pathogenesis and natural history. in Endocrinology 5th edn (eds. DeGroot, L.J. et al.) 10931117 (W.B. Saunders, 2005). Pathogenesis of non-insulin dependent (typ Continue reading >>

Biochemistry/regulation Of Glucose Transporter Translocator In Health And Diabetes

Biochemistry/regulation Of Glucose Transporter Translocator In Health And Diabetes

Due to the high level of biological importance that glucose plays in providing energy and a readily usable source of carbon, the mechanism of the transportation of glucose has elicited interest in the labs of researchers. For half a century scientists have been aware of insulin’s role in the uptake of glucose in the blood into surrounding tissues; more recently, however, scientists have pondered over what causes insulin-resistance. This study proposes that the mechanism of glucose transport involves the GLUT4 glucose transporter being stimulated by insulin, causing it to relocate and be absorbed into tissues. However, this mechanism is proposed to be negatively affected in the scenario of an excess of glucose that results from a consistently high calorie diet. NMR spectroscopy has confirmed that the extent in which insulin can cause glucose to be transported into the cell is impaired in cases of patients with type 2 diabetes. Some scientists have suggested that this could be the result of overloading a system that has evolved and favored the ability to maintain a storage of energy; that is, the body is unsure what to do in a situation of “over-nutrition” because it has adapted to survive in situations of unpredictable food availability. The body obtains its energy from the food it consumes, which is broken down into its simplest components. In the case of complex carbohydrates, the large polymers are broken down into glucose. The presence of glucose in the blood causes the release of the hormone insulin, which is secreted from the beta cells of the pancreas. Once in the bloodstream, insulin signal s the cells to store glucose as glycogen, which can be accessed as needed. When the cells need access to this energy storage deposit, the hormone glucagon is released, s Continue reading >>

Glucose Transporters In Diabetic Nephropathy

Glucose Transporters In Diabetic Nephropathy

Glucose transporters in diabetic nephropathy Changes in glucose transporter expression in glomerular cells occur early in diabetes. These changes, especially the GLUT1 increase in mesangial cells, appear to play a pathogenic role in the development of ECM expansion and perhaps other features of diabetic nephropathy. In addition, it appears that at least some diabetic patients may be predisposed to(More) American journal of physiology. Renal physiology American journal of physiology. Renal physiology Evidence for a novel TGF - b 1 - independent mechanism of fibrosis in mesangial cells overexpressing glucose transporters An - tisense - GLUT 1 protects mesangial cells from d - glucose - induced transporter and fibronectin expression P Gunning, J Leavitt, G Muscat, SY Ng, L Kedes Genetic variation of glucose transporter-1 (GLUT1) and albuminuria in the atherosclerosis risk in communities study. Diabetes 53:A200 (abstract Transcriptional control of metabolic regulation genes by carbohydrates Human podocytes rapidly utilize glucose by both GLUT 1 and GLUT 4 in response to insulin , with significant differences in glucose transporter levels occurring in diabetic nephropathy M Schiffer, M Ranalletta, K Susztak, JM Charron, EP Bottinger Localization of the GLUT 8 glucose transporter in the kidney and regulation in vivo in non - diabetic and diabetic conditions Continue reading >>

Pdb-101: Glucose Transporters

Pdb-101: Glucose Transporters

Glucose transporters deliver glucose molecules one-by-one across cell membranes. GLUT3 is shown on the left in the open outward conformation, and GLUT1 is shown on the right in an open inward conformation. Glucose is the fuel that powers most of the biosphere. Plants build it using energy from the sun, store it in starches and use it to build their infrastructure of cellulose. The glucose we eat is broken down through glycolysis and used to power the many processes of our cells. Thus, it is essential to supply each of our cells with a steady stream of glucose. Glucose is delivered throughout the body by the blood, and each cell gathers what it needs using glucose transporters. Glucose transporters manage the traffic of glucose across the cell's outer membrane. They act by alternating between two states. First, the transporter has an opening facing the outside of the cell, and it picks up a molecule of glucose. Then it shifts shape, and opens towards the inside, releasing glucose into the cell. Glucose transporters generally act passively: since glucose is rapidly phosphorylated by hexokinase , the concentration of free glucose in the cytoplasm is generally very low, and the higher concentration of glucose in the blood drives transport of glucose into the cell. The human genome encodes 14 similar transporters that deliver glucose and other sugars into different types of cells. For instance, GLUT1 (shown here from PDB entry 4pyp ) manages the basal levels of glucose uptake and is very common in red blood cells. GLUT2 helps control the flow of glucose in and out of liver cells, and pancreatic beta cells use it to monitor the level of glucose in the blood, releasing insulin when the level rises. Nerve cells in the brain require a constant supply of glucose, so they use GLU Continue reading >>

Role Of Glucose Transport Proteins In Diabetes Mellitus Garvey, W Timothy Indiana University-purdue University At Indianapolis, Indianapolis, In, United States

Role Of Glucose Transport Proteins In Diabetes Mellitus Garvey, W Timothy Indiana University-purdue University At Indianapolis, Indianapolis, In, United States

Role of Glucose Transport Proteins in Diabetes Mellitus Insulin resistance is central to the pathogenesis of Type II diabetes (NIDDM), and is largely due to decreased activity of the glucose transport system in target tissue. However, the mechanisms responsible for reduced transport activity are unknown. In pre- liminary studies, we found both cellular depletion and impaired function of glucose transport proteins causing insulin resistance in adipocytes isolated from these patients. Therefore, in the current proposal, we will extensively examine the role of glucose transporters in the cellular insulin resistance of NIDDM, by measuring their number, structure, function, and regulation in target tissue. In adipocytes from control and NIDDM subjects, we will use both cytochalasin B binding and immunologic methods to measure the number and cellular distribution of transporters under basal conditions as well as insulin's ability to recruit intracellular carriers to the cell-surface. Function will be assessed by correlating numbers of cell-surface transporters with glucose transport rates in intact cells, and by correlating glucose transporter number and functional activity of transporters isolated from various subcellular and membrane fractions and then reconstituted into synthetic phospholipid vesicles. The Km and Vmax of substrate uptake will also be measured in whole cells since defects in these functional parameters have mechanistic implications. To test for structural abnormalities, we will combine SDS-PAGE and isoelectric focusing to determine the MW, charge heterogeneity, and extent of post-translational glycosylation of photolabeled transporters, as well as measure the non-enzymatic glycosylation of transporters using an antibody specific for glycosyl-lysine adducts Continue reading >>

Regulation Of Glucose Transporters In Diabetes.

Regulation Of Glucose Transporters In Diabetes.

Regulation of glucose transporters in diabetes. Metabolic Unit, Rambam Medical Center, Haifa, Israel. It is now widely accepted that insulin stimulates glucose metabolism in its target tissues via recruitment of transporters from a large intracellular pool to the plasma membrane. Recent studies, however, suggest a two-step model for insulin action, of transporter translocation and transporter activation. Data confirming this hypothesis for the first time are presented. It is shown that insulin significantly enhances the intrinsic activity of glucose transporters in human and rat adipose cells, in physiological as well as in diabetic state. The functional activity of transporters is impaired in the diabetic state, but surprisingly, 'diabetic' transporters exhibit normal or even enhanced intrinsic activity. In both noninsulin-dependent diabetes mellitus and streptozotocin-diabetic rats, insulin resistance is associated with 50% transporter depletion in the intracellular pool, thus leading to a decreased number of transporters appearing in the plasma membrane in response to insulin. It is concluded that impaired glucose transport in diabetes is secondary (1) to intracellular transporter depletion, and (2) to the presence of inhibitory factors interfering with the full expression of glucose transporters at the plasma membrane, thus contributing to postreceptor insulin resistance. Continue reading >>

A High Fat Diet Impairs Stimulation Of Glucose Transport In Muscle

A High Fat Diet Impairs Stimulation Of Glucose Transport In Muscle

A High Fat Diet Impairs Stimulation of Glucose Transport in Muscle FUNCTIONAL EVALUATION OF POTENTIAL MECHANISMS * A high fat diet causes resistance of skeletal muscle glucose transport to insulin and contractions. We tested the hypothesis that fat feeding causes a change in plasma membrane composition that interferes with functioning of glucose transporters and/or insulin receptors. Epitrochlearis muscles of rats fed a high (50% of calories) fat diet for 8 weeks showed 50% decreases in insulin- and contraction-stimulated 3-O-methylglucose transport. Similar decreases in stimulated glucose transport activity occurred in muscles of wild-type mice with 4 weeks of fat feeding. In contrast, GLUT1 overexpressing muscles of transgenic mice fed a high fat diet showed no decreases in their high rates of glucose transport, providing evidence against impaired glucose transporter function. Insulin-stimulated system A amino acid transport, insulin receptor (IR) tyrosine kinase activity, and insulin-stimulated IR and IRS-1 tyrosine phosphorylation were all normal in muscles of rats fed the high fat diet for 8 weeks. However, after 30 weeks on the high fat diet, there was a significant reduction in insulin-stimulated tyrosine phosphorylation in muscle. The increases in GLUT4 at the cell surface induced by insulin or muscle contractions, measured with the 3H-labeled 2-N-4-(1-azi-2,2,2-trifluoroethyl)-benzoyl-1,3-bis-(d-mannose-4-yloxy)-2-propylamine photolabel, were 2636% smaller in muscles of the 8-week high fat-fed rats as compared with control rats. Our findings provide evidence that (a) impairment of muscle glucose transport by 8 weeks of high fat feeding is not due to plasma membrane composition-related reductions in glucose transporter or insulin receptor function, (b) a defect Continue reading >>

Payperview: Glucose Transporters: Their Abnormalities And Significance In Type 2 Diabetes And Cancer - Karger Publishers

Payperview: Glucose Transporters: Their Abnormalities And Significance In Type 2 Diabetes And Cancer - Karger Publishers

I have read the Karger Terms and Conditions and agree. Glucose, the major substrate for energy production in mammalian cells, is transported into the cell via facilitative glucose transporters (GLUT). The GLUT family consists of 14 members, which differ in their tissue distribution and substrate specificity. Expression of several GLUTs is controlled by hormones and environmental factors and differential expression is involved in various disease states such as diabetes and cancer. Insulin-stimulated glucose uptake in skeletal muscle and adipose tissue is critical for reducing post-prandial blood glucose concentrations and the dysregulation of this process is one hallmark of insulin resistance and type 2 diabetes. Type 2 diabetes is also associated with -cell failure that is characterized by the inability to secrete sufficient insulin in response to glucose. Impairment in glucose-sensing contributes to -cell dysfunction. GLUT2, and the glucose phosphorylating enzyme glucokinase, are key elements for glucose-sensing of the pancreatic -cell, the initial event in the pathway for glucose-stimulated insulin secretion. In the insulin-resistant state, e.g. induced by a high-fat diet, expression of both GLUT2 and glucokinase is reduced thereby impairing glucose-stimulated insulin secretion. The majority of cancers and isolated cancer cell lines overexpress the GLUT family members which are present in the respective tissue of origin under non-cancerous conditions. Moreover, due to the requirement of energy to feed uncontrolled proliferation, cancer cells often express GLUT proteins which would not be present in these tissues under normal conditions. This overexpression is predominantly associated with the likelihood of metastasis and hence poor patient prognosis. Continue reading >>

Glucose And Lipid Transporters Roles In Type 2 Diabetes

Glucose And Lipid Transporters Roles In Type 2 Diabetes

Glucose and Lipid Transporters Roles in Type 2 Diabetes San Diego Supercomputer Center, UC San Diego, USA These authors contributed equally to this work. These authors contributed equally to this work. San Diego Supercomputer Center, UC San Diego, USA Department of Neurosciences, UC San Diego, USA Type 2 diabetes is a chronic condition encompassing many metabolic processes throughout the body. Glucose and lipid transporters are involved in many of these critical metabolic processes and pathways, and are linked to the development and symptoms of type 2 diabetes. Therapeutic opportunities utilizing these transporters have already begun with the gliflozin drug class of inhibitors of sodium glucose linked co-transporters (SGLT). A range of transporter families: SLC5A (SGLT), SLC2A (GLUT), and ATP binding cassette (ABC) transporters are either connected to glucose or cholesterol homeostasis, significant in a systemic disease like diabetes type 2. Elucidating the roles of these transporters in type 2 diabetes is vital in establishing new and effective options for treatment. Sodium glucose linked co-transporters (SGLT) Sodium glucose linked co-transporters (SGLT) are members of the large solute carrier family of membrane transporter proteins (SLC). The SLC family contains hundreds of members and has three main families involved in glucose transport: SLC2, SLC5, and SLC50. Specifically, the SGLT class of transporters are encoded by the SLC5 gene type. There are twelve different transporter proteins encoded by the SLC5 genes, with six of them going under the alias of SGLT. The SLC5 family (Table 1) are membrane transporters with nearly all being involved in forms of glucose transport and homeostasis, transporting sugars such as glucose, mannose, and myo inositol and located in Continue reading >>

Regulation Of Glucose Transporter Translocation In Health And Diabetes

Regulation Of Glucose Transporter Translocation In Health And Diabetes

Regulation of Glucose Transporter Translocation in Health and Diabetes Vol. 81:507-532 (Volume publication date July 2012) First published online as a Review in Advance on April 5, 2012 Section of Endocrinology and Metabolism, Department of Internal Medicine, and Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06520-8020; email: [emailprotected] To enhance glucose uptake into muscle and fat cells, insulin stimulates the translocation of GLUT4 glucose transporters from intracellular membranes to the cell surface. This response requires the intersection of insulin signaling and vesicle trafficking pathways, and it is compromised in the setting of overnutrition to cause insulin resistance. Insulin signals through AS160/Tbc1D4 and Tbc1D1 to modulate Rab GTPases and through the Rho GTPase TC10 to act on other targets. In unstimulated cells, GLUT4 is incorporated into specialized storage vesicles containing IRAP, LRP1, sortilin, and VAMP2, which are sequestered by TUG, Ubc9, and other proteins. Insulin mobilizes these vesicles directly to the plasma membrane, and it modulates the trafficking itinerary so that cargo recycles from endosomes during ongoing insulin exposure. Knowledge of how signaling and trafficking pathways are coordinated will be essential to understanding the pathogenesis of diabetes and the metabolic syndrome and may also inform a wide range of other physiologies. The Cas9 protein (CRISPR-associated protein 9), derived from type II CRISPR (clustered regularly interspaced short palindromic repeats) bacterial immune systems, is emerging as a powerful tool for engineering the genome in diverse organisms. As an RNA-... Read More Figure 1: CRISPR-associated protein 9 (Cas9)-mediated sequence-specific genomic editing. (a) Co Continue reading >>

Frontiers | Glucose Transporters In Diabetic Kidney Diseasefriends Or Foes? | Endocrinology

Frontiers | Glucose Transporters In Diabetic Kidney Diseasefriends Or Foes? | Endocrinology

Front. Endocrinol., 09 April 2018 | Glucose Transporters in Diabetic Kidney DiseaseFriends or Foes? Department of Pathology, University of Helsinki, Helsinki, Finland Diabetic kidney disease (DKD) is a major microvascular complication of diabetes and a common cause of end-stage renal disease worldwide. DKD manifests as an increased urinary protein excretion (albuminuria). Multiple studies have shown that insulin resistance correlates with the development of albuminuria in non-diabetic and diabetic patients. There is also accumulating evidence that glomerular epithelial cells or podocytes are insulin sensitive and that insulin signaling in podocytes is essential for maintaining normal kidney function. At the cellular level, the mechanisms leading to the development of insulin resistance include mutations in the insulin receptor gene, impairments in the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway, or perturbations in the trafficking of glucose transporters (GLUTs), which mediate the uptake of glucose into cells. Podocytes express several GLUTs, including GLUT1, GLUT2, GLUT3, GLUT4, and GLUT8. Of these, the most studied ones are GLUT1 and GLUT4, both shown to be insulin responsive in podocytes. In the basal state, GLUT4 is preferentially located in perinuclear and cytosolic vesicular structures and to a lesser extent at the plasma membrane. After insulin stimulation, GLUT4 is sorted into GLUT4-containing vesicles (GCVs) that translocate to the plasma membrane. GCV trafficking consists of several steps, including approaching of the GCVs to the plasma membrane, tethering, and docking, after which the lipid bilayers of the GCVs and the plasma membrane fuse, delivering GLUT4 to the cell surface for glucose uptake into the cell. Studies have revealed novel molecular Continue reading >>

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