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Sodium Glucose Transporter Mechanism

Cell And Molecular Biology Of Na+/glucose Symport

Cell And Molecular Biology Of Na+/glucose Symport

Cell and Molecular Biology of Na+/Glucose Symport Part of the Membrane Transport in Biology book series (MEMBRANE, volume 5) Renal proximal tubule and intestinal epithelial cells contain apical membrane transporters (symporters) which catalyze the coupled translocation of glucose and Na+ in a symport (cotransport) mechanism [55]. The Na+/glucose symporter is restricted to the apical membrane in these epithelia, where it mediates the uphill movement of glucose across the apical membrane, against its concentration gradient. The energy source for this process, termed secondary active transport, is the transmembrane Na+ gradient generated by the ATP-driven Na+ pump (the Na+, K+, ATPase) localized on the basolateral membrane of these polarized epithelia. A Na+-independent passive glucose transporter localized in the basolateral membrane mediates the downhill exit of glucose at the basolateral cell surface. Working together, these two unrelated and mechanistically distinct glucose transporters mediate the transepithelial transport of glucose from the apical (luminal) side to the basolateral side of the epithelium (Fig. 1). While nonepithelial cell types lack Na+/glucose symporters, a similar Na+/symport mechanism is used to drive active uptake of certain amino acids and phosphate ion [7]. Brush Border MembraneFacilitative Glucose TransporterIntestinal Brush Border MembraneRadiation InactivationHexamethylene Bisacetamide These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Amsler K Cook JS (1982) Development of Na+-dependent hexose transport in a cultured line Continue reading >>

Sodium-glucose Co-transporter Inhibitors: Mechanisms Of Action

Sodium-glucose Co-transporter Inhibitors: Mechanisms Of Action

Subscribe to other NPS MedicineWise information I would like to receive regular email updates on NPS MedicineWise CPD activities and resources I have read the privacy policy and accept the terms of use Sodium-glucose co-transporter inhibitors: Mechanisms of action Sodium-glucose co-transporter inhibitors: Mechanisms of action Aust Prescr 2013;37:14-626 Nov 2013DOI: 10.18773/austprescr.2014.005 Sodium-glucose co-transporter 2 inhibitors are a new class of drug for the treatment of type 2 diabetes. They lower plasma glucose concentrations by increasing renal excretion of glucose. This class of drugs reduces glucose reabsorption in the kidney and lowers plasma glucose independent of changes in insulin concentrations or peripheral insulin resistance. They have a low risk of hypoglycaemia when used as monotherapy. The known adverse effects of the sodium-glucose co-transporter 2 inhibitors are related to their mechanism of action. They include an increased risk of dehydration and genital and urinary tract infections because of the increase in urinary glucose. See also "Sodium-glucose co-transporter inhibitors: clinical applications". Aust Prescr 2014;37:17-20 Current treatment options for type 2 diabetes focus on reducing insulin resistance, enhancing insulin secretion or providing exogenous insulin. However, the kidneys play an important role in glucose homeostasis. Increasing the excretion of glucose could lower blood glucose. This can be achieved by inhibiting the sodium-glucose co-transporter (SGLT). At normal concentrations of plasma glucose, the kidneys actively reabsorb almost all filtered glucose (approximately 180 g/day) with less than 1% excreted in the urine. 1 Glycosuria occurs when plasma glucose concentrations exceed the glucose reabsorbing capacity of the prox Continue reading >>

Sodium-glucose Transport Proteins

Sodium-glucose Transport Proteins

solute carrier family 5 (sodium/glucose cotransporter), member 1 solute carrier family 5 (sodium/glucose cotransporter), member 2 solute carrier family 5 (low affinity glucose cotransporter), member four Sodium-dependent glucose cotransporters (or sodium-glucose linked transporter, SGLT) are a family of glucose transporter found in the intestinal mucosa ( enterocytes ) of the small intestine (SGLT1) and the proximal tubule of the nephron ( SGLT2 in PCT and SGLT1 in PST ). They contribute to renal glucose reabsorption . In the kidneys, 100% of the filtered glucose in the glomerulus has to be reabsorbed along the nephron (98% in PCT , via SGLT2). If the plasma glucose concentration is too high ( hyperglycemia ), glucose is excreted in urine ( glucosuria ) because SGLT are saturated with the filtered glucose. Glucose is never secreted by a healthy nephron . The two most well known members of SGLT family are SGLT1 and SGLT2, which are members of the SLC5A gene family. In addition to SGLT1 and SGLT2, there are five other members in the human protein family SLC5A, several of which may also be sodium-glucose transporters. [1] SGLT2 inhibitors, also called gliflozins, [4] are used in the treatment of type 2 diabetes . Examples include dapagliflozin (Farxiga in US, Forxiga in EU), canagliflozin (Invokana) and empagliflozin (Jardiance). Firstly, an Na+/K+ ATPase pump on the basolateral membrane of the proximal tubule cell uses ATP molecules to move 3 sodium ions outward into the blood, while bringing in 2 potassium ions. This action creates a downhill sodium ion gradient from the outside to the inside of the proximal tubule cell (that is, in comparison to both the blood and the tubule itself). The SGLT proteins use the energy from this downhill sodium ion gradient created by the Continue reading >>

Sglt2 Inhibitors: A New Class Of Diabetes Medications

Sglt2 Inhibitors: A New Class Of Diabetes Medications

Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a new class of diabetic medications indicated only for the treatment of type 2 diabetes. In conjunction with exercise and a healthy diet, they can improve glycemic control. They have been studied alone and with other medications including metformin, sulfonylureas, nizagara 100, pioglitazone, and insulin. Editor’s Note: Since we first looked at this new drug class in April 2013, numerous studies have been done on the benefits and risks of the SGLT2 inhibitors. See below for a roundup of the new information, including the latest investigational drug in this class, Ertugliflozin. How SGLT2 Inhibitors Work SGLT2 is a protein in humans that facilitates glucose reabsorption in the kidney. SGLT2 inhibitors block the reabsorption of glucose in the kidney, increase glucose excretion, and lower blood glucose levels. SGLT2 is a low-affinity, high capacity glucose transporter located in the proximal tubule in the kidneys. It is responsible for 90% of glucose reabsorption. Inhibition of SGLT2 leads to the decrease in blood glucose due to the increase in renal glucose excretion. The mechanism of action of this new class of drugs also offers further glucose control by allowing increased insulin sensitivity and uptake of glucose in the muscle cells, decreased gluconeogenesis and improved first phase insulin release from the beta cells. It is proposed that in prehistoric times, we developed an elegant system for maximizing energy conservation and storage, due to lack of consistent food supplies. This system included reducing the activity of our neurological endocrine system to slow metabolism and conserve the stored energy in our bodies, as well as a method to increase reabsorption of excess glucose that was removed by the kidneys Continue reading >>

Sodium-glucose Cotransport Inhibitors: Mechanisms, Metabolic Effects And Implications For The Treatment Of Diabetic Patients With Chronic Kidney Disease

Sodium-glucose Cotransport Inhibitors: Mechanisms, Metabolic Effects And Implications For The Treatment Of Diabetic Patients With Chronic Kidney Disease

Sodium-glucose cotransport inhibitors: mechanisms, metabolic effects and implications for the treatment of diabetic patients with chronic kidney disease Department of Nephrology and Hypertension, Diabetes and Endocrinology Correspondence and offprint requests to: Peter R. Mertens; E-mail: [email protected] Search for other works by this author on: Department of Nephrology and Hypertension, Diabetes and Endocrinology Nephrology Dialysis Transplantation, Volume 30, Issue 8, 1 August 2015, Pages 12721276, George Vlotides, Peter R. Mertens; Sodium-glucose cotransport inhibitors: mechanisms, metabolic effects and implications for the treatment of diabetic patients with chronic kidney disease, Nephrology Dialysis Transplantation, Volume 30, Issue 8, 1 August 2015, Pages 12721276, Remarkable progress has been achieved in the field of diabetes with the development of incretin analogues, dipeptidyl peptidase IV inhibitors and novel insulin analogues; nevertheless, there is an unmet need for additional therapeutic options. Individualization of HbA1c target levels is a recent progress within the field. Approximately 50% of diabetics do not reach a previously aspired treatment goal of glycosylated HbA1 levels below 7% and often face a vicious circle with accelerated weight gain. Current antidiabetic therapeutics mainly target the decline in insulin secretion and ameliorate insulin resistance. In this regard a new generation of drugs, denoted gliflozines, that specifically interfere with sodium-glucose cotransporters (SGLT)-2 and exhibit a favourable impact on glucose metabolism in patients with type 2 diabetes are emerging as hopeful avenues. The resultant negative energy balance caused by glucosuria results in long-term weight losses, significantly reduced HbA1c levels ap Continue reading >>

Biology Of Human Sodium Glucose Transporters

Biology Of Human Sodium Glucose Transporters

Biology of Human Sodium Glucose Transporters There are two classes of glucose transporters involved in glucose homeostasis in the body, the facilitated transporters or uniporters (GLUTs) and the active transporters or symporters (SGLTs). The energy for active glucose transport is provided by the sodium gradient across the cell membrane, the Na+ glucose cotransport hypothesis first proposed in 1960 by Crane. Since the cloning of SGLT1 in 1987, there have been advances in the genetics, molecular biology, biochemistry, biophysics, and structure of SGLTs. There are 12 members of the human SGLT (SLC5) gene family, including cotransporters for sugars, anions, vitamins, and short-chain fatty acids. Here we give a personal review of these advances. The SGLTs belong to a structural class of membrane proteins from unrelated gene families of antiporters and Na+ and H+ symporters. This class shares a common atomic architecture and a common transport mechanism. SGLTs also function as water and urea channels, glucose sensors, and coupled-water and urea transporters. We also discuss the physiology and pathophysiology of SGLTs, e.g., glucose galactose malabsorption and familial renal glycosuria, and briefly report on targeting of SGLTs for new therapies for diabetes. Sodium-glucose transporters, also known as Na+/glucose cotransporters or symporters (SGLTs), have a historical place in the field of membrane transport. Half a century ago it was established that glucose transport across the small intestine occurred by active transport, i.e., the sugar could be absorbed uphill against its concentration gradient both in vivo and in vitro, and this uptake was blocked by metabolic poisons. Nonmetabolized glucose analogs were also actively transported, and the process was located at the brush Continue reading >>

Glucose Transporter - An Overview | Sciencedirect Topics

Glucose Transporter - An Overview | Sciencedirect Topics

R.Wayne Albers, ... George J. Siegel, in Basic Neurochemistry (Eighth Edition) , 2012 Brain capillary endothelial cells and some neurons express a Na-dependent D-glucose symporter SGLT1 (SLC5A1) was the first characterized of the large SLC5 family of Na+-dependent symporters that transport various solutes and ions into cells (Vemula et al., 2009). In brain vascular endothelium, SGLT1 expression is limited to the luminal membranes of brain capillary endothelial cells. This suggests that SGLT1 and GLUT1 (glucose transporter 1) are both involved in glucose transport from blood into capillary endothelia, whereas glucose efflux from the endothelia into astrocytes and neurons depends primarily on GLUT1. The low affinity of GLUT1 for intracellular glucose (Km ~25mmol/l) may require SGLT1 on the luminal membrane to accumulate sufficiently high endothelial intracellular glucose to maintain an adequate rate of supply to the astrocytic endfeet. Rebecca A. Simmons, in Fetal and Neonatal Physiology (Fifth Edition) , 2017 GLUTs have acquired distinct physiologic and biochemical properties that allow them to serve specific functions in the tissues in which they are expressed. An understanding of the mechanisms underlying tissue-specific expression of these transporters will facilitate an understanding of in vivo glucose utilization and clearance processes that occur normally and in disease states. Although studies in adults provide insight into the regulation of glucose transport, similar studies are required in the fetus and newborn to understand fully the role of the glucose transporter in fetal and neonatal development. Finally, it is likely that epigenetic mechanisms regulate expression and possibly function of GLUTs and we look forward in the coming years to further elucidation Continue reading >>

Sodium-glucose Cotransporter 2 Inhibitors: An Overview

Sodium-glucose Cotransporter 2 Inhibitors: An Overview

Sodium-Glucose Cotransporter 2 Inhibitors: An Overview Georgia CampusPhiladelphia College of Osteopathic Medicine School of Pharmacy Georgia CampusPhiladelphia College of Osteopathic Medicine School of Pharmacy ABSTRACT: The management of type 2 diabetes (T2DM) has evolved significantly over the past several decades. One of the newest additions to antidiabetic therapy is a sodium-glucose cotransporter 2 (SGLT2) inhibitor with a unique mechanism that targets the kidneys ability to reabsorb filtered glucose. In addition to providing glycemic control, this class has a unique mechanism of action associated with blood pressure reduction, weight loss, and potential cardiovascular benefits; however, the FDA is closely monitoring the use of these drugs based on increased safety concerns. The benefits and risks of SGLT2 inhibitors should be carefully considered. Selected patients with T2DM can benefit from SGLT2 inhibitor therapy. Diabetes, a devastating disease affecting more than 29 million Americans, is a growing epidemic and the leading cause of end-stage renal disease, lower-limb amputation, and blindness in the United States. In addition, cardiovascular (CV) events are highly prevalent in patients with diabetes.1 Metformin is the recommended first-line drug for type 2 diabetes (T2DM) patients with poor glycemic control. However, the glycemic response produced by metformin is typically inadequate in the long-term management of diabetes, and patients will eventually require additional treatments. The need for newer agents to treat T2DM is now being recognized. Most agents used for T2DM either improve the bodys sensitivity to insulin or increase pancreatic secretion of insulin. Improved understanding of the mechanisms involved in glucose reabsorption through the kidneys has Continue reading >>

Sodium-glucose Symporter

Sodium-glucose Symporter

Sodium - glucose Symporter is a transmembrane protein and is an example of sodium-driven Secondary active transport that occurs in the epithelial cells of the small intestines [1] . The sodium-glucose symporter is found on the Apical membrane of the epithelal cells [2] . The sodium and glucose bind to the symporter and are simultaneously both co-transported into the epithelial cells. The sodium driven-glucose symporter uses the potential free energy stored in the sodium electrochemical gradient (low sodium concentration inside the epithelial cells) established by Sodium-potassium pump [3] . Therefore, the sodium influx from the lumen to the epithelial cell is coupled with glucose transport. Alberts et al. Molecular Biology of The Cell (6th Edition), Garland Sciences; New York: 2015 (page 605) Alberts et al. Molecular Biology of The Cell (6th Edition), Garland science; New York: 2015 (page 605) Alberts et al. Molecular Biology of The Cell (6th Edition), Garland Science; New York: 2015 (page 606-608) Continue reading >>

Glucose Transporter Proteins

Glucose Transporter Proteins

Glucose serves as a major source of energy for metabolic processes in mammalian cells. Since polar molecules cannot be transported across the plasma membrane, carrier proteins called glucose transporters are needed for cellular uptake. Glucose transporters are found in the plasma membrane where they bind to glucose and enable its transport across the lipid bilayer. They can be divided into two classes: the sodium-glucose cotransporters or symporters (SGLTs) and the facilitative glucose transporters (GLUTs). SGLTs are expressed by cells in the small intestine and in the renal proximal tubules. These proteins mediate the active transport of glucose against an electrochemical gradient. Glucose in the intestinal lumen or the nephrons is transported against its concentration gradient by another transport mechanism, where glucose uptake is coupled with the uptake of sodium ions that are also being transported down their concentration gradient. The human SGLT family is made up of twelve members involved in the transport of glucose, anions, fatty acids and vitamins. Two of the main members responsible for glucose transport are SGLT1 and SGLT2. SGLT1 is a 664-amino acid protein serving as the primary transporter of glucose in the intestine. SGLT2 is located in cells that line the proximal tubule, where it aids reabsorption of glucose from renal fluid, to prevent glucose being eliminated in the urine. Facilitative glucose transporters (GLUTs) Research reveals how bacteria prepare sticky adhesion protein The second group of glucose transporters, the GLUT family, is made up of 14 members. These are responsible for the bidirectional transport of glucose in tissues and cells. This involvesusing facilitative diffusion to carry glucose down a concentration gradient, into the cell. The Continue reading >>

Sglt2 Inhibitors (gliflozins)

Sglt2 Inhibitors (gliflozins)

SGLT2 inhibitors help the kidneys lower blood glucose levels Sodium-glucose co-transporter-2 (SGLT2) inhibitors are a new group of oral medications used for treating type 2 diabetes . The drugs work by helping the kidneys to lower blood glucose levels . SGLT2 inhibitors have been approved for use as a treatment for diabetes since 2013. They are taken once a day with or without food. SGLT2 inhibitors work by preventing the kidneys from reabsorbing glucose back into the blood. This allows the kidneys to lower blood glucose levels and the excess glucose in the blood is removed from the body via urine. The kidneys work by filtering glucose out of the blood and then reabsorbing glucose back into the blood. The proteins that reabsorb glucose are called sodium-glucose transport proteins. SGLT2 inhibitors block these proteins which means less glucose gets reabsorbed back into the blood and gets passed out of the body via the urine. SGLT2 inhibitors may be suitable for people with type 2 diabetes that have high blood glucose levels despite being on a medication regimen such as metformin and insulin. SGLT2 inhibitors are not recommended for prescribing to people with kidney disease (nephropathy) as kidney disease prevents the drug from working sufficiently well. What are the benefits of SGLT2 inhibitors? SGLT2 inhibitors help to remove glucose from the blood and therefore help to lower blood glucose levels. By removing glucose from the body, SGLT2 inhibitors can also have benefits for weight loss . As the drugs cause more glucose to be excreted in the urine, there is a higher chance of getting genital and urinary tract infections . These side effects are more common in women than in men. Taking SGLT2 inhibitors with insulin, sulphonylureas or glinides may increase the risk of hy Continue reading >>

Sglt2 Inhibitors, A New Approach In Diabetes Treatment

Sglt2 Inhibitors, A New Approach In Diabetes Treatment

Transporters involved in the mechanism of tubular glucose reabsorption are separated into two main families: the SGLTs secondary active Na+/D-glucose co-transporters, located at the brush border of tubular cells and the GLUTs facilitated diffusion glucose transporters located at the basolateral membrane of tubular cells.[ 1 ] The SGLTs belong to the SLC5 gene family that includes more than 220 members both in animal and human genome.[ 22 ] The human members of SLC5 gene family code protein transporters are listed in Table 1 .[ 22 , 23 ] As for the renal tubules, early in vitro perfusion studies demonstrated that tubular glucose reabsorption was facilitated by two different transporters.[ 24 ] A low-affinity/high capacity Na+-coupled glucose transporter in S1 segments of proximal tubules (Km for D-glucose of 1.64 mM and a maximal transport rate Jmax of 83 pmol/min per mm) and a high-affinity/low capacity NA+-coupled glucose transporter located in S3 segments (Km for D-glucose of 0.35 mM and a maximal transport rate Jmax of 7.9 pmol/min/mm).[ 24 ] Further glucose uptake studies of Turner et al.[ 25 , 26 ] into brush border membrane vesicles from rabbit and human kidney cortex were in accordance with the model of two different Na+/glucose co-transporters and demonstrated that the one at the early S1/2 tubular segments exhibits low affinity (Km of 6 mM) and 1: 1 Na: glucose coupling and the other at the S3 segment presents high affinity (Km of 0.3 mM) and 2: 1 coupling.[ 25 , 26 ] It was also identified that SGLT2 and SGLT1 meet these transporter features, respectively (Figure 1).[ 2729 ] Recent in vitro studies in cultured human embryonic kidney cells[ 30 ] have shown that affinity for D-glucose one of the two stereoisomers of glucose is almost similar for SGLT1 and 2 (5 Continue reading >>

Potassium And Sodium Dependent Glucose Transport: Implications For Cystic Fibrosis

Potassium And Sodium Dependent Glucose Transport: Implications For Cystic Fibrosis

Editor,—In cystic fibrosis intestine there is an increase in the rate of sodium coupled glucose absorption,1 which exacerbates the characteristic luminal dehydration of this disease resulting from the failure of chloride secretion. The mechanism for the sodium dependent uptake of sugars from the small intestine is now well established, but early studies of its cation dependency revealed that replacement of external sodium with potassium had a greater inhibitory effect than replacement with urea or Tris.2 This was explained as competition between sodium and potassium for a common binding site on the glucose transporter and it was argued that intracellular potassium might therefore displace sodium and sugar from the carrier and promote further transport by returning the carrier to a conformation suitable for membrane recycling.2 Since it has recently been reported that cystic fibrosis enterocytes may possess higher intracellular potassium concentrations than non-cystic fibrosis cells,3 it is possible that enhanced sodium/glucose absorption in this disease could be a secondary effect of abnormalities in cellular potassium handling. The purpose of this study was to test whether potassium may have a direct effect on active sodium/glucose uptake using intestinal brush border membrane vesicles (BBMVs). BBMVs were prepared from rat jejunal mucosal scrapes using a magnesium precipitation technique.4 Human BBMVs were prepared in a similar manner, using operative sections of distal ileum taken from patients presenting with intestinal obstruction. All human tissues were morphologically normal and each specimen was obtained from an individual patient. BBMVs were loaded with a buffer containing additional potassium chloride or osmotically equivalent amounts of potassium gluconate, Continue reading >>

Functional Role Of Glucose Metabolism, Osmotic Stress, And Sodium-glucose Cotransporter Isoform-mediated Transport On Na+/h+ Exchanger Isoform 3 Activity In The Renal Proximal Tubule

Functional Role Of Glucose Metabolism, Osmotic Stress, And Sodium-glucose Cotransporter Isoform-mediated Transport On Na+/h+ Exchanger Isoform 3 Activity In The Renal Proximal Tubule

Glucose Modulates NHE3-Dependent JHCO3 in the Renal PT As an initial approach to study the effect of glucose on NHE3-mediated bicarbonate reabsorption, Wistar rats were subjected to stationary microperfusion in vivo, and their PTs were perfused with solutions containing different concentrations of glucose or a control solution (CTRL; solution without any transported sugar) ( Concise Methods ). As shown in Figure 1A , the rate of bicarbonate flux (JHCO3) in the PTs perfused with 5 mM glucose (GLU) was significantly higher than in CTRL-perfused tubules (1.9030.083 versus 2.7790.093 nmol/cm2 per second). A progressive inhibition of JHCO3 was found after the perfusion of higher glucose concentrations (1.1250.13 and 1.250.16 nmol/cm2 per second for GLU40 and GLU60, respectively). Because the stimulatory effect was observed only on perfusion of GLU5 and the maximum inhibitory effect occurred on GLU40 perfusion, these concentrations were used in all the following experiments. Representative curves of pH changes are given in Supplemental Figure 1 . Model of how physiological and supraphysiological concentrations of glucose modulate NHE3 activity in the renal PT. Perfused GLU enters the PT cell through SGLT1 and/or SGLT2. Intracellularly, it is metabolized by glucose metabolism through the action of hexokinase. Glucose metabolism stimulates the exchanger. The perfusion of supraphysiological concentrations of glucose (GLU) increases glucose uptake through SGLT2, the low-affinity, high-capacity glucose transporter, because the Km of this transporter is higher than the Km of physiological glucose concentration. Glucose uptake is known to be accompanied by water flow, and as such, glucose uptake promotes cell swelling and NHE3 inhibition. AQ, aquaporin. With regard to the effects o Continue reading >>

Sodium-glucose Cotransport

Sodium-glucose Cotransport

aInterPrET Center, Department of Biomedicine, Aarhus University, Aarhus, Denmark bVA San Diego Healthcare System, San Diego bVA San Diego Healthcare System, San Diego cDepartment of Medicine, University of California San Diego, La Jolla, California, USA aInterPrET Center, Department of Biomedicine, Aarhus University, Aarhus, Denmark bVA San Diego Healthcare System, San Diego cDepartment of Medicine, University of California San Diego, La Jolla, California, USA Correspondence to Dr Timo Rieg, Department of Medicine, Division of Nephrology-Hypertension, University of California San Diego & VA San Diego Healthcare System, 3350 La Jolla Village Drive (9151), San Diego, CA 92161, USA. Tel: +1 858 552 8585 x5944; fax: +1 858 642 1438; [email protected] The publisher's final edited version of this article is available at Curr Opin Nephrol Hypertens See other articles in PMC that cite the published article. Sodium-glucose cotransporters (SGLTs) are important mediators of glucose uptake across apical cell membranes. SGLT1 mediates almost all sodium-dependent glucose uptake in the small intestine, while in the kidney SGLT2, and to a lesser extent SGLT1, account for more than 90% and nearly 3%, respectively, of glucose reabsorption from the glomerular ultrafiltrate. Although the recent availability of SGLT2 inhibitors for the treatment of diabetes mellitus has increased the number of clinical studies, this review has a focus on mechanisms contributing to the cellular regulation of SGLTs. Studies have focused on the regulation of SGLT expression under different physiological/pathophysiological conditions, for example diet, age or diabetes mellitus. Several studies provide evidence of SGLT regulation via cyclic adenosine monophosphate/protein kinase A, protein kinase C, glucagon-like Continue reading >>

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