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SGLT1, SGLT2 and GLUT2 have roles in renal glucose handling [review]
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An inhibitor of the renal sodium/glucose cotransporter 2 (SGLT2), dapagliflozin, successfully prevented the development of cardiomyopathy in SKO mice. This is particularly relevant, given that SGLT2i treatment reduces cardiovascular event in T2DM patients. [review]
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SGLT2-I therapy is a potential new strategy for the treatment of HCC.
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Data suggest expression of SGLT1 is markedly increased in kidney of patients with type 2 diabetes as compared to control subjects; SGLT1 mRNA is highly and significantly correlated with fasting and postprandial plasma glucose and HbA1c. In contrast, data suggest SGLT2 and GLUT2 mRNA in kidney are down-regulated in type 2 diabetes, but not to statistically significant level. (GLUT2 = glucose transporter type 2)
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Data suggest that SGLT2 expression is higher in control kidney than in kidney from subjects with type 2 diabetes; SGLT1 expression in kidney tended in the same direction; SGLT2 appears to be localized to tubular brush-border membranes; unaffected renal tissues were obtained from subjects undergoing unilateral nephrectomy for renal carcinomas.
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Sodium-glucose cotransporter-2 (SGLT2) is selectively expressed in the human kidney, where it executes reabsorption of filtered glucose with a high capacity; it may be overactive in patients with diabetes, especially in the early, hyperfiltering stage of the disease. As a therapeutic target, SGLT2 has been successfully engaged by orally active, selective agents. [review]
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In this study, more than 90% of patients were on Forxiga or Invokana. Merck and Pfizer are also collaborating to bring an SGLT2 rival drug, ertugliflozin, to market as well as on two combinations containing the drug to treat type 2 diabetes.
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Canagliflozin, an orally active inhibitor of sodium glucose co-transporter 2, is approved for the treatment of type-2 diabetes mellitus. Food did not affect canagliflozin pharmacokinetics.
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C-peptide-based measurements of insulin secretion are appropriate for assessing beta-cell function in SGLT2 inhibitor canagliflozin-treated participants.
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The novel pathogenic SLC5A2 mutation p.S293C was responsible for the onset of FRG
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Molecular Interaction of Anti-Diabetic Drugs With Acetylcholinesterase and Sodium Glucose Co-Transporter 2.
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the key pharmacodynamic effects of SGLT2 inhibitors and the clinical evidence that support the rationale for the use of SGLT2 inhibitors in patients with HF who have T2D. Because these favorable effects presumably occur independent of blood glucose lowering, we also explore the potential use of SGLT2 inhibition in patients without T2D with HF or at risk of HF, such as in patients with coronary artery disease
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Results provide evidence that common genetic variants in the SLC5A2 gene do not affect diabetes-related metabolic traits in subjects at increased risk of type 2 diabetes.
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SGLT2/MAP17 functions as a low-affinity Na(+)-glucose cotransporter in the kidney.
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reported nominal effects of individual SLC5A2 variants on fasting and post-challenge glucose levels may probably not be mediated by altered glucagon release
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Findings suggest that there are subtypes of T2DM characterized by different urinary glucose excretion and cardiovascular risk factors. SLC5A2 and HNF1A mutations partially explain renal glycosuria in patients with T2DM.
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SGLT2 inhibitors combined with insulin might be an efficient and safe treatment modality for T1DM patients.
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Data suggest that, by shunting substantial amounts of carbohydrate into urine, SGLT2-mediated glycosuria results in a progressive shift in energy metabolism toward fatty substrates; studies were conducted in subjects with/without diabetes type 2 treated with SGLT2 antagonist and hypoglycemic agent empagliflozin.
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Studies indicate that Sodium-glucose cotransporter 2 (SGLT2)T2 inhibitors are promising antidiabetic agents that are gaining attention in both clinical medicine and basic research.
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Data suggest that ketoacidosis (ketonuria/ketonemia) associated with the use of sodium-glucose cotransporter 2 protein (SGLT-2) inhibitors needs further research.
