Solute Carrier Family 5 (Sodium/glucose Cotransporter), Member 2 (SLC5A2) ELISA Kits

Cow (Bovine) Solute Carrier Family 5 (Sodium/glucose Cotransporter), Member 2 (SLC5A2) interaction partners

1. cloning and distribution of SGLT2 mRNA expression in bovine tissues; SGLT2 mRNA was detected predominantly in the kidney; expression of SGLT2 mRNA in mammary gland increased more than 10-fold from late pregnancy to early lactation

Human Solute Carrier Family 5 (Sodium/glucose Cotransporter), Member 2 (SLC5A2) interaction partners

1. Membrane-associated protein 17 (MAP17) is shown to colocalize and coimmunoprecipitate with sodium/glucose cotransporter 2 (SGLT2).

2. Tissue-specific nucleosome occupancy plays an important role in the regulation of SGLT2 gene expression in renal proximal tubular epithelial cells.

3. ten novel SLC5A2 mutations and determination of the renal threshold for glucose excretion in Chinese patients with familial renal glucosuria

4. Results show that SGLT2 is upregulated in non-small cell lung cancer (NSCLC) patient samples and cell lines. Its 3'UTR is the direct target of miR-296.

5. SGLT1, SGLT2 and GLUT2 have roles in renal glucose handling [review]

6. 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]

7. SGLT2-I therapy is a potential new strategy for the treatment of HCC.

8. 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)

9. 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.

10. 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]

11. 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.

12. 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.

13. C-peptide-based measurements of insulin secretion are appropriate for assessing beta-cell function in SGLT2 inhibitor canagliflozin-treated participants.

14. The novel pathogenic SLC5A2 mutation p.S293C was responsible for the onset of FRG

15. Molecular Interaction of Anti-Diabetic Drugs With Acetylcholinesterase and Sodium Glucose Co-Transporter 2.

16. 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

17. 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.

18. SGLT2/MAP17 functions as a low-affinity Na(+)-glucose cotransporter in the kidney.

19. reported nominal effects of individual SLC5A2 variants on fasting and post-challenge glucose levels may probably not be mediated by altered glucagon release

20. 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.

Mouse (Murine) Solute Carrier Family 5 (Sodium/glucose Cotransporter), Member 2 (SLC5A2) interaction partners

1. 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]

2. By studying glucagon secretion in cultured alpha cells, a role was revealed for SGLT1 in modulating the promoter effect of Dapagliflozin (a highly selective SGLT2 inhibitor) on glucagon release.

3. SGLT-2 inhibition with dapagliflozin reduces the activation of the Nlrp3/ASC inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 inhibitor Saxagliptin.

4. Taken together, it was concluded that the effect of SGLT2 inhibition on weight loss is in part mediated via the liver-brain-adipose neurocircuitry.

5. Tofogliflozin, a selective inhibitor of sodium-glucose cotransporter 2, suppress albuminuria and tubulointerstitial injury in obese and type 2 diabetic mice. Inhibition of glucose entry into tubular cells by tofogliflozin may exert renoprotective properties in diabetes.

6. SGLT2 inhibition induced gluconeogenesis mainly in the kidney, whereas for low carbohydrate diet, it was predominantly in the liver.

7. Suggest SGLT2 inhibitor pragliflozin may be effective when administered as part of a combination regimen in the treatment of type 2 diabetes.

8. these results suggest that SGLT2i treatment acutely suppresses energy expenditure in BAT via regulation of an inter-organ neural network consisting of the common hepatic vagal branch and sympathetic nerves.

9. In conclusion, SGLT2 inhibitor luseogliflozin ameliorates glycemic control and thus exerts protective effects on pancreatic beta-cell mass and function.

10. SGLT2 can transport gentamicin and contribute to gentamicin-induced cytotoxicity.

11. SGLT2 is inhibited with dapagliflozin in pancreatic alpha cells, which triggers glucagon secretion

12. DNA sequencing of SGLT2 in SAMP10/TaSlc mice revealed a single nucleotide deletion of guanine at 1236, which resulted in a frameshift mutation that produced a truncated protein.

13. Improved glycemic control in mice lacking Sglt1 and Sglt2.

14. Prevention of renal glucose reabsorption by SGLT2 deletion reduced hyperglycemia, improved glucose intolerance, and increased glucose-stimulated insulin secretion in vivo.

15. SGLT2 mediates glucose reabsorption in the early proximal tubule and most of the glucose reabsorption by the kidney, overall.