| First Author | Zhao Y | Year | 2016 |
| Journal | Cell Metab | Volume | 23 |
| Issue | 4 | Pages | 699-711 |
| PubMed ID | 27053360 | Mgi Jnum | J:235404 |
| Mgi Id | MGI:5796241 | Doi | 10.1016/j.cmet.2016.02.019 |
| Citation | Zhao Y, et al. (2016) Sodium Intake Regulates Glucose Homeostasis through the PPARdelta/Adiponectin-Mediated SGLT2 Pathway. Cell Metab 23(4):699-711 |
| abstractText | High sodium intake is a major risk factor for developing hypertension in diabetes. Promotion of sodium excretion reduces cardiometabolic lesions in diabetes. However, the interaction between sodium intake and glucose homeostasis remains elusive. Here, we report that high sodium intake remarkably increased natriuresis in wild-type mice, but this effect was blunted in adipose-specific PPARdelta knockout mice and diabetic mice. PPARdelta activation in perirenal fat by agonist or high sodium intake inhibited renal sodium-glucose cotransporter 2 (SGLT2) function, which is mediated by increased production of adipose adiponectin. In addition, high salt intake-induced natriuresis was impaired in diabetic states because of renal SGLT2 dysfunction. Type 2 diabetic patients with uncontrolled hyperglycemia had less natriuresis that was correlated to their plasma adiponectin levels. Our findings provide insights into the distinctive role of the PPARdelta/adiponectin/SGLT2 pathway in the regulation of sodium and glucose homeostasis. |
