Renal olfactory receptor 1393 contributes to the progression of type 2 diabetes in a diet-induced obesity model

摘要

Glucose reabsorp-tion in the proximal tubule (via Sgltl and Sglt2) has emerged as an important contributor to the development of diabetes. Inhibition of Sglt2 is accepted as a viable therapeutic treatment option for patients with type 2 diabetes and has been shown to delay development of diabetic kidney disease. We hypothesized that Olfrl 393 may contribute to the progression of type 2 diabetes, particularly the development of hyperfiltration, which has been linked to increased Na~+ reabsorp-tion in the proximal tubule via the Sglts. To test this hypothesis, Olfrl 393 wild-type (WT) and knockout (KO) mice were challenged with a high-fat diet to induce early-stage type 2 diabetes. After 16 wk on the high-fat diet, fasting blood glucose values were increased and glucose tolerance was impaired in the male WT mice. Both of these effects were significantly blunted in the male KO mice.