盐摄入通过PPARδ／脂联素介导的SGLT2通路调控糖稳态  

Sodium Intake Regulates Glucose Homeostasis through the PPARδ/Adiponectin-Mediated SGLT2 Pathway

作　　者：Yu Zhao Peng Gao Fang Sun Qiang Li Jing Chen Hao Yu Li Li Xing Wei Hongbo He Zongshi Lu Xiao Wei Bin Wang Yuanting Cui Shiqiang Xiong Qianhui Shang Aimin Xu Yu Huang Daoyan Liu 祝之明[2,3] 

机构地区：[1]不详 [2]第三军医大学大坪医院全军高血压代谢病中心 [3]美国北卡大学

出　　处：《科学新闻》2017年第4期71-71,共1页Science News

基　　金：973计划;国家自然科学基金的资助

摘　　要：高盐摄入是糖尿病发生高血压的主要危险因素．促进肾脏盐排泄可减少糖尿病的心血管损害，但摄盐与糖稳态的相互作用尚不清楚。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 PPARδ knockout mice and diabetic mice. PPARδ 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 PPARδ/adiponectin/SGLT2 pathway in the regulation of sodium and glucose homeostasis.

关 键 词：糖尿病 PPARΔ 脂联素 盐 通路 危险因素 相互作用 心血管 

分 类 号：G804.7[文化科学—运动人体科学]