文章简介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。本研究发现高盐摄入能显著增加野生型小鼠肾脏盐排泄,但此效应在脂肪特异性敲除PPARδ或者糖尿病小鼠中受到抑制。肾周脂肪的PPARδ受激动剂或高盐摄入的激活能通过促进脂肪组织分泌脂联素抑制肾脏钠糖共 INTRODUCTION High salt intake is a major risk factor for the development of hypertension in hypertension. Promoting renal salt excretion can reduce the cardiovascular damage of diabetes, but the interaction between salt intake and sugar homeostasis is not clear. This study found that high salt intake significantly increased renal excretion of salt in wild-type mice, but this effect was suppressed in fat-specific knockout PPARδ or diabetic mice. Perinatal fat PPARδ activation by agonists or high salt intake of adiponectin by inhibiting the secretion of adiponectin inhibition of renal sodium