Abstract：
: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.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Zhao Y,Gao P,Sun F,Li Q,Chen J,Yu H,Li L,Wei X,He H,Lu Z,Wei X,Wang B,Cui Y,Xiong S,Shang Q,Xu A,Huang Y,Liu D,Zhu Zdoi
10.1016/j.cmet.2016.02.019subject
Has Abstractpub_date
2016-04-12 00:00:00pages
699-711issue
4eissn
1550-4131issn
1932-7420pii
S1550-4131(16)30068-7journal_volume
23pub_type
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