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NFAT5 参与了钠促进 GLP-1 分泌的过程。

NFAT5 Is Involved in GRP-Enhanced Secretion of GLP-1 by Sodium.

机构信息

Division of Renal Diseases & Hypertension, The George Washington University School of Medicine & Health Science, Washington, DC 20052, USA.

Department of Hypertension, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Henan University People's Hospital, Zhengzhou 450003, China.

出版信息

Int J Mol Sci. 2021 Apr 12;22(8):3951. doi: 10.3390/ijms22083951.

DOI:10.3390/ijms22083951
PMID:33921209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8069329/
Abstract

Gastrin, secreted by G-cells, and glucagon-like peptide-1 (GLP-1), secreted by L-cells, may participate in the regulation of sodium balance. We studied the effect of sodium in mice in vivo and mouse ileum and human L-cells, on GLP-1 secretion, and the role of NFAT5 and gastrin-releasing peptide receptor (GRPR) in this process. A high-sodium diet increases serum GLP-1 levels in mice. Increasing sodium concentration stimulates GLP-1 secretion from mouse ileum and L-cells. GRP enhances the high sodium-induced increase in GLP-1 secretion. High sodium increases cellular GLP-1 expression, while low and high sodium concentrations increase NFAT5 and GRPR expression. Silencing NFAT5 in L-cells abrogates the stimulatory effect of GRP on the high sodium-induced GLP-1 secretion and protein expression, and the sodium-induced increase in GRPR expression. GLP-1 and gastrin decrease the expression of Na-K/ATPase and increase the phosphorylation of sodium/hydrogen exchanger type 3 (NHE3) in human renal proximal tubule cells (hRPTCs). This study gives a new perspective on the mechanisms of GLP-1 secretion, especially that engendered by ingested sodium, and the ability of GLP-1, with gastrin, to decrease Na-K/ATPase expression and NHE3 function in hRPTCs. These results may contribute to the better utilization of current and future GLP-1-based drugs in the treatment of hypertension.

摘要

胃泌素由 G 细胞分泌，胰高血糖素样肽-1（GLP-1）由 L 细胞分泌，可能参与钠平衡的调节。我们研究了体内钠对小鼠、小鼠回肠和人 L 细胞 GLP-1 分泌的影响，以及 NFAT5 和胃泌素释放肽受体（GRPR）在这一过程中的作用。高钠饮食会增加小鼠血清中的 GLP-1 水平。增加钠浓度可刺激小鼠回肠和 L 细胞中 GLP-1 的分泌。GRP 增强了高钠诱导的 GLP-1 分泌增加。高钠增加细胞内 GLP-1 的表达，而低钠和高钠浓度增加 NFAT5 和 GRPR 的表达。在 L 细胞中沉默 NFAT5 可消除 GRP 对高钠诱导的 GLP-1 分泌和蛋白表达以及钠诱导的 GRPR 表达增加的刺激作用。GLP-1 和胃泌素降低了人肾近端小管细胞（hRPTC）中钠钾/ATP 酶的表达，并增加了钠/氢交换体 3（NHE3）的磷酸化。本研究为 GLP-1 分泌的机制提供了新的视角，特别是摄入的钠引起的 GLP-1 分泌机制，以及 GLP-1 与胃泌素降低 hRPTC 中钠钾/ATP 酶表达和 NHE3 功能的能力。这些结果可能有助于更好地利用当前和未来基于 GLP-1 的药物治疗高血压。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3878/8069329/d99dc4a120ae/ijms-22-03951-g008.jpg
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