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内皮细胞中 C 型利钠肽的过表达可预防饮食诱导肥胖期间的胰岛素抵抗和炎症。

Overexpression of C-type Natriuretic Peptide in Endothelial Cells Protects against Insulin Resistance and Inflammation during Diet-induced Obesity.

机构信息

Department of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.

Department of Regenerative Medicine and Tissue Engineering, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.

出版信息

Sci Rep. 2017 Aug 29;7(1):9807. doi: 10.1038/s41598-017-10240-1.

DOI:10.1038/s41598-017-10240-1
PMID:28852070
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5574992/
Abstract

The endogenous peptide C-type natriuretic peptide (CNP) binds its receptor, guanylyl cyclase B (GCB), and is expressed by endothelial cells in diverse tissues. Because the endothelial cells of visceral adipose tissue have recently been reported to play a role in lipid metabolism and inflammation, we investigated the effects of CNP on features of obesity by using transgenic (Tg) mice in which CNP was placed under the control of the Tie2 promoter and was thus overexpressed in endothelial cells (E-CNP). Here we show that increased brown adipose tissue thermogenesis in E-CNP Tg mice increased energy expenditure, decreased mesenteric white adipose tissue (MesWAT) fat weight and adipocyte hypertrophy, and prevented the development of fatty liver. Furthermore, CNP overexpression improved glucose tolerance, decreased insulin resistance, and inhibited macrophage infiltration in MesWAT, thus suppressing pro-inflammation during high-fat diet-induced obesity. Our findings indicate an important role for the CNP produced by the endothelial cells in the regulation of MesWAT hypertrophy, insulin resistance, and inflammation during high-fat diet-induced obesity.

摘要

内源性肽 C 型利钠肽（CNP）与其受体鸟苷酸环化酶 B（GCB）结合，并由不同组织的内皮细胞表达。由于内脏脂肪组织的内皮细胞最近被报道在脂质代谢和炎症中发挥作用，因此我们通过使用内皮细胞中过表达 CNP 的转基因（Tg）小鼠研究了 CNP 对肥胖特征的影响，其中 CNP 受 Tie2 启动子的控制。在这里，我们表明 E-CNP Tg 小鼠棕色脂肪组织产热增加会增加能量消耗，减少肠系膜白色脂肪组织（MesWAT）脂肪重量和脂肪细胞肥大，并防止脂肪肝的发生。此外，CNP 的过表达改善了葡萄糖耐量，降低了胰岛素抵抗，并抑制了 MesWAT 中的巨噬细胞浸润，从而抑制了高脂肪饮食诱导肥胖期间的促炎反应。我们的研究结果表明，内皮细胞产生的 CNP 在调节高脂肪饮食诱导肥胖期间的 MesWAT 肥大、胰岛素抵抗和炎症方面发挥着重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/ca73b71c7fd8/41598_2017_10240_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/a7e430abf0c0/41598_2017_10240_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/f34888105307/41598_2017_10240_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/3e67bd8fdd19/41598_2017_10240_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/79d3a0f7be1a/41598_2017_10240_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/3fe7032fceca/41598_2017_10240_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/36c3ce73dc18/41598_2017_10240_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/e7813e5202ec/41598_2017_10240_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/ca73b71c7fd8/41598_2017_10240_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/a7e430abf0c0/41598_2017_10240_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/f34888105307/41598_2017_10240_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/3e67bd8fdd19/41598_2017_10240_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/79d3a0f7be1a/41598_2017_10240_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/3fe7032fceca/41598_2017_10240_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/36c3ce73dc18/41598_2017_10240_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/e7813e5202ec/41598_2017_10240_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f19e/5574992/ca73b71c7fd8/41598_2017_10240_Fig8_HTML.jpg

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[3]
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[4]
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[7]
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[8]
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[10]
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本文引用的文献

[1]
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Food Funct. 2017-2-22

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Endothelium-Derived C-Type Natriuretic Peptide Contributes to Blood Pressure Regulation by Maintaining Endothelial Integrity.

Hypertension. 2017-2

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Biochem Biophys Res Commun. 2016-11-11

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Respir Res. 2016-2-19

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EMBO Rep. 2015-8

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Arterioscler Thromb Vasc Biol. 2014-8

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