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

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

内皮细胞中c型纳特里尿肽的过表达可在饮食诱导的肥胖症过程中防止胰岛素抵抗和炎症。

DOI:
10.1038/s41598-017-10240-1
复制
发表时间:
2017-08-29
期刊:
影响因子:
4.6
通讯作者:
Kangawa K
Kangawa K
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Bae CR;Hino J;Hosoda H;Arai Y;Son C;Makino H;Tokudome T;Tomita T;Kimura T;Nojiri T;Hosoda K;Miyazato M;Kangawa K

文献摘要

参考文献

被引文献

相似文献

内源性肽C型利钠肽(CNP)与其受体鸟苷酸环化酶B(GCB)结合,并由多种组织中的内皮细胞表达。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起作用,我们通过使用转基因(Tg)小鼠研究了CNP对肥胖特征的影响,其中CNP被置于Tie2启动子的控制下,从而在内皮细胞(E-CNP)中过表达。在这里,我们表明,增加棕色脂肪组织产热E-CNP Tg小鼠增加能量消耗,减少肠系膜白色脂肪组织(MesWAT)脂肪重量和脂肪细胞肥大,并防止脂肪肝的发展。此外,CNP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,从而抑制了高脂饮食诱导的肥胖期间的促炎症。我们的研究结果表明,在高脂饮食诱导的肥胖过程中,内皮细胞产生的CNP在调节MesWAT肥大、胰岛素抵抗和炎症中起重要作用。
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.
DOI: 10.1186/s12931-016-0335-6
发表时间: 2016-02-19
影响因子: 5.8
作者:
Kimura T;Nojiri T;Hino J;Hosoda H;Miura K;Shintani Y;Inoue M;Zenitani M;Takabatake H;Miyazato M;Okumura M;Kangawa K
通讯作者: Kangawa K
DOI: 10.1210/en.141.10.3807
发表时间: 2000-10-01
期刊: ENDOCRINOLOGY
影响因子: 4.8
作者:
Chusho, H;Ogawa, Y;Nakao, K
通讯作者: Nakao, K
DOI: 10.1161/01.cir.78.6.1401
发表时间: 1988-12-01
期刊: CIRCULATION
影响因子: 37.8
作者:
HIRATA, Y;ISHII, M;MATSUO, H
通讯作者: MATSUO, H
DOI: 10.1161/atvbaha.114.303029
发表时间: 2014-08
期刊: Arteriosclerosis, thrombosis, and vascular biology
影响因子: --
作者:
Brown NK;Zhou Z;Zhang J;Zeng R;Wu J;Eitzman DT;Chen YE;Chang L
通讯作者: Chang L
DOI: 10.1161/01.atv.21.6.930
发表时间: 2001-06-01
影响因子: 8.7
作者:
Doi, K;Ikeda, T;Nakao, K
通讯作者: Nakao, K