JBC：脂肪细胞分泌的一种激素或可缓解心肌梗塞

5月18日，日本名古屋大学的一个研究小组在新一期美国《生物化学期刊》（Journal of  Biological Chemistry）网络版上报告说，他们在老鼠实验中发现，脂肪细胞分泌的一种激素具有缓解心肌梗塞的效果。

心肌梗塞是由于动脉硬化导致血管堵塞、血液流动停滞、营养和氧气无法充分达到心脏引起心肌细胞坏死所致。有报告显示，脂肪细胞分泌的一种名为“CTRP9”的激素具有减缓血管收缩的作用。

研究人员用这种物质对32只有心肌梗塞症状的老鼠进行实验。他们给一些老鼠注射“CTRP9”激素，并在24小时后分析其心脏的变化，结果发现注射了“CTRP9”激素的老鼠因心肌梗塞而坏死的心肌细胞比没有注射的老鼠少30%左右。

研究小组还发现，肥胖老鼠血液中的这种激素含量只有健康老鼠的一半左右。研究人员认为，“CTRP9”激素减少容易引发心肌梗塞，因此正确减肥并提升该激素水平有助于保护心脏。（生物谷Bioon.com）

doi:10.1074/jbc.M112.357939 jbc.M112.357939.
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CTRP9 protects against myocardial injury following ischemia-reperfusion through AMPK-dependent mechanism

Takahiro Kambara1, Koji Ohashi2, Rei Shibata1, Yasuhiro Ogura2, Sonomi Maruyama2, Takashi Enomoto2, Yusuke Uemura2, Yuuki Shimizu2, Daisuke Yuasa2, Kazuhiro Matsuo2, Megumi Miyabe2, Yoshiyuki Kataoka2, Toyoaki Murohara2 and Noriyuki Ouchi2,*

Ischemic heart disease is the major cause of death in Western countries. C1q/TNF-related protein (CTRP) 9 is a fat-derived plasma protein that has salutary effects on glucose metabolism and vascular function. However, the functional role of CTRP9 in ischemic heart disease has not been clarified. Here we examined the regulation of CTRP9 in response to acute cardiac injury and investigated whether CTRP9 modulates cardiac damage after ischemia and reperfusion. Myocardial ischemia-reperfusion injury resulted in reduced plasma CTRP9 levels and increased plasma free fatty acid levels, which were accompanied by decrease in CTRP9 expression and increase in NADPH oxidase component expression in fat tissue. Treatment of cultured adipocytes with palmitic acid or hydrogen peroxide reduced CTRP9 expression. Systemic administration of CTRP9 to wild-type mice, before the induction of ischemia or at the time of reperfusion, led to a reduction of myocardial infarct size following ischemia-reperfusion. Administration of CTRP9 also attenuated myocyte apoptosis in ischemic heart, which was accompanied by increased phosphorylation of AMP-activated protein kinase (AMPK). Treatment of cardiac myocytes with CTRP9 protein reduced apoptosis in response to hypoxia/reoxygenation and stimulated the AMPK phosphorylation. Blockade of AMPK activity reversed the suppressive actions of CTRP9 on cardiomyocyte apoptosis. Knockdown of adiponectin-receptor 1 diminished CTRP9-induced increases in AMPK phosphorylation and survival of cardiac myocytes. Our data suggest that CTRP9 protects against acute cardiac injury following ischemia-reperfusion via an AMPK-dependent mechanism.