L-arginine promotes gut hormone release and reduces food intake in rodents.
L-arginine promotes gut hormone release and reduces food intake in rodents.
复制标题
DOI：
10.1111/dom.12644
复制
发表时间：
2016-05
期刊：
影响因子：
--
通讯作者：
Murphy KG
中科院分区：
文献类型：
--
作者：
Alamshah A;McGavigan AK;Spreckley E;Kinsey-Jones JS;Amin A;Tough IR;O'Hara HC;Moolla A;Banks K;France R;Hyberg G;Norton M;Cheong W;Lehmann A;Bloom SR;Cox HM;Murphy KG
研究L -精氨酸（L - Arg）对啮齿动物的厌食作用。我们研究了L -精氨酸对食物摄入的影响，以及啮齿动物厌食肠道激素胰高血糖素样肽- 1 （GLP - 1）和肽YY （PYY）、G -蛋白偶联受体家族C组6成员A （GPRC6A）和迷走神经在介导这些影响中的作用。口服L - Arg减少了啮齿动物的食物摄入量，并长期减少了饮食诱导的肥胖小鼠的累积食物摄入量。小鼠GPRC6A的缺乏和大鼠膈下迷走神经移行不影响这些厌食作用。L -精氨酸刺激GLP - 1和PYY在体内和体外释放。GLP‐1和PYY受体的药物阻断不影响L‐精氨酸的厌食效果。L -精氨酸介导的PYY释放调节净离子在肠道粘膜上的转运。经脑室和腹腔注射L - Arg可抑制大鼠的食物摄入。L -精氨酸减少了啮齿动物的食物摄入量，刺激了肠道激素的释放。L -精氨酸的厌食作用不太可能由GLP - 1和PYY介导，不需要GPRC6A信号传导，也不通过迷走神经介导。L - Arg的体外注射和i.p.抑制了大鼠的食物摄入，表明L - Arg可能作用于大脑来影响食物摄入。需要进一步的工作来确定L -精氨酸抑制食物摄入的机制及其在治疗肥胖方面的应用。
To investigate the anorectic effect of L‐arginine (L‐Arg) in rodents. We investigated the effects of L‐Arg on food intake, and the role of the anorectic gut hormones glucagon‐like peptide‐1 (GLP‐1) and peptide YY (PYY), the G‐protein‐coupled receptor family C group 6 member A (GPRC6A) and the vagus nerve in mediating these effects in rodents. Oral gavage of L‐Arg reduced food intake in rodents, and chronically reduced cumulative food intake in diet‐induced obese mice. Lack of the GPRC6A in mice and subdiaphragmatic vagal deafferentation in rats did not influence these anorectic effects. L‐Arg stimulated GLP‐1 and PYY release in vitro and in vivo. Pharmacological blockade of GLP‐1 and PYY receptors did not influence the anorectic effect of L‐Arg. L‐Arg‐mediated PYY release modulated net ion transport across the gut mucosa. Intracerebroventricular (i.c.v.) and intraperitoneal (i.p.) administration of L‐Arg suppressed food intake in rats. L‐Arg reduced food intake and stimulated gut hormone release in rodents. The anorectic effect of L‐Arg is unlikely to be mediated by GLP‐1 and PYY, does not require GPRC6A signalling and is not mediated via the vagus. I.c.v. and i.p. administration of L‐Arg suppressed food intake in rats, suggesting that L‐Arg may act on the brain to influence food intake. Further work is required to determine the mechanisms by which L‐Arg suppresses food intake and its utility in the treatment of obesity.