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肥胖症患者摄食后内源性大麻素食欲肽和厌食肽的同时失调。

Simultaneous postprandial deregulation of the orexigenic endocannabinoid anandamide and the anorexigenic peptide YY in obesity.

机构信息

Group Energy Balance and Obesity, INSERM U862, Neurocentre Magendie, Bordeaux, France.

出版信息

Int J Obes (Lond). 2012 Jun;36(6):880-5. doi: 10.1038/ijo.2011.165. Epub 2011 Aug 16.

DOI:10.1038/ijo.2011.165
PMID:21844878
Abstract

BACKGROUND

The endocannabinoid system is a potential pharmacotherapy target for obesity. However, the role of this system in human food intake regulation is currently unknown.

METHODS

To test whether circulating endocannabinoids might functionally respond to food intake and verify whether these orexigenic signals are deregulated in obesity alongside with anorexigenic ones, we measured plasma anandamide (AEA), 2-arachidonoylglycerol (2-AG) and peptide YY (PYY) changes in response to a meal in 12 normal-weight and 12 non-diabetic, insulin-resistant obese individuals.

RESULTS

Both normal-weight and obese subjects had a significant preprandial AEA peak. Postprandially, AEA levels significantly decreased in normal-weight, whereas no significant changes were observed in obese subjects. Similarly, PYY levels significantly increased in normal-weight subjects only. No meal-related changes were found for 2-AG. Postprandial AEA and PYY changes inversely correlated with waist circumference, and independently explained 20.7 and 21.3% of waist variance. Multiple regression analysis showed that postprandial AEA and PYY changes explained 34% of waist variance, with 8.2% of the variance commonly explained.

CONCLUSION

These findings suggest that AEA might be a physiological meal initiator in humans and furthermore show that postprandially AEA and PYY are concomitantly deregulated in obesity.

摘要

背景

内源性大麻素系统是肥胖症潜在的药物治疗靶点。然而,该系统在人类食物摄入调节中的作用目前尚不清楚。

方法

为了测试循环内源性大麻素是否可能对食物摄入产生功能性反应,并验证这些食欲刺激信号是否与厌食信号一起在肥胖症中失调,我们测量了 12 名正常体重和 12 名非糖尿病、胰岛素抵抗肥胖个体在进食前后血浆花生四烯酸酰胺(AEA)、2-花生四烯酸甘油(2-AG)和肽 YY(PYY)的变化。

结果

正常体重和肥胖组受试者均有显著的餐前 AEA 峰值。正常体重组餐后 AEA 水平显著下降,而肥胖组无明显变化。同样,PYY 水平仅在正常体重组显著增加。2-AG 无与进餐相关的变化。餐后 AEA 和 PYY 的变化与腰围呈负相关,分别独立解释了腰围变化的 20.7%和 21.3%。多元回归分析显示,餐后 AEA 和 PYY 的变化解释了腰围变化的 34%,其中 8.2%的方差是共同解释的。

结论

这些发现表明,AEA 可能是人类生理进餐的启动者,此外还表明,肥胖症患者餐后 AEA 和 PYY 同时失调。

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