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下丘脑弓状核参与介导电针对肥胖大鼠的饱食效应。

Arcuate nucleus of hypothalamus is involved in mediating the satiety effect of electroacupuncture in obese rats.

机构信息

Neuroscience Research Institute, Peking University, Beijing 100083, PR China.

出版信息

Peptides. 2011 Dec;32(12):2394-9. doi: 10.1016/j.peptides.2011.10.019. Epub 2011 Oct 25.

Abstract

Obesity is a major health problem in the world. Since effective remedies are rare, researchers are trying to discover new therapies for obesity, and acupuncture is among the most popular alternative approaches. This study investigated the anti-obesity mechanisms of EA, using a rat model of diet-induced obesity. After feeding with a high-fat diet for 9 weeks, a number of rats who gained weight that surpassed the maximal body weight of rats in the chow-fed group were considered obese and employed in the study. A 2 Hz EA treatment at the acupoints ST36/SP6 with the intensity increasing stepwise from 0.5-1-1.5 mA was given once a day for 30 min. Rats treated with EA showed significantly decreased food intake and reduced body weight compared with the rats in DIO and restraint group. EA treatment increased peptide levels of α-MSH and mRNA levels of its precursor POMC in the arcuate nuclear of hypothalamus (ARH) neurons. In addition, the cerebral spinal fluid (CSF) content of α-MSH was elevated by EA application. ARH lesions by monosodium glutamate abolished the inhibition effect of EA on food intake and body weight. A non-acupoint stimulation did not show the benefit effect on food intake inhibition and body weight reduction compared with restraint and ST36/SP6 EA treatment. We concluded that EA treatment at ST36/SP6 acted through ARH to significantly inhibit food intake and body weight gain when fed a high-fat diet and that the stimulation of α-MSH expression and release might be involved in the mechanism.

摘要

肥胖是全球范围内的一个主要健康问题。由于有效的治疗方法很少,研究人员正在努力寻找治疗肥胖的新方法,而针灸是最受欢迎的替代方法之一。本研究通过高脂肪饮食诱导肥胖的大鼠模型,探讨了电针对肥胖的治疗机制。经过 9 周的高脂饮食喂养后,体重超过正常饮食喂养组大鼠最大体重的一些大鼠被认为是肥胖的,并被纳入研究。每天给予 2 Hz 的电针对双侧足三里(ST36)和三阴交(SP6)穴位刺激,强度从 0.5 mA 逐渐增加至 1 mA 和 1.5 mA,每次刺激 30 分钟。与 DIO 组和束缚组相比,电针治疗组大鼠的食物摄入量显著减少,体重降低。电针治疗组大鼠下丘脑弓状核神经元的肽水平α-MSH 和前体 POMC 的 mRNA 水平增加。此外,电针治疗还增加了脑脊液(CSF)中α-MSH 的含量。谷氨酸单钠引起的 ARH 损伤消除了电针对食物摄入和体重的抑制作用。与束缚和 ST36/SP6 电针治疗相比,非穴位刺激对抑制食物摄入和减轻体重没有益处。我们得出结论,电针 ST36/SP6 治疗通过 ARH 发挥作用,显著抑制高脂肪饮食喂养大鼠的食物摄入和体重增加,而刺激α-MSH 的表达和释放可能参与了这一机制。

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