Veterans Research and Education Foundation and Transneuronix Research Lab, VA Medical Center, Oklahoma City, OK, USA.
Int J Obes (Lond). 2009 Aug;33(8):817-23. doi: 10.1038/ijo.2009.123. Epub 2009 Jun 23.
Intestinal electric stimulation (IES) is proposed as a potential tool for the treatment of morbid obesity. Our earlier study showed that IES with one pair of electrodes accelerated intestinal transit and decreased fat absorption in a segment of the jejunum in anesthetized rats. The aims of this study were to assess the effects of IES on whole gut transit and fat absorption in conscious rats, to examine the effects of multi-pairs IES and to explore the cholinergic mechanism behind the effects of IES.
Thirty-eight male rats implanted with serosal electrodes were randomized into five groups: control without IES, two- or three-pairs IES with short pulses, atropine and atropine plus IES. The whole gut transit and fat remained and emptied from the gut were analyzed after continuous 2-h IES.
Two- and three-pairs IES significantly accelerated phenol red (PR, marker used for transit) excretion (analysis of variance (ANOVA), P<0.001). No significant difference was found between two- and three-pairs IES. Two-pairs IES significantly increased the excretion of fat (P<0.05). Atropine significantly blocked the accelerated transit induced by IES (ANOVA, P<0.001). Correlation was found between the percentage of PR and fat retained in the whole gut (r=0.497, P<0.01).
IES accelerates whole gut transit and promotes fat excrement in conscious rats, and these effects are mediated through the cholinergic nerves. These findings are in support of the concept that IES may be a promising treatment option for obesity.
肠道电刺激(IES)被提议作为治疗病态肥胖的潜在工具。我们之前的研究表明,在麻醉大鼠的一段空肠中,使用一对电极进行 IES 可加速肠道转运并减少脂肪吸收。本研究的目的是评估 IES 对清醒大鼠全肠道转运和脂肪吸收的影响,研究多对电极的影响,并探讨 IES 作用背后的胆碱能机制。
38 只植入浆膜电极的雄性大鼠随机分为五组:无 IES 的对照组、短脉冲的两对对电极或三对对电极、阿托品和阿托品加 IES。连续 2 小时 IES 后,分析全肠道转运和脂肪从肠道中排空和残留的情况。
两对对电极和三对对电极均显著加速了酚红(PR,用于转运的标志物)的排泄(方差分析(ANOVA),P<0.001)。两对对电极和三对对电极之间没有显著差异。两对对电极显著增加了脂肪的排泄(P<0.05)。阿托品显著阻断了 IES 引起的转运加速(ANOVA,P<0.001)。PR 和全肠道中脂肪残留的百分比之间存在相关性(r=0.497,P<0.01)。
IES 可加速清醒大鼠的全肠道转运并促进脂肪排泄,这些作用是通过胆碱能神经介导的。这些发现支持 IES 可能是肥胖治疗的一种有前途的选择的概念。