Zheng Jolene, DiLorenzo Daniel J, McLaughlin Leslie, Roberts Andrew T, Greenway Frank L
Veterinary Science Department, Louisiana State University AgCenter, Baton Rouge, LA 70803, USA.
Med Hypotheses. 2009 Jun;72(6):706-10. doi: 10.1016/j.mehy.2008.12.046. Epub 2009 Feb 25.
Sympathetic activity and obesity have a reciprocal relationship. Firstly, hypothalamic obesity is associated with decreased sympathetic activity. Caffeine and ephedrine increase sympathetic activity and induce weight loss, of which 25% is due to increased metabolic rate and 75% is due to a reciprocally decreased food intake. Secondly, hormones and drugs that affect body weight have an inverse relationship between food intake and metabolic rate. Neuropeptide Y decreases sympathetic activity and increases food intake and body weight. Thirdly, a gastric pacemaker Transcend and vagotomy increase the ratio of sympathetic to parasympathetic activation, decrease food intake, and block gut satiety hormones. Weight loss with the pacemaker or vagotomy is variable. Significant weight reduction is seen only in a small group of those treated. This suggests that activation of the sympathetic arm of the autonomic nervous system may be most important for weight loss. Systemic sympathetic activation causes weight loss in obese patients, but side effects limited its use. We hypothesize that selective local electrical sympathetic stimulation of the upper gastrointestinal tract may induce weight loss and offer a safer, yet effective, obesity treatment. Celiac ganglia delivers sympathetic innervation to the upper gastrointestinal tract. Voltage regulated electrical simulation of the rat celiac ganglia increased metabolic rate in a dose-dependent manner. Stimulation of 6, 3, or 1.5 V increased metabolic rate 15.6%, 6.2%, and 5%, respectively in a single rat. These responses support our hypothesis that selective sympathetic stimulation of the upper GI tract may treat obesity while avoiding side effects of systemic sympathetic activation.
交感神经活动与肥胖之间存在相互关系。首先，下丘脑性肥胖与交感神经活动降低有关。咖啡因和麻黄碱可增加交感神经活动并导致体重减轻，其中25%归因于代谢率增加，75%归因于食物摄入量相应减少。其次，影响体重的激素和药物在食物摄入量和代谢率之间存在相反关系。神经肽Y会降低交感神经活动，增加食物摄入量和体重。第三，胃起搏器Transcend和迷走神经切断术会增加交感神经与副交感神经激活的比例，减少食物摄入量，并阻断肠道饱腹感激素。使用起搏器或迷走神经切断术减肥的效果因人而异。仅在一小部分接受治疗的患者中出现显著体重减轻。这表明自主神经系统交感神经分支的激活可能对减肥最为重要。全身性交感神经激活可使肥胖患者体重减轻，但副作用限制了其应用。我们假设对上消化道进行选择性局部电交感神经刺激可能会导致体重减轻，并提供一种更安全且有效的肥胖治疗方法。腹腔神经节为上消化道提供交感神经支配。对大鼠腹腔神经节进行电压调节电刺激可使代谢率呈剂量依赖性增加。在一只大鼠中，分别施加6V、3V或1.5V的刺激可使代谢率分别提高15.6%、6.2%和5%。这些反应支持了我们的假设，即对上消化道进行选择性交感神经刺激可能治疗肥胖，同时避免全身性交感神经激活的副作用。
