Furness J B, Koopmans H S, Robbins H L, Clerc N, Tobin J M, Morris M J
Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Australia.
Auton Neurosci. 2001 Sep 17;92(1-2):28-36. doi: 10.1016/S1566-0702(01)00311-3.
Truncal vagotomy can cause reduced food intake and weight loss in humans and laboratory animals. In order to investigate some of the factors that might contribute to this effect, we studied changes in ingestive behaviour, whole body and organ weights, serum leptin and hypothalamic neuropeptide Y in rats with bilateral vagal section, bilateral splanchnic nerve section and combined vagotomy plus splanchnectomy. Pyloromyotomy was combined with vagotomy to lessen effects of vagotomy on gastric emptying. Animals with vagotomy or vagotomy plus splanchnectomy lost weight and decreased their daily food intake relative to animals with splanchnectomy alone, rats with bilateral sham exposure of one or both nerve, or rats with pyloromyotomy alone. Serum leptin and white fat mass, 4 weeks after vagotomy, were about 20% of the values in the sham-operated animals at this time. No effect for splanchnic nerve section alone was observed. Pyloromyotomy caused no reduction in weight or fat mass, but reduced serum leptin. Following vagotomy with or without splanchnic nerve section, neuropeptide Y was elevated in the arcuate nucleus relative to values for the other four groups. Changes in neuropeptide Y were inversely correlated with levels of serum leptin. It is concluded that the effect of vagotomy could be due to the loss of a feeding signal carried by vagal afferent neurons, or to changed humoral signals, for example, increased production of a satiety hormone. However, it cannot be attributed to signals that reduce feeding (for example, gastric distension) reaching the central nervous system via the splanchnic nerves. The changes were sufficient to cause weight loss even though serum leptin was decreased, a change that would be expected to increase food intake.
迷走神经干切断术可导致人类和实验动物食物摄入量减少及体重减轻。为了探究可能导致这种效应的一些因素，我们研究了双侧迷走神经切断、双侧内脏神经切断以及迷走神经切断加内脏神经切除术大鼠的摄食行为、全身和器官重量、血清瘦素和下丘脑神经肽Y的变化。幽门肌切开术与迷走神经切断术联合进行，以减轻迷走神经切断术对胃排空的影响。与仅接受内脏神经切除术的动物、一侧或双侧神经进行双侧假暴露的大鼠或仅接受幽门肌切开术的大鼠相比，接受迷走神经切断术或迷走神经切断加内脏神经切除术的动物体重减轻，每日食物摄入量减少。迷走神经切断术后4周，血清瘦素和白色脂肪量约为此时假手术动物值的20%。未观察到单纯内脏神经切断术有任何效果。幽门肌切开术未导致体重或脂肪量减少，但降低了血清瘦素。在进行或未进行内脏神经切断术的迷走神经切断术后，相对于其他四组的值，弓状核中的神经肽Y升高。神经肽Y的变化与血清瘦素水平呈负相关。得出的结论是，迷走神经切断术的效应可能是由于迷走神经传入神经元携带的进食信号丧失，或者是由于体液信号改变，例如饱腹感激素产生增加。然而，它不能归因于通过内脏神经到达中枢神经系统的减少进食的信号（例如胃扩张）。即使血清瘦素降低，这些变化也足以导致体重减轻，而血清瘦素降低本应会增加食物摄入量。
