Effects of vagal and splanchnic section on food intake, weight, serum leptin and hypothalamic neuropeptide Y in rat

Citation
Jb. Furness et al., Effects of vagal and splanchnic section on food intake, weight, serum leptin and hypothalamic neuropeptide Y in rat, AUTON NEURO, 92(1-2), 2001, pp. 28-36
Citations number
40
Categorie Soggetti
Neurosciences & Behavoir
Journal title
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
ISSN journal
15660702 → ACNP
Volume
92
Issue
1-2
Year of publication
2001
Pages
28 - 36
Database
ISI
SICI code
1566-0702(20010917)92:1-2<28:EOVASS>2.0.ZU;2-F
Abstract
Truncal vagotomy can cause reduced food intake and weight loss in humans an d laboratory animals. In order to investigate some of the factors that migh t contribute to this effect, we studied changes in ingestive behaviour, who le body and organ weights, serum leptin and hypothalamic neuropeptide Y in rats with bilateral vagal section, bilateral splanchnic nerve section and c ombined vagotomy plus splanchnectomy. Pyloromyotomy was combined,with vagot omy to lessen effects of vagotomy on gastric emptying. Animals with vagotom y or vagotomy plus splanchnectomy lost weight and decreased their daily foo d intake relative to animals with splanchnectomy alone, rats with bilateral sham exposure of one or both nerve; or rats with pyloromyotomy alone. Seru m 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 weig ht or fat mass, but reduced serum leptin. Following vagotomy with or withou t splanchnic nerve section, neuropeptide Y was elevated in the arcuate nucl eus 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 f eeding signal carried by vagal afferent neurons, or to changed humoral sign als, for example, increased production of a satiety hormone. However, it ca nnot be attributed to signals that reduce feeding (for example, gastric dis tension) 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. (C) 200 1 Elsevier Science B.V. All rights reserved.