title: Effects of vagal and splanchnic section on food intake, weight, serum leptin and hypothalamic neuropeptide Y in rat.
abstract: 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.
authors.affiliation: Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Australia. j.furness@unimelb.edu.au
authors.forename: J B
authors.initials: JB
authors.lastname: Furness
authors.forename: H S
authors.initials: HS
authors.lastname: Koopmans
authors.forename: H L
authors.initials: HL
authors.lastname: Robbins
authors.forename: N
authors.initials: N
authors.lastname: Clerc
authors.forename: J M
authors.initials: JM
authors.lastname: Tobin
authors.forename: M J
authors.initials: MJ
authors.lastname: Morris
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology; D000818:Animals; D001835:Body Weight / Q000502:physiology; D015740:Calcitonin Gene-Related Peptide / Q000032:analysis; D004435:Eating / Q000502:physiology; D005260:Female; D007031:Hypothalamus / Q000737:chemistry*; D007150:Immunohistochemistry; D020738:Leptin / Q000097:blood*; D009197:Myenteric Plexus / Q000737:chemistry / Q000166:cytology; D009412:Nerve Fibers / Q000737:chemistry; D009478:Neuropeptide Y / Q000032:analysis*; D009929:Organ Size / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012528:Satiety Response / Q000502:physiology; D013153:Splanchnic Nerves / Q000502:physiology* / Q000601:surgery; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology* / Q000601:surgery
chemical_list: D020738:Leptin; D009478:Neuropeptide Y; D015740:Calcitonin Gene-Related Peptide