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
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
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