Regeneration may mediate the sparing of VMH obesity observed with prior vagotomy.
The extent to which the vagus nerve is involved in mediating the development of obesity in animals with lesions of the ventromedial hypothalamus (VMH) was determined. Female rats were given either VMH lesions or sham lesions 100 days after they had received vagotomy with pyloroplasty, sham vagotomy with pyloroplasty, or sham vagotomy with sham pyloroplasty. For the first 7 postlesion wk, the animals were fed a wet mash diet, then they were maintained on a high-fat diet for 10 wk, and finally they were fed a highly palatable supermarket diet for 4 wk. VMH-lesioned animals with prior vagotomy and pyloroplasty displayed 65% of the obesity observed in lesioned animals with prior sham vagotomy. This expression was increased to 72% of the full VMH obesity during the supermarket diet phase. Assessment of vagotomy suggested that vagal regeneration and, in some cases, recovery of vagally stimulated insulin secretion had occurred. This reorganization may have contributed to the residual obesity expressed in VMH-lesioned animals with prior vagotomy.
D000818:Animals; D004558:Electric Stimulation; D004947:Esophagus / Q000294:innervation; D005260:Female; D007033:Hypothalamus, Middle / Q000502:physiology*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D009416:Nerve Regeneration; D009765:Obesity / Q000209:etiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012038:Regeneration; D013997:Time Factors; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology
D007328:Insulin