title: Decreased apoptosis and increased ornithine decarboxylase activity in the intestinal mucosa of rats with bilateral ventromedial hypothalamus lesions.
abstract: BACKGROUND
  It has not been clearly demonstrated whether the ventromedial hypothalamus regulates intestinal cell growth. Ornithine decarboxylase is a key enzyme in polyamine synthesis, which plays an important role in intestinal mucosal growth. The aim of this study was to investigate whether bilateral ventromedial hypothalamus lesions affect mucosal cell growth. This was done by evaluating ornithine decarboxylase activity and apoptosis in rat small intestines.
  
  
  METHODS
  Bilateral ventromedial hypothalamus lesions were produced by thermocoagulation, done with rats under halothane anesthesia 7 days before the experiments. Rats with lesions were pair-fed with sham-operated rats. Total (truncal) vagotomy was performed before the development of ventromedial hypothalamus lesions. Ornithine decarboxylase activity and apoptosis were evaluated in the jejunal mucosa.
  
  
  RESULTS
  Ornithine decarboxylase activity in the jejunal mucosa increased significantly 1 week after the development of the bilateral ventromedial lesions, and was attenuated by truncal vagotomy. Apoptosis in the jejunal mucosa was suppressed in rats with ventromedial hypothalamus lesions. In contrast to the effect on ornithine decarboxylase activity, the truncal vagotomies had no effect on apoptosis in rats with lesions. Apoptosis increased in the sham-operated rats after 24-h and 48-h fasting. Apoptosis in the jejunal mucosa of rats with ventromedial hypothalamus lesions did not increase after 24-h fasting. After 48-h fasting, jejunal apoptosis increased in rats with lesions, but not markedly.
  
  
  CONCLUSIONS
  The ventromedial hypothalamus may regulate cell growth in the intestinal mucosa partly through the vagal nerve; however, the vagal nerve was not related to intestinal apoptosis controlled by the ventromedial hypothalamus.
authors.affiliation: Department of Internal Medicine, Saga Medical School, Saga, 849-8501, Japan.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Sakata
authors.forename: Akifumi
authors.initials: A
authors.lastname: Ootani
authors.forename: Takehiro
authors.initials: T
authors.lastname: Fujise
authors.forename: Yasuhisa
authors.initials: Y
authors.lastname: Sakata
authors.forename: Bin
authors.initials: B
authors.lastname: Wu
authors.forename: Seiji
authors.initials: S
authors.lastname: Tsunada
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Iwakiri
authors.forename: Kazuma
authors.initials: K
authors.lastname: Fujimoto
authors.forename: Takemasa
authors.initials: T
authors.lastname: Shiraishi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D053938:DNA Fragmentation; D004564:Electrocoagulation; D004587:Electrophoresis, Agar Gel; D007033:Hypothalamus, Middle / Q000502:physiology*; D007413:Intestinal Mucosa / Q000294:innervation / Q000378:metabolism*; D007583:Jejunum / Q000294:innervation / Q000378:metabolism / Q000473:pathology; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D051381:Rats; D015167:Vagotomy, Truncal
chemical_list: D009955:Ornithine Decarboxylase