Download PDF
Horm Metab Res 1982; 14(8): 392-395
DOI: 10.1055/s-2007-1019027
© Georg Thieme Verlag, Stuttgart · New York

Starvation Increases Gastrointestinal Somatostatin in Normal and Obese Zucker Rats: A Possible Regulatory Mechanism

Nancy R. Voyles, Sissay Awoke, Angel Wade, S. J. Bhathena, S. S. Smith, Lillian Recant
  • Veterans Administration Medical Center, Washington, D.C., U.S.A.
Further Information

Publication History

1981

1981

Publication Date:
14 March 2008 (online)

Also available at
  PDF Download  Permissions and Reprints

Summary

Normal, male Sprague-Dawley (S-D) rats and female, lean and obese Zucker rats were studied in the fed state and after 48 hours of food deprivation. Somatostatin-like immunoreactivity (SLI) was measured from acetic acid extracts of oesophagus-cardia, stomach, small and large intestine, pancreas, hypothalamus, pituitary and cerebellum. Within the CNS, the highest levels of SLI were found in the hypothalamus, while in the gut, these levels were highest in the stomach and pancreas. All Zucker rats displayed higher hypothalamic levels of SLI than did S-D rats. Obese Zucker rats in the fed state differed from their lean littermates in that SLI levels were lower in oesophagus-cardia, stomach and hypothalamus, while being higher in pancreas and pituitary. The response to starvation in both obese and lean Zucker rats was qualitatively similar, and included significant increases in stomach and oesophagus-cardia SLI, but with a significant fall in hypothalamic SLI. We have concluded that the increase in gastrointestinal SLI with starvation in Zucker as well as in S-D rats may represent a significant regulatory mechanism in nutrient homeostasis. We postulate that gastric SLI may decrease the availability of intestinal insulin secretagogues in the fasting state. This adaptive mechanism appears to be intact in the obese Zucker rat.

Key-Words:

Gastrointestinal Somatostatin - CNS - Somatostatin - Starvation - Zucker Rats - Obesity

      >