AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 5 1219-R1224, Copyright © 1989 by American Physiological Society
Bombesin affects feeding independent of a gastric mechanism or site of action
A. M. Hostetler, P. R. McHugh and T. H. Moran
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Peripherally administered bombesin has been demonstrated to inhibit food
intake in a variety of species. Although the behavioral actions of bombesin
are well characterized, neither the site of action nor mechanism through
which bombesin affects feeding has been demonstrated. To test the
hypothesis that bombesin's feeding effects are through a gastric inhibitory
mechanism or a gastric site of action we examined the potential
relationship between the inhibition of gastric emptying and the inhibition
of intake produced across a dose range of bombesin and compared the
relative potency of bombesin analogues for inhibiting feeding with their
affinity for gastric bombesin receptors. Comparisons of the inhibitions of
gastric emptying and feeding produced by 2, 4, 8, or 16 micrograms/kg of
bombesin revealed no relationship, and, in fact, no gastric inhibitory
action was evident. The feeding inhibitory actions of dose ranges (100
pmol-100 nmol) of litorin, ranatensin, acetylated gastrin-releasing
peptide-(20-27) [AcGRP-(20-27)] and bombesin-(8-14) fragment were assessed
and compared with bombesin. These compounds inhibited feeding with a
relative potency of bombesin greater than AcGRP-(20-27) greater than
ranatensin greater than litorin greater than bombesin-(8-14). This rank
order of potency differed from the relative affinity of these compounds for
gastric bombesin receptors for which all of these compounds except
bombesin-(8-14) have a greater affinity than does bombesin. The results of
these two experiments suggest that bombesin's satiety actions are not
mediated by a gastric inhibitory mechanism or through a gastric site of
action.
