Neuroendocrine and autonomic regulation of ingestive behaviour in the golden hamster (Mesocricetus auratus)

Miceli, Mario (1984) Neuroendocrine and autonomic regulation of ingestive behaviour in the golden hamster (Mesocricetus auratus). Doctoral (PhD) thesis, Memorial University of Newfoundland.

[English] PDF (Migrated (PDF/A Conversion) from original format: (application/pdf)) - Accepted Version Available under License - The author retains copyright ownership and moral rights in this thesis. Neither the thesis nor substantial extracts from it may be printed or otherwise reproduced without the author's permission. Download (29MB) [English] PDF - Accepted Version Available under License - The author retains copyright ownership and moral rights in this thesis. Neither the thesis nor substantial extracts from it may be printed or otherwise reproduced without the author's permission. (Original Version)

Abstract

Certain prandially released peptide hormones have been proposed to act as physiological satiety stimuli. It has been demonstrated in a variety of species that injection of these hormones reduces feeding in otherwise hungry animals. These peptides, however, were not previously tested in Syrian hamsters, a species known to have physiological feeding controls different from those of many other animals. The first series of experiments examined whether putative satiety hormones reduce feeding in this species. Feeding in fasted hamsters was measured after peripheral injections of cholecystokinin octapeptide (CCK-8), bombesin (BBS), thyrotropin releasing hormone (TRH), and calcitonin (CT) , Each of these peptides reduced feeding in hamsters, but with varying degrees of specificity. CCK-8 and BBS, but not TRH and CT, appeared to reduce feeding specifically. Intraventricular CCK-8, BBS, and CT also decreased feeding in fasted hamsters. Effective central doses of BBS and CT were considerably lower than effective peripheral doses, thus indicating a central site of action for these peptides. Comparable amounts of CCK-8 were required to suppress feeding by either intraventricular or peripheral routes of administration. -- In a second series of experiments it was found that peripheral CCK-8 injections also reduced gastric emptying. Since gastric distention is a well-known satiety stimulus which is enhanced by reduced gastric emptying, it was possible that CCK-8 reduced feeding indirectly by facilitating gastric distention. The sham-feeding paradigm, in which orally ingested liquid diet passes out of a gastric fistula (thereby eliminating gastric distention), was used to assess this possibility. The relative efficacy of peripherally injected CCK-8 was tested in hamsters with chronic gastric fistulas during sham- and real-feeding (the fistula is closed and the stomach distends) sessions. Although CCK-8 did decrease sham-feeding, the magnitude of the decrement was small and not statistically reliable. In contrast, peripheral injections of CCK-8 produced a robust and reliable suppression of real-feeding. It is concluded that inhibition of gastric emptying and the ensuing gastric distention contribute to the satiety effect of peripherally administered CCK. -- A third series of experiments investigated the role of the abdominal vagus in CCK-8s inhibition of feeding. Total abdominal vagotomy completely blocked feeding suppression by a relatively low intraperitoneal dose of CCK-8. This blocking effect appeared to be specific to CCK-8, as vagotomized hamsters showed the usual feeding suppression in response to peripherally administered doses of BBS, CT, and TRH. In a second experiment vagotomized hamsters were completely unresponsive to relatively low doses of CCK (<_ 6.0 ug/kg) but did show feeding suppression in response to larger doses (_> 8.0 pg/kg). Selective gastric vagotomy also attenuated feeding suppression in response to CCK-8 but not as effectively as total abdominal vagotomy. These findings suggest that vagal fibres (probably afferents) are necessary for feeding suppression following low doses of exogenous CCK, and by inference, for eeding suppression by endogenous!y released gut-CCK. The gastric division of the vagus plays a major role in CCK's inhibition of feeding, but other abdominal divisions are also relevant. Extra-vagal sites of CCK action in the control of feeding (possibly in the brain) are indicated, since vagotomized hamsters reduced feeding after the larger CCK-8 doses. -- These findings in the hamster are discussed in relation to the sites and mechanisms of peptide action in the control of feeding in other species.

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