Elevation of plasma cholecystokinin concentration following a meal is increased by gonadectomy in male cats

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Abstract:

Summary

An overweight or obese body condition commonly develops after gonadectomy (GX) in domestic cats. The cause appears to be a rapid, quantal (approximately 12%), increase in food intake that is sustained and probably mediated by withdrawal of gonadal hormone. Recently, an interaction of gonadal hormone and cholecystokinin (CCK) effectiveness has been suggested. A reduction in the satiating potency of intestinal CCK was presently hypothesized to contribute to the disturbance of food intake control caused by GX in domestic cats. Pre- and post-prandial intestinal CCK secretion as indicated by plasma CCK concentrations were determined in 16 adult male cats (5.1 ± 0.1 kg) 8 weeks before and 57 weeks after eight of the cats were gonadectomized. During ad libitum intake of a commercial dry, expanded diet, body weight increased from 22% to 28% in gonadectomized cats and was unchanged in intact cats. Baseline CCK concentrations were not different between gonadectomized and intact cats. Amounts of diet ingested during CCK determinations were 15–19% of daily metabolizable energy requirement and were not different between gonadectomized and intact cats. The post-prandial area under the curve (AUC; 0–400 min) CCK concentration increased linearly with meal size (p < 0.01) and was not correlated with body weight. Area under the curve CCK concentration, when normalized for meal size, was 34% greater (p < 0.01) in gonadectomized cats than that in intact cats. The findings indicate GX increases meal-induced intestinal CCK secretion and therefore, do not support the study hypothesis. The findings indicate GX may slow digestion and absorption and attenuate inhibition of food intake by CCK.

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1439-0396.2005.00581.x

Affiliations: 1: Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO, USA and 2: Department of Molecular Biosciences, University of California, Davis, CA, USA

Publication date: April 1, 2006

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