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Am J Physiol Regul Integr Comp Physiol 295: R76-R81, 2008. First published May 14, 2008; doi:10.1152/ajpregu.90327.2008
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APPETITE, OBESITY, AND DIGESTION

Salmon calcitonin reduces food intake through changes in meal sizes in male rhesus monkeys

Nicholas T. Bello, Matthew H. Kemm, and Timothy H. Moran

Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland

Submitted 31 March 2008 ; accepted in final form 13 May 2008

Amylinergic mechanisms are believed to be involved in the control of appetite. This study examined the effects of the amylin agonist, salmon calcitonin, on food intake and meal patterns in adult male rhesus monkeys. Fifteen minutes before the onset of their 6-h daily feeding period, monkeys received intramuscular injections of various doses of salmon calcitonin (0.032, 0.056, 0.1, 0.32, and 1 µg/kg) or saline. Salmon calcitonin dose dependently reduced total daily and hourly food intake, with significant decreases at the 0.1, 0.32, and 1 µg/kg doses. Daily food intake was reduced by ~35%, 62%, and 96%, at these doses, respectively. An analysis of meal patterns revealed that size of the first meal was significantly reduced across the dose range of 0.056 to 1 µg/kg, while average meal size was reduced with the 0.32 and 1 µg/kg doses. Meal number was only affected at the 1 µg/kg dose. Repeated 5-day administration of the 0.1 µg/kg dose resulted in a reduction in daily food intake only on injection day 2, while significant reductions in food intake were observed on all five injection days with a 0.32 µg/kg dose. Daily food intake was also reduced for 1 day after the termination of the 5-day injections of the 0.32 µg/kg salmon calcitonin dose. These sustained reductions in intake were expressed through decreases in meal size. These data demonstrate that salmon calcitonin acutely and consistently decreases food intake mainly through reductions in meal sizes in nonhuman primates.

satiation; islet amyloid polypeptide; calcitonin-gene related peptides



Address for reprint requests and other correspondence: N. T. Bello, Dept. of Psychiatry and Behavioral Sciences, Johns Hopkins Univ. School of Medicine, Ross 618, 720 Rutland Ave., Baltimore, MD 21205 (e-mail: ntbello{at}jhmi.edu)







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