Abstract
Cholecystokinin (CCK) has been shown to elicit insulin secretion and increased insulin availability has been shown to correlate with increased satiety attributed to reduced size of spontaneously occurring meals. The present experiment, however, clearly showed that CCK was effective in suppressing food ingestion in free-fed rats independent of the animal's level of insulin. Rats were tested with 1, 2 and 4 μg/kg of CCK-octapeptide (Sincalide, Squibb) during a baseline (pancreatic-normal) period, an insulin-poor state (streptozotocin diabetic) and an insulin clamped condition (diabetic treated by a minipump). CCK produced a highly significant ( p<0.01) reduction of food intake compared to saline, control injections regardless of the insulin conditions of the animals. Higher doses of CCK were more effective than lower doses during all three periods of study. CCK and hyperinsulinemia function independently if they produce satiety or reductions in food intake.
Published Version
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