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AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 6 1313-R1317, Copyright © 1989 by American Physiological Society
ARTICLES |
D. P. Figlewicz, A. J. Sipols, D. Porte Jr, S. C. Woods and R. A. Liddle
Department of Psychology, University of Washington, Seattle 98195.
To evaluate the role of cholecystokinin (CCK) as a physiological regulator of meal size and gastric emptying in the baboon, we measured plasma CCK bioactivity during 30-min meals alone and after intravenous or intraventricular infusions of CCK COOH-terminal octapeptide (CCK-8). Both intravenous (2 micrograms/kg) and intraventricular (1 microgram/kg) CCK-8 administration resulted in plasma CCK elevations comparable with normal prandial CCK levels: peak plasma levels were 4.1 +/- 0.9, 7.1 +/- 1.1, and 4.9 +/- 2.2 pM for pooled intravenous and intraventricular control, intravenous, and intraventricular conditions. Also, both treatments appeared to reduce gastric emptying as indicated by a significant suppression of postprandial plasma insulin and glucose levels. However, only intraventricular CCK reliably reduced meal size (percent of control meal size was 91 +/- 5% or 43 +/- 19% with intravenous or intraventricular CCK). We conclude that circulating endogenous CCK is a potent postprandial endocrine regulator of gastric emptying. However, the ability of CCK to decrease meal size may require direct interaction with the central nervous system.
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