AJP - Endocrinology and Metabolism, Vol 244, Issue 1 61-E65, Copyright © 1983 by American Physiological Society
Hyperphagia during lactation: satiety response to CCK and growth of the pancreas
C. L. McLaughlin, C. A. Baile and S. R. Peikin
Cholecystokinin (CCK) secreted from the duodenum during feeding has been
shown to elicit satiety and stimulate growth of the pancreas in addition to
affecting gastrointestinal function. In previous experiments hyperphagic
Zucker obese rats were less sensitive to the effects of CCK on satiety and
had a smaller pancreas than normal-weight rats. In the present experiments
with hyperphagic lactating Zucker rats, the food intake response to
exogenously administered CCK and the size and composition of the pancreas
were measured. Food intakes after a 2-h fast were not decreased by 4.0 or
8.0 micrograms/kg CCK-8 during wk 1, 2, or 3 of lactation. However, in the
same rats 2 wk after pups were weaned, 4.0 and 8.0 micrograms/kg CCK-8
decreased food intake 32% (2.1 +/- 0.4 vs. 3.1 +/- 0.3 g, paired t = 2.33,
P less than 0.03) and 52% (1.5 +/- 0.2 vs. 3.1 +/- 0.5 g, paired t = 3.48,
P less than 0.006). On day 18 of lactation, pancreas weight was increased
41% (1.38 +/- 0.05 vs. 0.98 +/- 0.02 g, paired t = 2.68, P less than 0.02)
and contents of DNA, RNA, and protein were increased 57, 57, and 73%,
respectively. Thus, hyperphagia in lactating female rats was associated
with 1) decreased sensitivity to the satiety effect of CCK similar to that
in hyperphagic obese rats and 2) hypertrophy of the pancreas in contrast to
decreased pancreas size in obese rats.
