AJP - Gastrointestinal and Liver Physiology, Vol 249, Issue 2 161-G167, Copyright © 1985 by American Physiological Society
Role of small intestine in pathogenesis of hyperlipidemia in diabetic rats
D. A. Popper, Y. F. Shiau and M. Reed
The small intestine can utilize endogenous substrates for triglyceride
synthesis. In diabetes mellitus, potential endogenous substrates are
elevated. This study was designed to investigate whether intestinal
triglyceride production utilizing endogenous substrates contributes to the
pathogenesis of hyperlipidemia in diabetes. Intestinal fatty acid
esterification as well as activities of acyl-CoA synthetase and acyl-CoA
monoglyceride acyltransferase are the same in diabetic and control rats
when the results are expressed per milligram protein. However, due to
marked intestinal hypertrophy these activities are increased when the
results are expressed as per centimeter gut length. In the mesenteric lymph
fistula rat model, we found that during fasting diabetic rats have a
greater than twofold increase in triglyceride output that is carried mainly
by very low-density lipoproteins (VLDL). During lipid infusion, total
triglyceride fatty acid output was not different between diabetic and
control rats, although there were significant differences in the patterns
of partition of endogenous and exogenous triglyceride into chylomicrons and
VLDL. Endogenous triglyceride production did not increase in diabetic rats
during lipid infusion. In contrast, there was a substantial increase in
endogenous triglyceride production in the control group to a level
comparable with that of the diabetic rats. There was a significant
reduction in incorporation of exogenous triglyceride into chylomicrons in
diabetic rats.
