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D A Popper

Publications and source records attributed to D A Popper.

2 recordsLinked to original sources

Intestinal triglycerides are derived from both endogenous and exogenous sources.

Although studies have indicated that the small intestine is capable of utilizing endogenous substrates for triglyceride synthesis in the absence of dietary lipid, the importance of the endogenous contribution to total intestinal triglyceride production during absorption has not yet been defined. In this study we have examined the quantitative contribution of endogenous triglyceride production during different luminal lipid loads. By use of a mesenteric lymph fistula rat model with total parenteral nutritional support, mesenteric lymphatic triglyceride transport was investigated. Our results indicate that, during absorption, a substantial fraction (greater than 50%) of total triglyceride is derived from endogenous sources. Increased luminal fatty acid loads lead to an increase in both endogenous and exogenous triglyceride production. Incorporation of luminally infused oleic acid into triglyceride carried by chylomicrons is dependent on the luminal fatty acid load, while incorporation of oleic acid into very low-density lipoprotein (VLDL) triglyceride is saturable. We conclude that both chylomicron and VLDL are involved in transporting triglyceride derived from both endogenous and exogenous sources. The different patterns in the partition of endogenous and exogenous triglyceride into chylomicrons and VLDL suggest that these two lipid-carrying lipoproteins are probably packaged differently in the small intestine.

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Role of small intestine in pathogenesis of hyperlipidemia in diabetic rats.

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.

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