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Lipid metabolism in pregnancy 8. effects of dietary fat vs. carbohydrate on lipo protein and hepatic lipids and tissue tri glyceride lipases



Lipid metabolism in pregnancy 8. effects of dietary fat vs. carbohydrate on lipo protein and hepatic lipids and tissue tri glyceride lipases



Metabolism Clinical and Experimental 30(1): 27-35



Whether hypertriglyceridemia in the fed state in pregnancy is due to intolerance to exogenous fat, accumulation of endogenous triglycerides [TG] or to accumulation of remnants of d [density] < 1.006 lipoprotein metabolism was determined. Pregnant and nonpregnant rats were fed fat-free diets high in starch or sucrose, or diets containing fat or fat plus cholesterol for 12 days until gestational day 21 (term = 22 days). Blood was obtained 0, 4 or 8 h after removal of food from the cages. Lipid concentrations were determined in chylomicrons and very low, low and high density lipoproteins. Hypertriglyceridemia in pregnancy exists on both starch and sucrose containing fat-free diets and is exaggerated 4 and 8 h after food is removed from the cage. The TG rise occurs in d < 1.006 lipoproteins. With fat feeding, chylomicron TG concentrations are not significantly elevated in pregnant rats, 0 or 8 h postabsorptively despite greater food intake in pregnancy. Very low density lipoprotein (VLDL) TG concentrations are elevated at all times following fat feeding in pregnant compared to nonpregnant animals. A significant contribution of lipoprotein remnants to the TG rise in d < 1.006 lipoproteins seems unlikely since an isolated increase in VLDL cholesterol is not observed. No statistically significant accumulation of hepatic TG occurs on any diet in pregnancy. Diet-induced shifts in adipose tissue and muscle lipoprotein lipase activity are exaggerated in pregnancy while hepatic lipase is unaffected. Fetal weight is similar on all diets except sucrose where weight is reduced. Hypertriglyceridemia in fed pregnant rats is due to an increase in endogenous TG. Remnant lipid accumulation does not appear to contribute to the endogenous hypertriglyceridemia. There is no intolerance to exogenous (dietary) fat. The results are compatible with an unimpaired delivery of exogenous fat to fat oxidizing tissues thereby maximizing glucose availability for fetal growth.

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