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Feeding to mice of both basal as well as high sucrose diet led to increased levels of plasma triglycerides, which was associated with increased lecithin-cholesterol acyltransferase activity. Although males had significantly higher LCAT activity than females in all the dietary groups, sex difference in the plasma triglycerides was observed in high sucrose group only. Increase in plasma triglycerides in experimental groups was associated with an increase in LCAT activity.
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The effects of level and feeding frequency of retinoic acid (OIC) or retinyl acetate (YL) on the accumulation of lipids in the serum and liver of rats were investigated. Male Sprague-Dawley rats were fed ad libitum 1% cholesterol diets with or without supplemental OIC or YL. Vitamin A-fed groups included (per g of dry diet): 105 microgram of OIC or 113 microgram YL daily for 28 days, 735 microgram OIC or 791 microgram YL once each week for 28 days; and 735 or 105 microgram OIC on day 1 or 105 microgram OIC daily for the week experiment. Daily feeding of OIC or YL increased serum triglyceride concentrations as compared to conrols. Several days after removal of OIC or 1 week after removal of supplemental YL from the rat diets, serum triglyceride concentrations returned to basal levels. Cholesterol feeding elevated serum cholesterol as well as hepatic cholesterol, total lipids and vitamin A concentrations. Daily OIC feeding depressed serum and hepatic cholesterol concentrations. These results show that daily supplement of vitamin A increased serum triglycerides and reduced serum and hepatic cholesterol concentrations. Serum and liver alterations were dependent on continued feeding.
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Plasma triglyceride concentration and blood oxygen tension were measured in samples obtained by cordocentesis from 35 small- and 54 appropriate-for-gestational-age fetuses at 18 to 36 weeks' gestation. In the appropriate-for-gestational-age fetuses there was an exponential decrease in plasma triglycerides with gestation. Some small-for-gestational age fetuses were hypertriglyceridemic and the degree of this biochemical disturbance was significantly correlated with the degree of fetal hypoxemia.
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Three different assays for selective measurement of plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) were compared. These were: an immunochemical method based on enzyme antibody precipitation (IM), a procedure in which both enzymes were separated by affinity chromatography on small heparin--Sepharose columns (HS), and an assay in which one enzyme was inhibited by protamine sulfate (PS). Good correlations were found between the immunochemical and the heparin--Sepharose method, but not between these and the protamine sulfate assay procedure. The IM was then used to evaluate the effect of clofibrate on the two lipolytic enzymes. It was found that both in normals and in patients with Type IV hyperlipoproteinemia, clofibrate treatment leads to a specific increase of plasma LPL while H-TGL activity remains almost unaffected. The magnitude of the LPL response was different in normals and in patients with endogenous hyperlipoproteinemia. Furthermore, in normals the maximal increase of LPL activity was already reached one week after drug treatment was begun, while in hypertriglyceridemic patients, this effect was not evident prior to four weeks of clofibrate treatment. The marked enzyme increase following clofibrate administration indicates that an increased peripheral removal rate for triglycerides is one major mechanism responsible for the lipid-lowering effect of this drug.
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