The results suggest that mangiferin may ameliorate hypertriglyceridemia partly by modulating the expression levels of genes involved in lipid oxidation and lipogenesis.
To elucidate mechanisms responsible for the increased plasma triglyceride (TG) which occurs in diet-induced hypercholesterolemia in rabbits, albino rabbits were fed a 3% cholesterol diet for various durations, and the following determinations were carried out: plasma lipid levels; turnover rate of plasma TG (labeled very low density lipoprotein, or glycerol-2-3 H method); lipoprotein lipase activity of the heart and plasma; fatty acid and acetate incorporation into TG in the liver (homogenates and slices). Plasma levels of both free and esterified cholesterol and phospholipid increased rapidly, while TG increased relatively slowly during cholesterol feeding without change in hepatic TG synthesis. The fractional turnover was, on the other hand, depressed within a week. The decrease in plasma TG in response to a heparin injection was less in hypercholesterolemic rabbits than in normal animals. However, the measured activity of heart lipoprotein lipase of cholesterol-fed rabbits was higher than that of the control group. When the effects of two substrates (very low density lipoprotein from normo-and from hypercholesterolemic plasma) were compared, the apparent activity was lower with the latter. The degree of this inhibition was proportional to the amount of cholesterol in the lipoproteins. The inhibition of lipoprotein lipase activity was also observed with the addition of cholesterol to activated Ediol, but not with addition of esterified cholesterol. Lineweaver-Burk plots were constructed using partially purified plasma lipoprotein lipase, and Km values for Ediol, Ediol plus protamine sulphate, and Ediol plus cholesterol were calculated. The presence of cholesterol in the substrate of lipoprotein lipase competitively inhibits the enzyme activity, and this is the mechanism of hyperglyceridemia observed in diet-induced hypercholesterolemic rabbits. ADDITIONAL KEY WORDS plasma lipoprotein lipase very low density lipoprotein plasma triglyceride turnover heart lipoprotein lipase cholesterol inhibition of lipoprotein lipase hepatic triglyceride synthesis • There are a number of clinical entities which accompany hypercholesterolemia, hyperglyceridemia, and defective postheparin lipolytic activity (1-4). Experimentally, when rabbits are fed a diet containing a high cholesterol content, not only does the plasma concentration of cholesterol increase, but an From the
Rabbits were fed a diet containing 3% cholesterol for 2–6 months. Total cholesterol, cholesterol ester, phospholipids, and triglycerides were increased in the plasma. Total cholesterol and cholesterol ester were also increased in the heart mitochondria and supernatant, and liver mitochondria, microsomes, and supernatant, but triglycerides and phospholipids in all cell fractions studied remained within the normal ranges. The respiratory control ratio, P/O ratio, and oxygen consumption of the cardiac and hepatic mitochondria were not affected by the increase in cholesterol content. Possible mechanisms responsible for the altered lipid composition in the cells of rabbits on a high-cholesterol diet, as well as that for the unchanged mitochondrial respiratory function are discussed.
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