Regulation of hepatic triglyceride synthesis in diabetic rats.

Abstract

A B S T R A C T The syntheses of triglyceride and its precursors were increased when liver homogenates of ketotic diabetic rats were incubated with [U-14C]-glycero 3-phosphate and cofactors. Triolein sonicates produced a concentration-dependent inhibition of the synthesis of both diglyceride and triglyceride, whereas monoolein sonicates had no effect. Rat In studies on the site of inhibition oftriglyceride synthesis in the overall biosynthetic pathway, serum very low density lipoproteins produced a concentrationdependent inhibition of liver cytosolic phosphatidate phosphohydrolase activity. A higher I50 value was obtained with the hepatic enzyme of the diabetic rats. This higher I50 value was reversed to control by insulin treatment of the diabetic rats. These results indicated that the activity of this enzyme was less sensitive to inhibition by very low density lipoproteins in the ketotic diabetic state. The reduced sensitivity ofphosphatidate phosphohydrolase activity to triglyceride inhibition observed in the present studies could explain our previous observation ofan increased rate oftriglyceride synthesis in ketotic diabetic liver homogenates.

Effects of vitamin B1, vitamin E and selenium on pregnancy and blood metabolites profile during non-breeding season and early prediction of pregnancy by thermographic monitoring in Merino ewes

“…Cholesterol metabolism also changed over time in both groups. Murthy and Shipp (1981) reported that cholesterol concentration was non-significantly higher during estrus. Cholesterol is a key component of steroid hormones.…”

Pathogenesis of alcoholic hepatic steatosis

“…These studies support a role for enhanced triacylglycerol synthesis in the pathogenesis of alcoholic steatosis. However, in animal studies the data suggests that as lipid accumulation progresses, hepatic triacylglycerol synthesis becomes depressed, possibly due to the inhibitory effect of very low density lipoprotein triacylglycerol on PAH activity (Murthy & Shipp, 1981). Recent evidence suggests that before incorporation into very low density lipoproteins cytosolic triacylglycerol must undergo lipolysis and subsequent re-esterification (Gibbons et al, 1994;Yang et al, 1995), impairment of this process may also contribute to hepatic lipid accumulation.…”