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J Belleville

Publications and source records attributed to J Belleville.

133 records · Page 8Linked to original sources

Hepatic steatosis and serum very low density lipoproteins during two types of protein malnutrition followed by balanced refeeding.

The relation of serum very low density lipoproteins (VLDL) to hepatic steatosis was studied during protein malnutrition followed by refeeding of a balanced diet in growing rats. A control group was fed a balanced diet containing 15% casein for 42 days. Two depleted groups were fed low protein diets containing 2% casein (group C) or 5% gluten (group GI) (protein malnutrition phase) for 28 days and then were fed the balanced diet for 14 days (refeeding phase). The concentrations of phospholipids and proteins in both liver and serum VLDL were decreased during protein malnutrition, whereas triacylglycerols, unesterified cholesterol, and cholesteryl esters were higher in the liver and lower in the serum VLDL in the C and GI groups compared with the control group. There was a significant inverse relation between serum VLDL apolipoproteins and liver triacylglycerols on the one hand and between serum VLDL triacylglycerols and liver triacylglycerols on the other hand, in both depleted groups, although this relation was less important in the GI group. The major fatty acid levels of liver triacylglycerols were negatively correlated with those of serum VLDL during protein malnutrition. Our results show that in spite of a similar fatty acid intake, protein malnutrition involved an important decrease in essential fatty acids in VLDL triacylglycerols and phospholipids. Moreover, triacylglycerol accumulation was accompanied by increases in unesterfied cholesterol and cholesteryl esters in the liver of rats fed low protein diets, especially with 5% gluten. Hence, the hepatic steatosis was not entirely attributable to impaired transport of triacylglycerols by VLDL.

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Time course of changes in rat serum lecithin-cholesterol acyl-transferase activity and high-density-lipoprotein composition during the consumption of two different low-protein diets followed by a balanced diet.

We studied the effects of low-protein diets on high-density-lipoprotein (HDL) composition and checked whether the changes observed were correlated with lecithin-cholesterol acyl-transferase (LCAT) activity. We also studied whether HDL lipid and protein compositions and LCAT activity were modified differently in growing rats during the consumption of two low-protein diets [2% casein (C) and 5% gluten (GI)] for 28 days, followed by the refeeding of a balanced diet containing 15% casein for 14 days. The control group was fed the balanced diet for 42 days. LCAT activity was determined by conversion of 3H-cholesterol into 3H-esterified cholesterol. The consumption of both protein-depleted diets highly decreased LCAT activity. At the end of the period of protein malnutrition, LCAT activity was only 22% and 13% of that of the control group in the C and GI groups, respectively. There was no significant difference between the two depleted diets. At day 3 of refeeding, values of both C and GI groups returned to control values. Despite the reduction in LCAT activity with both types of protein-depleted diets, HDL metabolism was not significantly impaired. This might be partly due to the maintenance of higher apolipoprotein A-I levels. The reduced LCAT activity could be attributable to reduced synthesis of LCAT in the liver during both protein-depleted diets.

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