[Gestational or essential hypertension in pregnant women limits the capacity to stock triglycerides by the placenta despite raised lipoprotein-lipase activity]. / L'hypertension gravidique ou essentielle chez la femme en gestation limite la capacité de stockage des triglycérides du placenta malgré une activité lipoprotéine lipase élevée.

Placenta lipoprotein lipase (LPL) activity as well as serum VLDL and placenta lipids composition were determined in pregnant hypertensive women at term. 46 patients aged from 29 +/- 2 years with gravidic hypertension (HTA-G) and 38 patients with essential hypertension (HTA-E) aged 30 +/- 1 years were compared with 20 normotensive women aged 27 +/- 1 years. Serum triacylglycerols (TG) concentrations were 1.3-fold higher in the both hypertensive patients compared with controls. However, serum phospholipids (PL) and total cholesterol (TC) values were similar in the three groups. VLDL mass and their apolipoproteins, unesterified cholesterol (UC) and cholesteryl esters (CE) contents were significantly increased in hypertensive women compared with controls. In HTA-G and HTA-E patients, respectively. TG-VLDL concentrations were increased by +43% and +36% compared with those of controls (P < 0.01). In placenta, the values were lower 2.2- and 1.9-fold for TG, 2.8 and 2.5-fold for PL and two- and threefold for TC, in HTA-G and HTA-E patients than in controls. Placenta LPL activity was 2.7-fold higher in HTA-G and HTA-E patients compared with that of controls. In conclusion, although placenta LPL activity is higher it is not permit a decrease of serum TG-VLDL on the one hand, and an increase of placenta ability in TG storage on the other hand.

Age-related changes in cholesterol metabolism in macrosomic offspring of rats with streptozotocin-induced diabetes.

The aim of this study was to determine the impact of diabetic macrosomia on cholesterol and lipoprotein metabolism. Age-related changes in the activities of serum LCAT, hepatic HMG-CoA reductase, cholesterol 7alpha-hydroxylase, and ACAT, the major enzymes involved in cholesterol metabolism, were determined in macrosomic offspring of streptozotocin-induced diabetic rats. Hepatic, serum, and lipoprotein cholesterol contents were also examined. Mild hyperglycemia in pregnant rats was induced by intraperitoneal injection of streptozotocin (40 mg/kg body weight) on day 5 of gestation. Control pregnant rats were injected with citrate buffer. At birth, macrosomic pups had higher serum, LDL-HDL(1), and HDL(2-3) cholesterol levels (P < 0.05) associated with increased LCAT activity (+57%) compared with control values. At 1 and 2 months of life, serum and lipoprotein cholesterol concentrations in macrosomic rats were similar to those of controls, whereas LCAT activity remained elevated about 1.5-fold. In addition, there was no change in hepatic cholesterol contents but hepatic HMG-CoA reductase, cholesterol 7alpha-hydroxylase, and ACAT activities were higher in both macrosomic males and females than in their respective controls (P < 0.01). By 3 months, macrosomic rats had developed hypercholesterolemia with a rise in all lipoproteins. Enzyme activities were still increased in these mature macrosomic rats, and hepatic cholesteryl esters were higher only in macrosomic females. These data demonstrate an overproduction, combined with overutilization, of cholesterol during the phase of rapid growth in macrosomic rats. However, cholesterol oversynthesis exceeded its removal and was a major contributor to hypercholesterolemia in adult macrosomic rats. In conclusion, macrosomia was associated with alterations in cholesterol metabolism through adulthood.

Low-protein diet prevents tissue lipoprotein lipase activity increase in growing rats.

The time course of changes in tissue lipolytic activities was studied in young rats during the consumption of a low-protein diet containing 50 g protein/kg (40 g wheat gluten +10 g casein/kg) for 28 d followed by balanced refeeding with 200 g protein/kg (160 g wheat gluten +40 g casein/kg) for 28 d. Lipoprotein lipase (LPL) activities were compared with the values of a control group fed a balanced diet containing 200 g protein/kg for 56 d. At the end of protein malnutrition period, the epididymal fat tissue LPL activity represented 36 %, and that of heart and gastrocnemius was 44 %, of those of the control group. These differences were accompanied by lower serum- and VLDL-triacylglycerols (TAG), respectively 47.6 % and 31 % of the control group values, probably resulting from reduced synthesis of VLDL-apolipoproteins (29 % of control group values), concomitant with liver lipid accumulation (4.8-fold) and little lipid storage in epididymal fat tissue. At day 2 of refeeding, there was no significant difference in liver and epididymal fat tissue LPL activities between experimental and control rats. At the end of the refeeding period, LPL activity of epididymal fat and liver lipolytic activity had increased and became similar to control group values. The consumption of a low-protein diet prevented the increase in extrahepatic LPL activities as observed in the control group. The alterations in LPL activity suggest that a low-protein diet limits lipid storage in adipose tissue due to reduced serum VLDL-TAG availability.

Rat plasma VLDL composition and concentration and hepatic lipase and lipoprotein lipase activities are impaired during two types of protein malnutrition and unaffected by balanced refeeding.

The relationships between VLDL concentrations and composition and changes in hepatic lipase and lipoprotein lipase activities were determined in rats, during the consumption of two low protein diets (2% casein or 5% gluten) (protein malnutrition) for 28 d, followed by the refeeding of a balanced diet for 14 d (15% casein) (refeeding). A control group was fed 15% casein for 42 d. In the control group, total lipolytic activity increased with age (r = 0.83, P < 0.001), whereas in both depleted groups, this activity remained low and stable throughout the period of protein malnutrition. At d 28 of protein malnutrition, plasma total lipolytic activities were significantly reduced in both depleted groups, (P < 0.05); hepatic lipase values represented 23% of the control value and lipoprotein lipase activity was about 11% of the control value. Moreover, lipid supply was even more dramatically diminished by the strong reduction in plasma VLDL concentration in both depleted groups. At d 14 of refeeding, lipoprotein lipase activities remained low in both depleted groups. Hepatic lipase activity was similar in the control and casein groups, but significantly higher in the gluten group. The VLDL composition varied significantly with each type of protein malnutrition and could be attributable to the different low levels of plasma VLDL-apolipoprotein C of rats fed both depleted protein diets, which involve an inhibiting or activating effect on lipoprotein lipase activity. Therefore, our results indicated that both protein-deficient diets investigated may diminish fatty acid supply in the various tissues involved.

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.