Impaired serum lipids and lipoproteins in fetal macrosomia related to maternal obesity.

The aim of this work was to determine lipoprotein metabolism alterations in macrosomic newborns and to see whether these lipoprotein abnormalities are parallel or not to those found in their obese or nonobese mothers. Serum lipids, apo A-I, apo B100, lipoproteins (VLDL, LDL, HDL2, and HDL3), and LCAT activity were investigated in obese and nonobese mothers and cord blood of their macrosomic or appropriate-for-gestational-age (AGA) newborns. Serum and VLDL triglyceride concentrations were higher in obese mothers of AGA newborns than in nonobese mothers. Serum triglyceride, VLDL, and apo B100 levels were higher, while serum apo A-I and HDL2 cholesterol concentrations were lower in obese mothers of macrosomic newborns than in the other groups. In their macrosomic newborns, serum lipid, lipoprotein, apo B100, and apo A-I levels were higher as compared with those of other newborns. Macrosomic newborns of nonobese mothers had lipoprotein profiles similar to those in AGA newborns. LCAT activity was similar in both mother groups and in both newborn groups. In conclusion, maternal obesity and fetal macrosomia were associated with lipoprotein abnormalities consistent with high atherogenic risk.

Changes in serum lipid and lipoprotein concentrations and compositions at birth and after 1 month of life in macrosomic infants of insulin-dependent diabetic mothers.

The aim of this study was to determine whether macrosomia related to maternal diabetes alters lipoprotein metabolism and whether these abnormalities still persist or regress after 1 month of life. Serum lipoprotein compositions and concentrations as well as serum lipid fatty acid compositions were investigated in macrosomic infants (birth weight = 4840 +/- 105 g at term) of insulin-dependent diabetic mothers at birth and after 1 month of life, and were compared to those of control infants (birth weight = 3400 +/- 198 g at term) of healthy mothers. Compared to controls, at birth, macrosomic newborns had higher serum lipids, apolipoprotein A-I and B-100, and lipoprotein (very low density lipoprotein, low density lipoprotein, high density lipoprotein-2 and high density lipoprotein-3) levels. Higher percentages of C18:2n-6 in serum triacylglycerols, phospholipids and cholesteryl esters were also observed. At day 30, in macrosomics, serum triacylglycerol, apo B-100, very low density lipoprotein and low density lipoprotein levels were still significantly higher. C18:2n-6 and C18:3n-3 contents in serum phospholipids, triacylglycerols and cholesteryl esters were reduced while C20:4n-6 and C22:6n-3 contents in serum phospholipids and cholesteryl esters were enhanced, compared to control values. Macrosomia was associated with alterations in lipoprotein compositions and concentrations at birth, some of which persisted after 1 month of life, and might play a role in the pathogenesis of diabetes and atherosclerosis in adult life.

Low birth weight at term impairs cord serum lipoprotein compositions and concentrations.

UNLABELLED: The purpose of this study was to determine the effect of low birth weight at term on serum lipoproteins. Lipid and apolipoprotein (apo) contents were investigated in cord sera of small-for-gestational-age (SGA) newborns at term (2290 g +/- 33 g) and compared with those of appropriate-for-gestational-age (AGA) newborns (3570 g +/- 93 g). In SGA newborns, VLDL amounts were twofold higher, whereas LDL, HDL2 and HDL3 contents were lower than in AGA newborns (-38%, -44% and -42%, respectively). VLDL-triacylglycerols (TG), apo B-100 and apo E were higher, while VLDL-apo C-II values were 39% lower in SGA newborns compared with those of AGA newborns. In SGA newborns, HDL2-apolipoprotein, phospholipid and cholesteryl ester levels were respectively reduced to 70%, 50% and 40% compared with AGA values. HDL3-apolipoprotein and phospholipid contents were also decreased in SGA newborns (-43% and -60%, respectively). The different HDL2 and HDL3-apolipoproteins (apo A-I, A-II, C-III and E) were significantly decreased in SGA newborns. CONCLUSION: Intra-uterine growth retardation was accompanied by alterations in apolipoproteins and lipid compositions in the four lipoprotein fractions, which may impair lipid metabolism. Follow up studies on lipoprotein patterns in SGA infants are required to investigate whether such abnormalities at birth lead to diseases in adulthood.

Serum lecithin: cholesterol acyltransferase activity and HDL2 and HDL3 composition in small for gestational age newborns.

The aim of this study was to determine serum lecithin: cholesterol acyltransferase (LCAT) activity in parallel with HDL2 and HDL3 composition in cord sera of small for gestational age (SGA) newborns, and to compare them with those obtained from appropriate for gestational age (AGA) newborns. LCAT activity was assayed by conversion of [3H]cholesterol to labelled cholesteryl ester. HDL2 and HDL3 were separated by ultracentrifugation. Serum cholesteryl ester, apolipoprotein (apo) A-I concentrations and LCAT activity were significantly lower (-47%, -18% and -56%, respectively), whereas serum triglyceride amounts were twofold higher in SGA newborns than in AGA newborns. In SGA newborns, HDL2 and HDL3 levels were low, and HDL3 and HDL2 phospholipid and HDL2-cholesteryl ester contents were diminished. HDL3-apo A-I, A-II, C-III and E values were lower in SGA newborns. In HDL2, apo A-I, A-II and E concentrations were decreased. Therefore, in SGA newborns, the reduced LCAT activity was associated with quantitative and qualitative changes in HDL2 and HDL3 particles.

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.

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.

Time course of changes in rat serum apolipoproteins during the consumption of different low protein diets followed by a balanced diet.

The effects of protein malnutrition (PM) followed by refeeding a balanced diet on apolipoprotein and lipid contents of the serum lipoproteins were studied in young Wistar male rats. The changes of serum apolipoproteins were compared with the appearance of fatty liver during PM and its disappearance during refeeding. The control group (T) was fed a balanced diet containing 15% casein for 42 d. Two depleted groups (C) and (G1) were fed for 28 d low protein diets containing 2% casein and 5% gluten, respectively, and then were fed the balanced diet for 14 d. During PM a concentration of triacylglycerols (TGs) in liver in the two depleted groups increased; the level in rats fed 2% casein was twice that in rats fed 5% gluten. There was a significant negative correlation between serum TGs and liver TGs. The serum apolipoproteins (apo) did not respond consistently. The high-density lipoproteins apo A-I, A-II and A-IV, which are more than 50% synthetized in the intestine, remained essentially unchanged, thus showing resistance to protein malnutrition. The very low density lipoproteins apo B and total apo C, which mainly originate from liver, were significantly lower in malnourished groups than in controls, while the liver TGs accumulated in malnourished groups. Only the levels of total apo C and apo B48 were correlated with hepatic TG steatosis during malnutrition and refeeding.

[Course of the levels of myofibrillar proteins in the cardiac ventricles of adult rats in protein malnutrition followed by a balanced diet]. / Evolution des teneurs en quelques protéines myofibrillaires des ventricules cardiaques du rat adulte au cours d'une malnutrition protéique suivie d'une réalimentation équilibrée.

Adult male Wistar rats weighing 320 +/- 20 g at the beginning of the experiment were divided into two equal lots. A reference lot (T) was fed on a balanced diet containing 23,5 p. 100 mixed protein, for 60 days. A deficient lot (E) was fed on a low protein diet (3 p. 100 cereal protein) for 30 days (malnutrition), then on a balanced diet for 30 days (refeeding). When the food intake was expressed in 100 g of body weight/day, both lots ate about the same amount throughout the experiment. On the contrary, the amount of N ingested/100 mg of body weight/day by the E rats was only 11 p. 100 of that of the T lot. After 30 days of refeeding, the mean weight of the E rats equalled 90 p. 100 of that of the T rats. In the E lot, during malnutrition, the nitrogen balances were always positive and their nitrogen CDU were ranged between 73-83 p. 100 in comparison with 86-88 p. 100 in the T lot. The protein concentration of cardiac ventricles was the similar in both lots of rats, during malnutrition and refeeding periods. On the contrary, the myofibrillar protein concentration was increased in the E rats during these two phases. After separation of subunits sizes of muscle proteins by sodium dodecyl sulphate gel electrophoresis, we observed that the concentrations of myosin, actin, troponin-tropomyosin complex, myosin light chains, evolved in the same way that the total myofibrillar proteins. A relative degree of cardiac myocontractile protein sparing is suggested in our chronic protein malnutrition of adult rats.