The aim of this study was to investigate the effect of dietary oxidized fats on the lipoprotein profile and the atherogenicity of LDL. Two experiments with male Sprague-Dawley rats were conducted. In Experiment 1, diets with either fresh fat or oxidized fat, prepared by heating at temperatures of 50, 105 or 190 degrees C, containing either 25 or 250 mg alpha-tocopherol equivalents/kg were used. In Experiment 2, diets with fresh or oxidized fat, heated at a temperature of 55 degrees C, containing 25 mg alpha-tocopherol equivalents/kg, were used. In Experiment 1, rats fed all types of oxidized fats had higher concentrations of HDL cholesterol and lower ratios between plasma and HDL cholesterol than rats fed the diet containing the fresh fat. As determined from the lag time, the susceptibility of LDL to copper-induced lipid peroxidation was higher in rats fed oxidized fats heated at 105 or 190 degrees C than in rats fed the diets containing the fresh fat or the oxidized fat treated at 50 degrees C, irrespective of the dietary vitamin E concentration. However, in Experiment 2, the composition of LDL apolipoproteins and uptake of LDL by macrophages were not different between rats fed the fresh fat diet and those fed the oxidized fat diet. We conclude that ingestion of oxidized fats does not adversely affect the lipoprotein profile in the rat model used, and does not cause modifications of apolipoproteins that would lead to enhanced uptake of LDL via macrophage scavenger receptors.

Background/Objectives: It has been shown that plasma carnitine concentrations markedly decline during gestation in women. The reason for this, however, is unknown. One objective of this study was to investigate the effect of carnitine supplementation on plasma carnitine concentrations in pregnant women. The second objective was to investigate the hypothesis that reduced plasma carnitine concentrations during gestation are caused by a reduced carnitine synthesis because of a diminished iron status. Subjects/Methods: Healthy pregnant women (n ¼ 26) were randomly assigned in two groups receiving either a L-carnitine supplement (500 mg L-carnitine per day as L-carnitine L-tartrate) (n ¼ 13) or placebo (n ¼ 13) from the 13th week of gestation to term. Results: In the control group, there was a marked reduction of plasma carnitine concentration from the 12th week of gestation to term. This reduction was prevented by the supplementation of carnitine. In the control group, there was a positive relationship between the parameters of iron status (mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and ferritin) and plasma concentration of carnitine (Po0.05). Moreover, there were inverse correlations between the concentrations of ferritin and the carnitine precursor g-butyrobetaine in plasma, and between g-butyrobetaine and carnitine in plasma (Po0.05).Conclusions: This study confirms that plasma carnitine concentrations decline in the course of pregnancy, an effect that can be prevented by the supplementation of carnitine. Data of this study, moreover, suggest that the decline of plasma carnitine concentration during pregnancy could be caused by a reduced rate of carnitine biosynthesis, possibly because of an inadequate iron status.

No abstract

Three experiments were carried out with rats (experiments 1 and 2) and guinea pigs (experiment 3) to study the effect of oxidized fats, in interaction with dietary concentrations of vitamins E and C, on the antioxidant status of erythrocytes and the rate of haemolysis. In experiment 1, diets with fresh or thermoxidized fats, containing either 25 or 250 mg alpha-tocopherol equivalents/kg were used; experiment 2 included diets with fresh or thermoxidized fats, containing 25 mg alpha-tocopherol equivalents/kg; in experiment 3, besides a control diet with a fresh fat, diets containing thermoxidized fats with various concentrations of Vitamin E (35 vs. 175 mg alpha-tocopherol equivalent/kg) and Vitamin C (300 vs. 1000 mg/kg) were used. Rats and guinea pigs fed diets with oxidized fats had reduced concentrations of glutathione in erythrocytes as compared with animals fed the fresh fat diets. In rats fed oxidized fats, the activity of catalase and in guinea pigs fed oxidized fats, the activity of glutathione peroxidase plus the concentration of alpha-tocopherol was reduced in erythrocytes as compared with animals fed the equivalent fresh fat diets. The concentrations of alpha-tocopherol in erythrocytes were increased by both, Vitamin E and Vitamin C while the concentrations of glutathione were independent of the concentrations of those vitamins in the diets. Erythrocytes of guinea pigs fed oxidized fats also showed an increased susceptibility to haemolysis during incubation in hypotonic salt solutions; this effect could be improved by increasing the concentrations of both, Vitamin E and Vitamin C. Parameters of in vivo haemolysis (activities of lactate dehydrogenase and acidic phosphatase and concentrations of potassium and free haemoglobin in plasma) were not adversely affected in rats and guinea pigs fed the oxidized fats as compared with animals fed the fresh fats. The study shows that dietary oxidized fats reduce the antioxidant status of erythrocytes and increase their susceptibility against haemolysis but do not increase the rate of haemolysis in vivo.

To investigate the effect of a dietary oxidized fat on the concentrations of cholesterol in liver, plasma, and lipoproteins and the susceptibility of low-density lipoproteins (LDL) to lipid peroxidation, and to explore the effects of vitamins E and C, male guinea pigs were divided into five groups. Four groups were fed diets with an oxidized fat supplemented with 35 or 175 mg alpha-tocopherol equivalents/kg and 300 or 1000 mg of vitamin C/kg for 29 days. One group, used as a control, was fed the same basal diet with fresh fat with 35 mg alpha-tocopherol equivalents/kg and 300 mg of vitamin C/kg. Guinea pigs fed the oxidized-fat diets, irrespective of dietary vitamin E and C concentrations, had significantly lower concentrations of total cholesterol in the liver and a lower concentration of cholesterol in LDL than the control animals fed the fresh fat. According to the lag time before onset of lipid peroxidation, LDL of guinea pigs fed the oxidized-fat diet with 35 mg alpha-tocopherol equivalents and 300 mg vitamin C/kg were significantly more susceptible to copper-induced lipid peroxidation than those of guinea pigs fed the fresh fat diet. Within the groups fed the oxidized fat diets, increasing the dietary vitamin E concentration from 35 to 175 mg/kg significantly (p < 0.05) and increasing the dietary vitamin C concentration from 300 to 1000 mg/kg in tendency (p < 0.10) reduced the susceptibility of LDL to oxidation. LDL of guinea pigs fed the oxidized fat diets with 175 mg alpha-tocopherol equivalents/kg were even more resistant to oxidation than LDL of guinea pigs fed the fresh diet. In conclusion, the study shows that dietary oxidized fat influences the cholesterol metabolism and the susceptibility of LDL to lipid peroxidation; the latter can be modified by dietary vitamins E and C.

Summary. 1. 24-h-fasted rats exhaled 35--37% of i.v. administered loads of labelled glucose, xylitol and fructose, and 20% of a sorbitol load as ir within a period of six hours. 2. Streptozotocin-diabetic rats exhaled under similar conditions only 11--18~ of these substrates as laCO 2. The rate of glucose oxidation was similar in both groups of animals when a correction for the different glucose pool size was applied, It is concluded that glucose oxidation to 14C0e takes place mainly in tissues which are not sensitive to insulin. 3. Urinary excretion of all substrates was 39--55% of the given dose in diabetic rats. The large difference of urinary carbon-14 between fasted and diabetic rats was due to the excretion of glucose-i~C by the diabetic rats. 4. Six hours after the administration of all four substrates, similar amounts of carbon-14 were recovered in serum, serum osazones, liver glycogen and total lipids and diaphragm glycogen within each group of animals. It is concluded that the similarities of the metabolism of all substrates is due to the rapid conversion of the substitute sugars to glucose.

The results demonstrated that supplementation of vitamins E and C improves the vitamin E status but does not prevent the formation of lipid oxidation products in the liver of guinea pigs fed oxidised fats.

Abstract. Young male rats metabolize xylitol, sorbitol and fructose with a half‐life of 165 seconds. Within 10 min. after the intravenous injection of a load of these substrates more than 70% of the carbon‐14 in plasma is present as 14C‐glucose. The labelling of plasma glucose from these substrates appears to be insulin‐independent. A small percentage of labelled xylitol, sorbitol and fructose is retained by the liver as glycogen and total lipids. In the normal rat, this process appears to be insulin‐independent. In the chronic streptozotocin‐diabetic rat, insulin acutely enhances glycogen synthesis from all three substrates and reduces their incorporation into total lipids. Once these substrates have been converted to glucose the further storage as muscle glycogen and adipose tissue total lipids is entirely dependent on insulin, both in the normal and in the streptozotocin‐diabetic rat. Fructose makes an exception since it is metabolized by adipose tissue independently of insulin. In the light of these results in the rat a re‐evaluation of the use of various carbohydrates and polyols in parenteral nutrition of normal and diabetic subjects appears desirable.