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Biomedical subjects

U M Houtsmuller

Publications and source records attributed to U M Houtsmuller.

At least 19 recordsLinked to original sources
PubMed1991

Increased n-3 polyunsaturated fatty acid content of red blood cells from fish oil-fed rabbits increases in vitro lipid peroxidation, but decreases hemolysis.

In view of a possible relationship between fish oil, lipid peroxidation, and atherosclerosis, the in vitro lipid peroxidation susceptibility of red blood cells (RBCs) from rabbits on conventional (-FO) and fish oil-enriched diets (+FO) was investigated. The diet caused substantial increases in the RBC concentrations of n-3 polyunsaturated fatty acids (PUFAs), in combination with decreases in the concentration of oleic acid (18:1) and linoleic acid (18:2). Cumene hydroperoxide-induced oxidative stress led to increased overall fatty acid peroxidation in +FO RBCs compared with with -FO RBCs, as quantitated by GLC fatty acid analysis. However, the increased overall susceptibility to lipid peroxidation of +FO RBCs was not reflected in increased peroxidation of every individual fatty acid. This was observed for endogenous arachidonic acid (20:4) as well as, in separate experiments, for exogenously added parinaric acid (PnA). The increased cumene hydroperoxide-induced PUFA oxidation in +FO RBCs was accompanied by a lesser extent of hemolysis. To account for these observations, it is proposed that the increased n-3 PUFA content of +FO RBCs serves as an oxidizable buffer. The present data suggest that oxidation of fatty acids can occur until a critically low level of intact phospholipid in the RBC membrane is reached, after which the membrane destabilizes and hemolysis occurs. At the same time, the PUFA buffer in +FO RBCs could also prevent oxidative damage to specific membrane proteins, which could also help prevent cell lysis.

Animals↗
PubMed1990

Evaluation of vitamin E requirement and food palatability in rabbits fed a purified diet with a high fish oil content.

The vitamin E requirement of rabbits fed a semi-synthetic diet containing high amounts of fish oil was studied. Three groups of 5 rabbits were fed fish oil diets containing, respectively, 50, 100 and 500 mg/kg vitamin E. Moreover diet palatability was evaluated by using different levels of grass meal: 0.5, 1 and 2%, respectively. Incorporation of 1% grass meal in the diet was sufficient to achieve acceptance of the fish oil diet. Increased vitamin E intake resulted in a dose-related rise in vitamin E levels in serum, blood platelets, liver and adipose tissue. The higher vitamin E intake was reflected by a twofold increase of vitamin E in serum, platelets and adipose tissue, and a tenfold increase in the liver. The adipose tissue revealed histopathological changes of yellow fat disease, mainly in the low-dose vitamin E group. In the liver microgranulomas of lipofuscin-laden macrophages were seen. Vitamin E was found to decrease but not to prevent the formation of these lesions. The results indicate that protection of marine oils against in vivo oxidation is problematic in the rabbit. It is questionable whether in this animal vitamin E is an adequate biological anti-oxidant for very long chain n-3 fatty acids.

Adipose Tissue↗
PubMed1989

Effect of dietary fats on linoleic acid metabolism. A radiolabel study in rats.

Effects on the linoleic acid metabolism in vivo of three dietary fats, rich in either oleic acid, trans fatty acids or alpha-linolenic acid, and all with the same linoleic acid content, were investigated in male Wistar rats. After 6 weeks of feeding, the rats were intubated with [1-14C]linoleic acid and [3H]oleic acid. The incorporation of these radiolabels into liver, heart and serum was investigated 2, 4, 8, 24 and 48 h after intubation. The amount of 14C-labelled arachidonic acid incorporated into the liver phospholipid of the group fed the oleic acid-rich diet was significantly higher than that of the other groups. However, compared to the trans fatty acids-containing diet, the oleic acid-rich diet induced only a slightly higher arachidonic acid level in the phospholipid fraction of the tissues as determined by GLC. Dietary alpha-linolenic acid more than halved the arachidonic acid levels. Our results do not support the hypothesis that the delta 6-desaturase system actually determines the polyunsaturated fatty acid levels in tissue lipids by regulating the amount of polyunsaturated fatty acids (e.g., arachidonic acid) synthesized. The biosynthesis of polyunsaturated fatty acids only is not sufficient to explain the complicated changes in fatty acid compositions as observed after feeding different dietary fats.

Animals↗
PubMed1989

Effects of varying the carbohydrate:fat ratio in a hot lunch on postprandial variables in male volunteers.

1. Healthy male volunteers consumed at noon, hot test meals with four different carbohydrate:fat ratios varying between 2.64 and 0.50, and composed of fried beefsteak, mashed potatoes, French beans, and a dessert of custard with mashed peaches. The energy content of the meals was 40% of the daily intake of the volunteers, estimated from their individual dietary histories. 2. Before, and at different times after the start of the meal, blood samples were taken and a number of indices of carbohydrate and lipid metabolism were determined in the samples, i.e. glucose, insulin, free fatty acid, free and total glycerol, free and total cholesterol, high-density-lipoprotein (HDL)-cholesterol and low-density-lipoprotein (LDL)-cholesterol. 3. Increasing the carbohydrate:fat ratio resulted in higher postprandial peaks of glucose and insulin. In addition, the peak area under the postprandial glucose curve showed a significant increase. The peak area under the postprandial insulin curve had also increased, indicating that a larger amount of insulin was secreted by the pancreas on increasing the carbohydrate content in the meal. There was no significant correlation between the height of the postprandial peak of blood glucose and the size of the meal. 4. All four meals caused elevated postprandial blood triacylglycerol levels. However, the decline of this elevated level took a much longer time after the meals with the lower carbohydrate:fat ratios, i.e. containing larger amounts of triacylglycerols. There was a significant decreasing linear relation between the carbohydrate content of the meals and the peak area under the postprandial triacylglycerol curve. Free glycerol and free fatty acids showed lower postprandial levels in the blood after the meals with the higher carbohydrate:fat ratios, and the peak areas of the postprandial curves of both variables displayed a significant decrease. Little or no effect of the meal carbohydrate:fat ratio was observed on the postprandial concentrations of total cholesterol, unesterified cholesterol, HDL-cholesterol or LDL-cholesterol.

Adult↗
PubMed1988

Linoleic acid requirement of rats fed trans fatty acids.

The amount of linoleic acid required to prevent undesirable effects of C18 trans fatty acids was investigated. In a first experiment, six groups of rats were fed diets with a high content of trans fatty acids (20% of energy [en%]), and increasing amounts of linoleic acid (0.4 to 7.1 en%). In a second experiment, four groups of rats were fed diets designed to compare trans fatty acids with saturated and cis-monounsaturated fatty acids of the same chain length at the 2 en% linoleic acid level. After 9-14 weeks, the oxygen uptake, lipid composition and ATP synthesis of heart and liver mitochondria were determined. The phospholipid composition of the mitochondria did not change, but the fatty acid compositions of the two main mitochondrial phospholipids were influenced by the dietary fats. Trans fatty acids were incorporated in all phospholipids investigated. The linoleic acid level in the phospholipids, irrespective of the dietary content of linoleic acid, increased on incorporation of trans fatty acids. The arachidonic acid level had decreased in most phospholipids in animals fed diets containing 2 en% linoleic acid. At higher linoleic acid intakes, the effect of trans fatty acids on the phospholipid arachidonic acid level diminished. However, in heart mitochondrial phosphatidylethanolamine, trans fatty acids significantly increased the arachidonic acid level. Despite these changes in composition, neither the amount of dietary linoleic acid nor the addition of trans fatty acids influenced the mitochondrial function. For rats, a level of 2 en% of linoleic acid is sufficient to prevent undesirable effects of high amounts of dietary C18 trans fatty acids on the mitochondrial function.

Animals↗
PubMed1988

Dietary influence on the insulin function in the epididymal fat cell of the Wistar rat. I. Effect of type of fat.

For at least 3-4 weeks, young male Wistar rats were fed semisynthetic diets containing sunflowerseed oil, palm oil, olive oil, linseed oil, cocoa butter and coconut oil as dietary fat. The type of dietary fat had little effect on body weight, epididymal fat pad weight and on the diameter of fat cells isolated from the epididymal fat pads, but the rats fed the linseed oil-containing diet had a lower epididymal fat pad weight. The fatty acid composition of the triacylglycerol fractions of the fat pads correlated well with those of the dietary fats. The correlations with the fatty acid composition of the phospholipids of the fat pads were less pronounced. High responses to insulin in the epididymal fat cells were obtained with sunflowerseed oil, linseed oil and olive oil, whereas low responses were found for cocoa butter, palm oil or coconut oil. Rather than the amount of polyunsaturated fatty acids or the ratio of polyunsaturated to saturated fatty acids, the amount of saturated fatty acids with 12, 14 or 16 carbon atoms appeared to be the most important parameter in determining the maximal insulin response. A negative correlation was found between the amount of saturated fatty acids in the diet and the extent of insulin response. The modulating effects of the dietary type of fat on the response to insulin cannot be fully explained by changes in the number of insulin receptors on the fat cell surface as determined by insulin binding but must, at least partially, be ascribed to postreceptor effects.

Adipose Tissue↗
PubMed1988

Effect of dietary fat composition on the metabolism of triacylglycerol-rich plasma lipoproteins in the postprandial phase in meal-fed rats.

Rats conditioned to eating fixed-size meals (meals at 7 AM and 7 PM), consuming diets rich in palm oil or sunflower seed oil, were used to study the metabolism of chylomicrons and hepatic very low density lipoproteins (VLDL) as a function of time after meal consumption. Rats fed a palm oil diet had higher serum triacylglycerol levels at 7 AM, before the meal (1.96 +/- 0.25 mM vs. 1.09 +/- 0.09 mM) and reached higher levels postprandially (4.32 +/- 0.48 mM vs. 2.87 +/- 0.18 mM) than sunflower seed oil-fed animals, due to higher levels of hepatic VLDL (at 7 AM) and higher levels of chylomicrons and hepatic VLDL (in the postprandial phase). These differences in serum triacylglycerol concentrations between the diets tested were found not to be due to differences in hepatic VLDL triacylglycerol secretion (similar rate for both dietary groups and not very much affected by meal consumption) or chylomicron triacylglycerol secretion (similar response profiles on both diets), pointing towards differences in plasma triacylglycerol catabolism. Subsequent double-label studies on triacylglycerol catabolism of chylomicrons from palm oil- and sunflower seed oil-fed animals in chow-fed recipients showed that palm oil triacyglycerol is catabolized slower than sunflower seed oil triacylglycerol. Furthermore, activities of postheparin plasma lipoprotein lipase tended to be higher in sunflower seed oil-fed animals. From these data we conclude that the relative hypertriglyceridemia found in palm oil-fed animals is due to less efficient catabolism and not to increased synthesis of plasma triacylglycerol.

Animals↗
PubMed1985

Identification, isolation and characterization of epidermal lipids containing linoleic acid.

Three specific linoleate-rich lipids have been identified in pig epidermis and are referred to as O-acylglucosyl ceramide, O-acyl ceramide, and O-acyl acid. The acid moiety is up to 70% linoleic acid and linked via the hydroxyl group of a omega-OH long-chain fatty acid, which itself is linked to sphingosine or glucosyl sphingosine. The identification of O-acyl ceramide confirmed the findings of another group, whereas the structural configuration of the O-acylglucosyl ceramide is different to previous reports. The identification of an O-acyl acid in epidermis is novel. Our evidence allows us to speculate that a hydroxylated derivative of the O-acyl ceramide may be intimately involved in the permeability barrier of skin, perhaps providing sufficient polarity to maintain a lamellar phase in the intercellular space of the lower stratum corneum region, and that it is specifically in this form that linoleic acid is involved in skin barrier function. Alternatively, or concurrently, this species may act as a signal for late keratinisation events.

Animals↗
PubMed1985

Metabolism of linoleic acid and other essential fatty acids in the epidermis of the rat.

Essential fatty acids are absolutely necessary for maintaining the proper condition of the water barrier (stratum compactum) in the skin. Even direct topical application of linoleic acid or any other Z,Z-(n-6, n-9)-fatty acid to the skin restores the barrier in essential fatty acid-deficient animals. In order to investigate the mechanism by which these polyunsaturated fatty acids exert their activity, radioactively labelled fatty acids were applied to the skin of the live animal and the epidermal lipids were analysed after 1-4 days. Much radioactivity was incorporated into two peculiar lipids, viz. acyl ceramide and acyl acid, which are characteristic of the barrier, in which linoleate was esterified to the end-position of very-long-chain (C30-34) unsaturated omega-hydroxy fatty acids. Strong evidence was obtained which showed that these lipids carry linoleate into the barrier layer where it is converted, probably by lipoxygenase(s), into a series of peroxidated lipids. The lipoxygenase inhibitor, eicosatetraynoic acid, prevents both oxygenation of the polyunsaturated fatty acid and the formation of a healthy skin. This peroxidation may supply the mediators which induce the proper differentiation of the epidermal cells into an effective stratum compactum and a horny layer.

Animals↗
PubMed1980

Effect of low cholesterol, linoleic acid enriched diet on thrombotic tendency and plasma lipoproteins in patients with angina pectoris.

Eighteen patients with an established angina pectoris aged 46-74 years were investigated. These patients received a low cholesterol, linoleic acid enriched diet during a period of three months. Of these patients seventeen terminated the three months period. The adherence to the diet was assessed by determining the fatty acid pattern in cholesterol and triglycerides. Both were found to increase significantly and to the same extend. When comparing the values between the entry to the study and after three months of dietetic intervention we found a significant improvement in the fibrinogen level, haematocrit, the aggregation of platelets, the PAT I test according to Breddin and in the test according to Wu and Hoak. However, the fibrinolytic activity before occlusion of an arm was disminished. The changes in ADP -, collagen -, adrenalin and thrombin induced platelet aggregation were not uniform. We found a significant lowering of VLDL, LDL, phospholipids and total cholesterol. HDL did not change significantly. It seems that the diet had a favourable effect on several thrombotic and lipoprotein parameters in these patients.

Aged↗
PubMed1979

Alteration of the lipase activities of muscle, adipose tissue and liver by rapeseed oil feeding of rats.

Feeding rapeseed oil, rich in erucic acid, for 4 days results in a significant increase of the lipoprotein lipase activities of heart and adipose tissue. The lipase activity of liver, which in earlier studies has been shown to be releasable by heparin perfusion, also increases by the dietary regimen. The increased lipoprotein lipase activity of heart may contribute to lipid accumulation in this organ. The higher intracellular lipid store probably results in higher (hormone-sensitive) tissue lipase activity. The increase of lipoprotein lipase of adipose tissue, however, is not accompanied by an increase of hormone-stimulated tissue lipase activity in fat cells. This activity may even become lower, and might contribute to the decrease of the lipid store in heart after an initial rapid phase of fat accumulation during erucic acid feeding.

Adipose Tissue↗