Changes in lipids in liver and serum of rats fed a histidine-excess diet or cholesterol-supplemented diets

The influence of dietary excess (5%) L-histidine on serum and liver lipids was examined in rats. Feeding a histidine-excess diet for 3, 6, 14 or 30 days caused growth retardation, hepatomegaly and decreased liver lipids throughout the period of the experiment. Hypercholesterolemia was observed after feeding a histidine-excess diet for 6 days; then serum cholesterol continuously increased for 30 days. Serum triglyceride on day 30 in rats fed the histidine-excess diet showed a significant decrease compared to rats fed the basal diet. Serum phospholipids of rats fed the histidine-excess diet for 7 or 14 days showed a significant increase compared to rats fed the basal diet. When rats were fed a basal, histidine-excess or cholesterol-supplemented diet (0.5% and 1.0% cholesterol) for 6 days, the distribution of serum high density (HDL), low density (LDL) and very low density lipoprotein cholesterol in rats fed the histidine-excess diet was similar to that of rats fed the basal diet, whereas LDL-cholesterol increased and HDL-cholesterol decreased in rats fed the cholesterol-supplemented diet.     

Dietary protein deficiency affects n−3 and n−6 polyunsaturated fatty acids hepatic storage and very low density lipoprotein transport in rats on different diets

Fatty livers and the similarity between the skin lesions in kwashiorkor and those described in experimental essential fatty acid (EFA) deficiency have led to the hypothesis that protein and EFA deficiencies may both occur in chronic malnutrition. The relationship between serum very low density lipoprotein (VLDL) and hepatic lipid composition was studied after 28 d of protein depletion to determine the interactions between dietary protein levels and EFA availability. Rats were fed purified diets containing 20 or 2% casein and 5% fat as either soybean oil rich in EFA, or salmon oil rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, or hydrogenated coconut, oil poor in EFA. Animals were divided into six groups, SOC (20% casein +5% soybean oil), SOd (2% casein +5% soybean oil), COC (20% casein +5% hydrogenated coconut oil), COd (2% casein + 5% hydrogenated coconut oil), SAC (20% casein +5% salmon oil) and SAd (2% casein +5% salmon oil). After 28 d, liver steatosis and reduced VLDL-phospholipid contents (P<0.001) were observed in protein-deficient rats. In protein deficiency, triacylglycerol and phospholipid fatty acid compositions in both liver and VLDL showed a decreased polyunsaturated-to-saturated fatty acid ratio. This ratio was higher with the salmon oil diets and lower with the hydrogenated coconut oil diets. Furthermore, independent of the oil in the diet, protein deficiency decreased linoleic and arachidonic acids in VLDL phospholipids. Conversely, despite decreased proportions of EPA at low protein levels, DHA levels remained higher in rats fed salmon oil diets. While in rats fed the hydrogenated coconut oil-fed diets the amount of 22∶5n−6 was lower in liver, it was higher in VLDL lipids at low protein levels. Both EPA and arachidonic acid are precursors of eicosanoids and their diminution may be related to certain clinical symptoms seen in infants suffering from kwashiorkor.     

Zinc deficiency and activities of lipogenic and glycolytic enzymes in liver of rats fed coconut oil or linseed oil

In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver, whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) (“coconut oil diet”) or linseed oil (80 g/kg) (“linseed oil diet”) as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver. The concentrations of serum lipids were elevated in zinc-deficient rats fed either type of dietary fat. These results demonstrate that fatty liver in zinc-deficient rats on the coconut oil diet is caused by elevated activities of lipogenic enzymes, and not by disturbed lipid secretion from liver. Dietary linseed oil prevents both the elevation of lipogenic enzyme activity and fatty liver in zinc-deficient rats.     

Fatty liver of growing rats fed excess lysine and its prevention by adenine or allopurinol

Weanling male Sprague-Dawley rats were fed ad libitum 15% casein diets with and without 5.0% lysine-HCl, 0.25% adenine sulfate or 0.1% allopurinol for 2 weeks. Addition of lysine alone depressed 2-week growth from 94 to 65 g, increased average daily urinary orotic acid excretion from 0.39 to 1.77 mg and increased the percentage of total liver lipids from 3.6 to 11.2. Adenine or allopurinol did not change growth but markedly enhanced lysine-induced orotic aciduria and completely prevented lysine-induced fatty livers. Reports by others show that adenine and allopurinol also prevent fatty livers of rats fed arginine-free diets or excess orotic acid. The authors conclude that lysine-induced orotic aciduria results from arginine deficiency caused by antagonism of arginine function by lysine, and that lysine-induced fatty liver probably results from a lesion identifical to that produced by feeding excess orotic acid.     

Effect of cocaine intake on the development of fatty liver in rats fed a low-protein diet

It has been shown that cocaine given in the diet is able to reduce fat accumulation in the liver of protein-malnourished rats (Arch. Latinoamer. Nutr. 19: 69-79, 1969). This study was, therefore, designed to approach the probable action of the drug upon the process (increased triglycerides synthesis and normal/decreased capacity for exporting triglycerides from the liver into the blood) which leads to an increased fat accumulation in the liver under this physiological condition. To accomplish this purpose, the total and fractioned lipids in the liver and total lipids as well as lipoproteins in serum were determined in female Wistar rats (120-130 g) fed either a 5% corn protein diet or a 20% casein diet, with and without cocaine (15 mg HCl cocaine/10 g of diet) for 18 days. The results, aside from confirming the reduction (p less than 0.001) of fat accumulation in the liver of rats fed on the 5% corn protein diet plus cocaine, revealed that this drug also reduced triglycerides concentration (significantly, (p less than 0.001, when results were calculated by difference, and slightly reduced them when results were determined) in this tissue. Nevertheless, it increases both total lipids (p less than 0.05) and triglycerides-rich pre-beta lipoprotein (p less than 0.10) levels in the serum of these animals. Otherwise, these lipidic parameters were not modified by cocaine in rats on the 20% casein diet, except for the total cholesterol level in liver and the cholesterol-rich beta lipoprotein level in serum. Respectively, these were slightly and significantly (p less than 0.001) reduced by the drug. These evidences and their statistical significance suggest that cocaine given chronically with the 5% corn-protein diet for 18 days, reduces at least partially (other biochemical event in the liver could have also accounted for its effect at this level) the liver fat accumulation, by increasing the triglycerides output from the liver into the blood. Elsewhere, cocaine appears to be able to induce some metabolic alterations in the hepatic cholesterol of well-nourished rats.     

The combined effects of dietary proteins and fish oil on cholesterol metabolism in rats of different ages

Male Sprague-Dawley rats at the ages of four weeks and nine months were fed purified diets containing 20% proteins either as casein (CAS), milk whey protein (WHY), or soybean protein (SOY) with 5% sardine oil for four weeks. The hypocholesterolemic effect of SOY was not statistically evident as compared to milk proteins at both ages, although serum cholesterol tended to be low in the SOY groups. A significant agedependent increase in serum cholesterol was observed in all dietary groups. Liver cholesterol concentrations were comparable in young rats, whereas in adults they were significantly lower in the SOY than in the CAS or WHY groups. At both ages, the activity of liver 3-hydroxy-3-methylglutaryl coenzyme A reductase tended to be higher in the SOY than in the other groups. Fecal steroid excretion was significantly higher in rats fed SOY than those fed either CAS or WHY, especially in adult rats. Significant age- and dietary protein-effects were observed in fatty acid profiles of liver microsomal phospholipids. Thus, the effects of dietary proteins on various lipid parameters were essentially maintained even when fish oil served as the source of dietary fat.     

The effect of fatty acid composition of rapeseed oil on plasma lipids and oxidative stability of low‐density lipoproteins in cholesterol‐fed hamsters

We studied the effect of four rapeseed oils with different fatty acid profiles on parameters implicated in the pathogenesis of atherosclerosis in humans in a model experiment with hamsters. The hamsters were divided into seven groups and fed a semi‐synthetic, cholesterol‐enriched diet (5 g/kg diet) containing 15% of the fat in question for a period of six weeks. The following rapeseed oils were used: (1) conventional rapeseed oil (6% saturated fatty acids [SFA], 64% monounsaturated fatty acids [MUFA], 18% linoleic acid [LA], 9% α‐linolenic acid [ALA]), (2) linoleic acid‐rich rapeseed oil (6% SFA, 61% MUFA, 28% LA, 2% ALA), (3) oleic acid‐rich rapeseed oil (6% SFA, 74% MUFA, 11% LA, 5% ALA), (4) myristic acid‐rich rapeseed oil (11% myristic acid, 35% SFA, 44% MUFA, 14% LA, 5% ALA). Sunflower oil, olive oil and lard were used as control fats. The concentrations of the lipids in the plasma, in the lipoprotein fractions and in the liver, the fatty acid composition of various tissues, the tocopherol status and the susceptibility of low‐density lipoproteins (LDL) to in vitro‐oxidation were determined. The concentrations of total cholesterol found in the plasma and in the LDL fraction and the ratios of LDL to HDL were similar after feeding the four different types of rapeseed oil, sunflower oil and olive oil. Lard produced the highest concentrations of cholesterol in plasma and the LDL fraction and the highest ratio of LDL to HDL. Feeding conventional, oleic acid‐ and myristic acid‐rich rapeseed oils resulted in markedly lower ratios of arachidonic to eicosapentaenoic acid in the lipids of the liver and the erythrocytes. This is considered beneficial for the formation of eicosanoids. The lag‐time before the onset of peroxidation of the LDL lipids, induced by copper ions, was not statistically significant between the seven hamster groups suggesting that the susceptibility of LDL to lipid peroxidation was similar after feeding all types of fat. Considering all parameters obtained in the used hamster model it is obvious that all four rapeseed oils are at least as favourable as olive oil or sunflower oil.     

Effect of the nature and amount of dietary energy on lipid composition of rat bone marrow

The effect of the nature and amount of dietary calories on the lipid composition of bone marrow of rats was studied. Male weanling rats were fed 3 isocaloric diets, containing high carbohydrate, normal protein, and high protein, and a fourth high fat diet for 49 days. Feeding of the high carbohydrate, high protein, and high fat diets caused a significant increase in the level of total lipids compared to the normal protein diet. This increase of total lipids was due primarily to the increase in the level of triglycerides. There was no significant difference in fatty acid composition of either nonpolar or polar lipids of bone marrow among rats fed high carbohydrate diet and those fed normal protein diet. A comparison of fatty acid compositions between bone marrow lipids of rats fed high protein diet and the other 2 isocaloric diets revealed that the proportion of palmitic acid was higher and the proportion of oleic acid was lower in animals fed high protein diet than in animals fed the other 2 diets. Compared to the 3 isocaloric low fat diets, dietary feeding of high fat diet caused a decrease in the proportion of palmitic and palmitoleic acids and an increase in the proportion of oleic and linoleic acids in total fatty acids of both nonpolar and polar lipids.     

Nutritional effects of mustard seed protein detoxified with aqueous isopropanol in young rats

The effect of removing anti‐nutritional factors from n‐hexane‐extracted mustard meal using 80% isopropanol (to reduce thioglucosides, phenolics, etc.) on growth, food efficiency ratio, serum and liver lipid profiles and protein content of young rats was examined. For this n‐hexane‐extracted mustard meal was extracted with 80% isopropanol giving a fraction with 68% protein and low residual thioglucoside (0.5%) as well as phenolic (0.3%) content. This isopropanol‐extracted mustard seed protein fraction reduced the growth of young rats slightly when compared with casein. The food efficiency ratio between rats fed isopropanol‐extracted mustard seed protein or casein did not differ, nor did the protein composition affect serum total cholesterol, triglyceride, HDL‐cholesterol, LDL‐cholesterol, VLDL‐cholesterol and LDL‐C/HDL‐C ratio. However, rats fed isopropanol‐extracted mustard seed protein showed a significantly lower (p<0.05) liver cholesterol concentration than rats fed casein. Liver triglyceride and phospholipid concentrations did not differ between rats fed the two proteins, nor was serum protein affected. This study indicates that extraction of hexane‐extracted mustard meal with 80% isopropanol reduced a number of anti‐nutritional factors like thioglucoside and phenolics. Furthermore the nutritional quality of mustard seed protein fraction is comparable to casein in respect to growth, food efficiency ratio, serum lipid and protein concentrations and organ weights.     

Response of plasma lipids to dietary cholesterol and wine polyphenols in rats fed polyunsaturated fat diets

This experiment was designed to evaluate the effects of dietary red wine phenolic compounds (WP) and cholesterol on lipid oxidation and transport in rats. For 5 wk, weanling rats were fed polyunsaturated fat diets (n−6/n−3=6.4) supplemented or not supplemented with either 3 g/kg diet of cholesterol, 5 g/kg diet of WP, or both. The concentrations of triacylglycerols (TAG, P<0.01) and cholesterol (P<0.0002) were reduced in fasting plasma of rats fed cholesterol despite the cholesterol enrichment of very low density lipoprotein + low density lipoprotein (VLDL+LDL). The response was due to the much lower plasma concentration of high density lipoprotein (HDL) (−35%, P<0.0001). In contrast, TAG and cholesteryl ester (CE) accumulated in liver (+120 and +450%, respectively, P<0.0001). However, the cholesterol content of liver microsomes was not affected. Dietary cholesterol altered the distribution of fatty acids mainly by reducing the ratio of arachidonic acid to linoleic acid (P<0.0001) in plasma VLDL+LDL (−35%) and HDL (−42%) and in liver TAG (−42%), CE (−78%), and phospholipids (−28%). Dietary WP had little or no effect on these variables. On the other hand, dietary cholesterol lowered the α-tocopherol concentration in VLDL+LDL (−40%, P<0.003) and in microsomes (−60%, P<0.0001). In contrast, dietary WP increased the concentration in microsomes (+21%, P<0.0001), but had no effect on the concentration in VLDL+LDL. Cholesterol feeding decreased (P<0.006) whereas WP feeding increased (P<0.0001) the resistance of VLDL+LDL to copper-induced oxidation. The production of conjugated dienes after 25 h of oxidation ranged between 650 (WP without cholesterol) and 2,560 (cholesterol without WP) μmol/g VLDL+LDL protein. These findings show that dietary WP were absorbed at sufficient levels to contribute to the protection of polyunsaturated fatty acids in plasma and membranes. They could also reduce the consumption of α-tocopherol and endogenous antioxidants. The responses suggest that, in humans, these substances may be beneficial by reducing the deleterious effects of a dietary overload of cholesterol.     

Hypolipidemic activity of the surfactants aminimides,and their effects on lipid metabolism of rodents

A series of short chain fatty acid derivatives of aminimides were shown to possess hypolipidemic activity in rats and mice. Most of the agents tested lowered both serum cholesterol and triglyceride levels by at least 30% in mice and were effective in hyperlipidemic induced mice. 1,1-Dimethyl-1-(2-hydroxypropyl)-amine mersitimide lowered serum cholesterol levels 41% and serum triglyceride levels 56% at 20 mg/kg/day I.P. after 16 days. The same agent was active orally when administered to rats with a 38% reduction in serum cholesterol and a 52% reduction in serum triglycerides after 14 days. The agents inhibited liver acetyl CoA synthetase, ATP dependent citrate lyase and phosphatidate phosphohydrolase activities in vitro and in vivo. Reduction of cholesterol, triglycerides, neutral lipids and phospholipid levels were noted in the livers of mice treated for 16 days. In rat studies, cholesterol, triglyceride and phospholipid levels were reduced in liver, small intestine and the feces after two weeks' dosing. The cholesterol content was reduced in the very low density lipoprotein (VLDL) and low density lipoprotein (LDL) fractions but elevated in the high density lipoproteins (HDL). Triglyceride levels were lowered in the VLDL, and neutral lipid levels were reduced in the chylomicron and VLDL fractions.     

Differential effects of dietary linoleic and α-linolenic acid on lipid metabolism in rat tissues

Comparative effects of feeding dietary linoleic (safflower oil) and α-linolenic (linseed oil) acids on the cholesterol content and fatty acid composition of plasma, liver, heart and epididymal fat pads of rats were examined. Animals fed hydrogenated beef tallow were used as isocaloric controls. Plasma cholesterol concentration was lower and the cholesterol level in liver increased in animals fed the safflower oil diet. Feeding the linseed oil diet was more effective in lowering plasma cholesterol content and did not result in cholesterol accumulation in the liver. The cholesterol concentration in heart and the epididymal fat pad was not affected by the type of dietary fatty acid fed. Arachidonic acid content of plasma lipids was significantly elevated in animals fed the safflower oil diet and remained unchanged by feeding the linseed oil diet, when compared with the isocaloric control animals fed hydrogenated beef tallow. Arachidonic acid content of liver and heart lipids was lower in animals fed diets containing safflower oil or linseed oil. Replacement of 50% of the safflower oil in the diet with linseed oil increased α-linolenic, docosapentaenoic and docosahexaenoic acids in plasma, liver, heart and epididymal fat pad lipids. These results suggest that dietary 18∶2ω6 shifts cholesterol from plasma to liver pools followed by redistribution of 20∶4ω6 from tissue to plasma pools. This redistribution pattern was not apparent when 18∶3ω3 was included in the diet.     

Studies on lipid biosynthesis and cholesterol content of liver and serum lipoproteins in rats fed various phthalate esters

The effect of various phthalate ester plasticizers on lipid metabolism in rats was studied in vivo and in vitro. Di-2-ethylhexyl phthalate (DEHP) and di-n-butyl phthalate (DBP) inhibited (30–70%) hepatic sterologenesis from¹⁴C-acetate and¹⁴C-mevalonate in liver minces from rats fed the phthalates at a level of 2.5 mmoles/100 g of chow diet for 21 days; inhibition of¹⁴C-acetate incorporation into phospholipids, triglycerides, and steryl esters was reduced (35–70%) by DEHP and DBP feeding. In addition, serum cholesterol was lowered ca. 14 mg/dl with dietary DEHP or DBP but not with dimethyl phthalate (DMP). Hepatic total cholesterol levels were reduced significantly (31%, P<0.001) by DMP but not by DBP or DEHP. In other studies with DEHP fed at the 0.5% level in chow diets (1.3 mmoles/100 g), the incorporation (esterification) of³H-oleate into di- and triglycerides was reduced ca. 40%. Furthermore, the addition of DEHP (2%, 5 mmoles/100 g) to a semisynthetic diet containing 10% fat (hydrogenated coconut oil) resulted in changes in serum lipoprotein composition. The percentage of serum cholesterol in LDL rose from 22% to 34% while that in HDL fell from 78% to 66%; these changes occurred without net changes in serum cholesterol levels. Possible mechanisms for the inhibitory effect of phthalates on hepatic lipid biosynthesis are discussed. These studies are in partial fulfillment of the requirements for a Doctorate degree in Medical Sciences, McMaster University, Hamilton, Ontario, Canada.     

The impact of dietary mono‐ and poly‐unsaturated fatty acids on risk factors for atherosclerosis in humans

The fatty acid composition of the diet has various effects on atherosclerosis risk factors. Dietary saturated fatty acids (SFA) and trans‐unsaturated fatty acids increase the low‐density lipoprotein (LDL)‐/high‐density lipoprotein (HDL)‐cholesterol ratio in serum, while these fats do not have a significant bearing on serum triglyceride levels. By contrast, dietary monounsaturated fatty acids (MUFA), n‐6 polyunsaturated fatty acids (PUFA), and α‐linolenic acid (C18:3n‐3) similarly reduce LDL cholesterol concentrations, while their influence on serum HDL cholesterol and triglycerides is not appreciable. Dietary long‐chain n‐3 PUFA slightly increase serum LDL cholesterol concentrations, but are nevertheless considered salubrious with regard to serum lipids due to the distinct triglyceride‐lowering effects. MUFA‐rich compared to n‐6 PUFA‐rich diets strongly reduce the in vitro oxidizability of LDL. The available studies on this subject also suggest that n‐3 PUFA in the small amounts usually present in the diet are not unduly harmful. These findings are consistent with reports from observational studies: the amount of SFA is positively and the amount of MUFA and n‐6 PUFA in the diet is inversely associated with the risk of cardiovascular disease in most epidemiological studies. The available studies have had an impact on current dietary guidelines, which unanimously recommend that most of the dietary fat should be in the form of MUFA, while the amount of SFA and trans fatty acids in the diet should be as low as possible.     

Enteral feeding a structured lipid emulsion containing fish oil prevents the fatty liver of sepsis

Fish oils (FO) have been shown to reduce plasma triglycerides (TG). In this study we evaluated whether enteral feeding with a structured lipid emulsion (SLE) containing FO and medium-chain triglycerides (MCT) would prevent the hypertriglyceridemia and fatty infiltration of the liver that develops during sepsis. For five days, male Lewis rats (275–300 g) were fed intragastrically a nutritionally complete diet containing a SLE or a similar diet with a soybean oil emulsion (SOE) in place of the SLE. On the fifth day, sepsis was induced by intravenously injecting 8×10⁷ liveEscherichia coli colonies/100 g b.w.; 24 h later the control SLE, septic SLE, control SOE, and septic SOE rats were sacrificed. Diet, but not treatment, had a significant effect on serum TG and free fatty acids (FFA). Feeding the SLE reduced the plasma FFA of the control and septic rats by more than 50% in comparison to both control and septic rats fed the SOE. Soleus muscle activity of lipoprotein lipase from the septic SLE rats was 44% higher than the control SLE rats. Soleus muscle from the septic SLE rats also had a twofold greater activity of lipoprotein lipase than the septic SOE rats. TG did not accumulate in the livers of the septic rats fed SLE when compared to the control SLE rats and the rats fed the SOE. Livers from the septic rats fed the SLE had a third of the TG that were present in the livers from the septic rats fed the SOE. The rate of incorporation of [¹⁴C]oleate into liver lipids was significantly lower in septic rats fed SLE than in those fed the SOE. TG esterification was 70% lower in the septic rats fed SLE rather than the SOE. Our findings suggest that the SLE with FO and MCT has a role in the prevention of the sepsis-associated fatty liver by reducing the biosynthesis of liver TG.     

Dietary proteins modulate the effects of fish oil on triglyceridemia in the rat

Sprague-Dawley rats were fed purified diets varying in both protein (20%) and lipid (11%) content for 28 d to verify the independent and interactive effects of dietary proteins and lipids on serum and hepatic lipids, and on tissue lipoprotein lipase (LPL) activity in both fasted and postprandial states. These diets consisted of either casein-menhaden oil, casein-coconut oil, soy protein-menhaden oil (SPMO), soy protein-coconut oil, cod protein-menhaden oil, or cod protein-coconut oil. A randomized 3×2 factorial design was used. A significant protein-lipid interaction was seen on serum triglyceride levels: menhaden oil, compared with coconut oil, induced a decrease in serum triglyceride levels when combined with soy protein but not when combined with cod protein and casein. The lower serum triglyceride concentrations observed in the SPMO-fed rats could be the result of decreased hepatic triglycerides when soy protein was compared with casein and when menhaden oil was compared with coconut oil. Total LPL activity in the heart was higher in menhaden oil-fed rats than in coconut oil-fed rats in the postprandial state. The higher LPL activity in the heart could, however, explain only 10% of the reduction of serum triglycerides, contributing slightly to the lowering effects of SPMO diet on serum triglycerides. Therefore, the present results indicate that dietary proteins can modulate the effects of fish oil on triglyceridemia in the rat, and that could be mainly related to specific alterations in hepatic lipid concentrations.     

Dietary effect of gamma-linolenic acid on the lipid profile of rat fed erucic acid rich oil

This study evaluated the effects of dietary supplementation of gamma-Linolenic acid (18:3n-6, GLA) on the lipid profile of serum and other tissues of rats fed erucic acid (C22:1) rich oil like mustard oil. The rats were fed diet containing 20% mustard oil as erucic acid rich oil and 20% groundnut oil as dietary fat. These groups were kept as reference groups. Another group fed diet containing 20% fat to which evening primrose oil as a source of GLA was blended with mustard oil and groundnut oil at 5% level. The feeding experiment was done for 4 weeks. In another set mustard oil fed group was kept as control while the experimental group was fed evening primrose oil as a source of GLA blended with mustard oil at 2.5% level. The feeding experiment was carried out for 12 weeks. The other dietary components remained same for all the groups. After the scheduled feeding period, it was found that there was no significant change in weight gain, food intake and food efficiency ratio. It was found that dietary GLA resulted in significant decrease in serum triglyceride (TG) and very low density lipoprotein (VLDL) cholesterol and significant increase in high density lipoprotein (HDL) cholesterol in serum in the experimental group. In liver total cholesterol (TC) is significantly higher and in heart and liver TG is significantly lower in GLA fed group.     

Serum cholesterol,triglycerides and total lipid fatty acids of rats in response to okra(hibiscus escuientus) seed oil

Tender pods of okra are commonly consumed vegetables in India. Okra seed kernel, like soybean, is a rich source of protein and fat. Its fat, with its appreciable linoleic acid content (>42%), prompted us to look into its metabolic utility in comparison with commonly consumed groundnut oil. Serum lipid profiles, with respect to cholesterol, triglycerides and total lipid fatty acids were determined in rats receiving okra seed oil at a level of 10% in the casein based diet which was adequate with respect to vitamins, minerals, etc. The control group received a casein based diet in which groundnut oil was the source of fat. Serum lipid profiles in this group were similarly monitored. The feeding trial was carried out for a period of 90 days. Results showed that serum cholesterol content of rats receiving okra seed oil was significantly lower compared to those consuming groundnut oil. A decreasing trend in total lipids as well as triglycerides was also evident in animals fed okra seed oil. Serum fatty acid profiles showed a relatively higher proportion of long chain and polyunsaturated fatty acids in this group as compared to the group receiving groundnut oil. These results indicate that okra seed oil consumption has a potential hypocholesterolemic effect. To whom correspondence to be addressed. ¹Part of this work was presented at 45th Annual Meeting of Oil Technologists Association of India, New Delhi-Feb. 9–10, 1990.     

Interaction Between Marginal Zinc and High Fat Supply on Lipid Metabolism and Growth of Weanling Rats

The impact of a moderate Zn deficiency on growth and plasma and liver lipids was investigated in two 4-week experiments with male weanling rats fed fat-enriched diets. Semisynthetic, approximately isocaloric diets containing 3% soybean oil were supplemented with either 7 or 100 mg Zn/kg diet and with 22% beef tallow (BT) or sunflower oil (SF). In Experiment 1, which compared the dietary fat level and the fat source in a factorial design of treatments, all diets were fed ad libitum to 6 × 8 animals, whereas intake of the high-Zn BT and SF diets was restricted in Experiment 2 (5 × 6 rats) to the level of intake of the respective low-Zn diets. The low-Zn SF diet consistently depressed food intake and final live weights of the animals to a greater extent than the other low-Zn diets, while intake and growth were comparable among the animals fed the high-Zn diets. The marginal Zn deficit per se did not alter plasma triglyceride and cholesterol concentrations nor hepatic concentrations of triglyceride, cholesterol and phospholipids. The fatty acid pattern of liver phospholipids did not indicate that chain elongation and desaturation of fatty acids was impaired by a lack of zinc. It was concluded that dietary energy and fat intake, and fat source have a greater effect on plasma and liver lipids than a moderate Zn deficiency. Marginally Zn-deficient diets enriched with sunflower oil as a major energy source cause a greater growth retardation than diets rich in carbohydrates or beef tallow.     

Deposition of dietary epoxides in tissues of rats

Epididymal fat pad lipids from rats fed trivernolin at the 4.8% level in the diet for 90 days were found to contain 6.1% epoxyoleic acid. No epoxides were detected in the serum lipids and only trace amounts were found in the liver lipids. TLC, GLC and a specific color reaction with picric acid were used to identify this fatty epoxide in the tissues. Epoxyoleic acid was shown to be present as a mixture of predominately monovernoloyl triglycerides with some divernoloyl triglycerides and small amounts of trivernolin. Lipase hydrolysis of the first two triglycerides has demonstrated that the vernoloyl groups are present mostly in the 1,3 positions. In a separate experiment, rats were fed cholesterol epoxide at the 0.5% and 1.5% levels in the diet for 90 days. TLC and GLC examination of lipids from these rats failed to reveal the presence of any cholesterol epoxide. Only one-half of the sterol fed could be accounted for in the fecal lipids. Presented in part at the AOCS Meeting, Chicago, October 1967.