Dietary single cell protein reduces fatty liver in obese Zucker rats

There is growing evidence that dietary proteins may interfere with lipid metabolism. We therefore examined the effects of feeding obese Zucker rats a single cell protein (SCP) with low ratios of methionine:glycine and lysine:arginine for 6 weeks. SCP feeding reduced the hepatic steatosis and lowered the plasma transaminase levels when compared with casein-fed rats (controls). The fatty acid oxidation was increased in liver mitochondria and peroxisomes, whereas the activities of enzymes involved in lipogenesis and TAG biosynthesis were unaffected. SCP feeding affected the fatty acid composition of liver lipids and plasma, and reduced the mRNA levels of the fatty acid desaturases. The decreased gene expression of stearoyl-CoA desaturase suggested that the fatty acids were directed towards oxidation rather than esterification as TAG. The decreased mRNA levels of VLDL-receptor and lipoprotein lipase in the liver after SCP feeding suggested that the uptake of TAG-rich lipoprotein to the liver was decreased. To conclude, the reduced fatty liver by SCP feeding may be caused by the increased capacity for fatty acid beta-oxidation in the liver, combined with changed fatty acid composition and possibly a reduced hepatic clearance of circulating VLDL. An increased awareness of the effect of dietary proteins on lipid metabolism could be of relevance in future dietary treatment of non-alcoholic fatty liver disease.     

Dietary effect of pomegranate seed oil rich in 9cis, 11trans, 13cis conjugated linolenic acid on lipid metabolism in obese,hyperlipidemic OLETF Rats

Conjugated fatty acid, the general term of positional and geometric isomers of polyunsaturated fatty acids with conjugated double bonds, has attracted considerable attention because of its potentially beneficial biological effects. In the present study, dietary effect of pomegranate seed oil rich in punicic acid (9 cis, 11 trans, 13 cis -conjugated linolenic acid; 9c, 11t, 13c-CLNA) on lipid metabolism was investigated in obese, hyperlipidemic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. After 2 weeks feeding period, OLETF rats revealed obesity and hyperlipidemia compared with their progenitor LETO rats. Feeding of the diet supplemented with 9% safflower oil and 1% pomegranate seed oil (9c, 11t, 13c-CLNA diet) did not affect abdominal white adipose tissue weights and serum lipid levels compared with the diet supplemented with 10% safflower oil (control diet) in OLETF rats. However, the accumulated hepatic triacylglycerol was markedly decreased by 9c, 11t, 13c-CLNA diet in OLETF rats. Activities of hepatic enzymes related to fatty acid synthesis and fatty acid β-oxidation were not altered by 9c, 11t, 13c-CLNA diet. Levels of monounsaturated fatty acid (MUFA), major storage form of fatty acid, in serum triacylglycerol were markedly higher in obese, hyperlipidemic OLETF rats than in lean LETO rats. In addition, 9c, 11t, 13c-CLNA diet significantly decreased MUFA levels in OLETF rats. This is the first study showing that 9c, 11t, 13c-CLNA suppresses delta-9 desaturation in vivo, and we suggest that the alleviation of hepatic triacylglycerol accumulation by 9c, 11t, 13c-CLNA diet was, at least in part, attributable to the suppression of delta-9 desaturation in OLETF rats.     

Age-related changes in fatty acids in obese offspring of streptozotocin-induced diabetic rats

OBJECTIVE: The long-term effects of fetal hyperinsulinemia, time course of changes in liver and very-low-density lipoprotein (VLDL) lipid levels and fatty acid compositions were investigated in obese offspring of streptozotocin-induced mildly diabetic rats. RESEARCH METHODS AND PROCEDURES: Mild hyperglycemia in pregnant rats was induced by intraperitoneal injection of streptozotocin on day 5 of gestation. Control pregnant rats were injected with citrate buffer. Liver and VLDL lipids and fatty acids were analyzed in offspring at different ages. RESULTS: At birth, obese pups had higher VLDL triglyceride levels, saturated fatty acids, and C20:4n-6. They also had lower C18:2n-6 proportions in VLDL triglycerides, phospholipids, and cholesteryl esters than controls pups. In 1-month-old male and female obese rats, VLDL and liver lipid amounts were similar to those in their respective controls; however, high levels of C18:2n-6 and C20:4n-6 were noted in liver and VLDL lipids. At the age of 2 months, liver and VLDL triglyceride levels were higher in obese females than in control females. Fatty acid abnormalities seen in obese rats included low C18:3n-3 and high C22:6n-3 proportions in liver triglycerides and phospholipids. At the age of 3 months, obese rats, both males and females, compared with control animals, had higher VLDL and hepatic lipids with reduced C20:4n-6 levels and polyunsaturated/saturated fatty acids ratios in hepatic and VLDL triglycerides and phospholipids. DISCUSSION: Fetal obesity, associated with alterations in VLDL lipid fatty acid composition, represents an important risk factor for adult obesity and diabetes.     

Thiamine prevents obesity and obesity-associated metabolic disorders in OLETF rats

We previously found that thiamine mitigates metabolic disorders in spontaneously hypertensive rats, harboring defects in glucose and fatty acid metabolism. Mutation of thiamine transporter gene SLC19A2 is linked to type 2 diabetes mellitus. The current study extends our hypothesis that thiamine intervention may impact metabolic abnormalities in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, exhibiting obesity and metabolic disorders similar to human metabolic syndrome. Male OLETF rats (4 wk old) were given free access to water containing either 0.2% or 0% of thiamine for 21 and 51 wk. At the end of treatment, blood parameters and cardiac functions were analyzed. After sacrifice, organs weights, histological findings, and hepatic pyruvate dehydrogenase (PDH) activity in the liver were evaluated. Thiamine intervention averted obesity and prevented metabolic disorders in OLETF rats which accompanied mitigation of reduced lipid oxidation and increased hepatic PDH activity. Histological evaluation revealed that thiamine alleviated adipocyte hypertrophy, steatosis in the liver, heart, and skeletal muscle, sinusoidal fibrosis with formation of basement membranes (called pseudocapillarization) which accompanied significantly reduced expression of laminin β1 and nidogen-1 mRNA, interstitial fibrosis in the heart and kidney, fatty degeneration in the pancreas, thickening of the basement membrane of the vasculature, and glomerulopathy and mononuclear cell infiltration in the kidney. Cardiac and renal functions were preserved in thiamine treatment. Thiamine has a potential to prevent obesity and metabolic disorders in OLETF rats.     

The form of dietary conjugated linoleic acid does not influence plasma and liver triacylglycerol concentrations in Syrian golden hamsters

Several studies have shown that conjugated linoleic acid (CLA) supplementation can improve the plasma lipid profile and thereby probably decrease the risk for development of atherosclerosis. The aim of the present study was to compare the effects on plasma and organ lipids of different dietary forms of CLA: triacylglycerol (TAG), diacylglycerol (DAG), monoacylglycerol (MAG), and fatty acid ethyl esters (FAEEs). DAG-, MAG-, and FAEE-CLA were produced by enzymatic interesterifications and all supplements were composed of a 1:1 mixture of the 2 major CLA isomers: cis-9, trans-11 and trans-10, cis-12. Male Syrian Golden hamsters were fed mildly atherogenic diets (10 g butter/100 g, 0.1 g cholesterol/100 g) supplemented with 0.5 g CLA/100 g or without CLA (control) for 8 wk. Liver weights were greater in the TAG- and FAEE-CLA groups than in the control group. In general, the form of CLA did not differentially affect plasma or liver cholesterol or plasma lipoprotein cholesterol concentrations, but only the TAG-CLA group had a higher final plasma TAG concentration than the control group. Both CLA isomers were incorporated into plasma, livers, and spleens. The results of the present study suggest that the form in which CLA is supplemented in the diet does not affect hamster plasma and liver TAG concentrations. The TAG-CLA form, a frequently used form of supplemental CLA, increases plasma TAG concentrations. If similar effects occur in humans, supplemental TAG-CLA cannot be considered to be beneficial given the relation between plasma TAG and the development of atherosclerosis.     

Trans-11 vaccenic acid dietary supplementation induces hypolipidemic effects in JCR:LA-cp rats

Trans-11 vaccenic acid [VA; 18:1(n-9)] is a positional and geometric isomer of oleic acid and is the precursor to conjugated linoleic acid (CLA) in humans. Despite VA being the predominant trans monoene in ruminant-derived lipids, very little is known about its nutritional bioactivity, particularly in conditions of chronic metabolic disorders, including obesity, insulin resistance, and/or dyslipidemia. The aim of this study was to assess the potential of VA to improve dyslipidemia, insulin sensitivity, or inflammatory status in obese and insulin-resistant JCR:LA-cp rats. The obese rats and age-matched lean littermates were fed a control diet or a control diet supplemented with 1.5% (wt:wt) VA for a period of 3 wk. The incorporation of VA and subsequent conversion to CLA in triglyceride was measured in adipose tissue. Glucose and insulin metabolism were assessed via a conscious adapted meal tolerance test procedure. Plasma lipids as well as serum inflammatory cytokine concentrations were measured by commercially available assays. VA supplementation did not result in any observable adverse health effects in either lean or obese JCR:LA-cp rats. After 3 wk of feeding, body weight, food intake, and glucose/insulin metabolism did not differ between VA-supplemented and control groups. The incorporation of VA and CLA into adipose triglycerides in obese rats fed VA increased by 1.5-fold and 6.5-fold, respectively, compared with obese rats fed the control diet. The most striking effect was a 40% decrease (P < 0.05) in fasting triglyceride concentrations in VA-treated obese rats relative to obese controls. Serum Il-10 concentration was decreased by VA, regardless of genotype (P < 0.05). In conclusion, short-term dietary supplementation of 1.5% VA did not result in any detrimental metabolic effects in JCR:LA-cp rats. In contrast, dietary VA had substantial hypo-triglyceridemic effects, suggesting a new bioactivity of this fatty acid that is typically found in ruminant-derived food products.     

Effects of conjugated linoleic acid on serum leptin concentration, body-fat accumulation, and beta-oxidation of fatty acid in OLETF rats

We investigated the efficacy of a 4-wk supplementation of conjugated linoleic acid (CLA) as free fatty acid (FFA) or triacylglycerol (TG) on serum leptin concentration, body-fat accumulation, and mitochondrial beta-oxidation in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. A significant reduction of serum leptin concentration (42%) and a decrease in the wet weights of perirenal, epididymal, and omental/visceral-adipose tissue in TG-CLA and FFA-CLA groups were found in comparison with the OLETF control group. Both forms of CLA supplementation produced a 5.2% decrease in body weight compared with the control even though food intake was similar in the OLETF groups. Moreover, both forms of CLA enhanced carnitine-palmitoyltransferase activity in brown adipose tissue, perirenal adipose tissue, red gastrocnemius muscle, and liver in comparison with the OLETF control group. Serum concentrations of non-esterified fatty acid and TG also were reduced in rats fed diets supplemented with TG-CLA and FFA-CLA.     

Fish Oil Decreases Hepatic Lipogenic Genes in Rats Fasted and Refed on a High Fructose Diet

Fasting and then refeeding on a high-carbohydrate diet increases serum and hepatic triacylglycerol (TAG) concentrations compared to standard diets. Fructose is a lipogenic monosaccharide which stimulates de novo fatty acid synthesis. Omega-3 (n-3) fatty acids stimulate hepatic β-oxidation, partitioning fatty acids away from TAG synthesis. This study investigated whether dietary n-3 fatty acids from fish oil (FO) improve the hepatic lipid metabolic response seen in rats fasted and then refed on a high-fructose diet. During the post-prandial (fed) period, rats fed a FO rich diet showed an increase in hepatic peroxisome proliferator-activated receptor α (PPAR-α) gene expression and decreased expression of carbohydrate responsive element binding protein (ChREBP), fatty acid synthase (FAS) and microsomal triglyceride transfer protein (MTTP). Feeding a FO rich diet for 7 days prior to 48 h of fasting resulted in lower hepatic TAG, lower PPAR-α expression and maintenance of hepatic n-3 fatty acid content. Refeeding on a high fructose diet promoted an increase in hepatic and serum TAG and in hepatic PPAR-α, ChREBP and MTTP expression. FO did not prevent the increase in serum and hepatic TAG after fructose refeeding, but did decrease hepatic expression of lipogenic genes and increased the n-3 fatty acid content of the liver. n-3 Fatty acids can modify some components of the hepatic lipid metabolic response to later feeding with a high fructose diet.     

Gamma-linolenic acid prevents conjugated linoleic acid-induced fatty liver in mice

OBJECTIVE: The present study was done to clarify the mechanism by which conjugated linoleic acid (CLA) induces fatty liver in mice and to attenuate this symptom by adding other dietary fatty acids. METHODS: Mice were given CLA short (12 h) or long (4 wk) term or given CLA with linoleic acid (LA) or gamma-linolenic acid (GLA) in the long term (4 wk). Total lipids, triacylglycerol, and prostaglandin E(2) (PGE(2)) levels in the liver were determined. RESULTS: A single administration of CLA significantly increased PGE(2) levels in the liver 12 h after administration. However, long-term administration of CLA significantly decreased the liver PGE(2) level and induced fatty liver. GLA increased PGE(2) levels, and coadministration with GLA, but not with LA, prevented the CLA-induced fatty liver. CONCLUSIONS: These data suggest that CLA initially stimulates PGE(2) production followed by depletion of PGE(2) sources in the liver. The fatty liver associated with PGE(2) reduction by CLA ingestion can be attenuated by GLA in mice.     

Dietary hydrogenated soybean oil affects lipid and vitamin E metabolism in rats

Fatty acids containing stearic acid, which are found in hydrogenated fat, may have a detrimental effect on the cholesterol and triacylglycerol (TAG) content of plasma lipoproteins, and on the absorption of fatty acids and fat-soluble vitamins. The aim of our study was to examine the tissue concentration of lipids and vitamins A and E after feeding a hydrogenated soybean oil (HSO) diet to rats. Twenty male Sprague-Dawley rats were randomly divided into two groups, fed on coconut oil (control) and HSO, respectively in amounts corresponding to 15% of the total feed. Plasma total cholesterol, VLDL- and LDL-cholesterol, lipid peroxidation and daily excretion of the TAG and cholesterol in feces were higher in the HSO than in the control group. TAG values in plasma and liver, and HDL-cholesterol levels in plasma were lower in the HSO than in the control group. The same was true for phospholipids in plasma and for saturated fatty acids, mono- and polyunsaturated fatty acids levels in the liver and vitamin E in plasma, LDL and adipose tissue. The results of this study provide new evidence concerning the effect of dietary hydrogenated fat on lipid, TAG and vitamin E status, which are important for maintenance of good health. Consumption of dietary HSO may be associated with cardiovascular disease.     

Arachidonic acid prevents fatty liver induced by conjugated linoleic acid in mice

Conjugated linoleic acid (CLA) has anti-obesity effects, but induces fatty liver in mice. The present study investigated whether co-administration of arachidonic acid (ARA) attenuates fat accumulation in the mouse liver induced by CLA. Male mice (8 weeks old) were given diets with either no addition of dietary fat (control), 3 % linoleic acid (LA), 3 % CLA, 3 % CLA+1 % ARA, or 3 % CLA+2 % ARA for 4 weeks. The perirenal fat weight in ARA-treated groups decreased similarly as with CLA alone, when compared to control or LA. Plasma TAG concentration was significantly higher in the CLA group than in either CLA+ARA group, while plasma cholesterol and NEFA concentrations did not vary among the groups. In contrast to visceral fat, liver weight was significantly higher in the CLA group than in the control or LA groups, and the effects of CLA were attenuated by ARA. TAG and cholesterol were markedly accumulated in the liver with dietary CLA, whereas co-administration with ARA, at either concentration, suppressed CLA-induced lipid accumulation. Liver PGE(2) was enhanced by a combination of CLA and ARA when compared with CLA alone, but PGE(1) level was not significantly different among groups. In conclusion, fatty liver induced by CLA was attenuated by co-administration with ARA, furthermore, a combination of these fatty acids maintained the anti-obese effect of CLA.     

Dietary conjugated linoleic acid alleviates nonalcoholic fatty liver disease in Zucker (fa/fa) rats

Nonalcoholic fatty liver disease (NAFLD) is the preferred term to describe the spectrum of liver damage ranging from hepatic steatosis to steatohepatitis, liver fibrosis, and cirrhosis, and it is emerging as the most common liver disease in industrialized countries. Thus, the discovery of food components that would ameliorate NAFLD is of interest. Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of linoleic acid, has attracted considerable attention because of its potentially beneficial biological effects both in vitro and in vivo. We tested whether dietary CLA protects Zucker (fa/fa) rats from hepatic injury. After 8 wk of feeding, hepatomegaly, hepatic triglyceride (TG) accumulation, and elevated hepatic injury markers in plasma were markedly alleviated in CLA-fed Zucker rats compared with linoleic acid-fed (control) rats. These effects were attributed in part to the enhanced hepatic activities of carnitine palmitoyltransferase, a key enzyme of fatty acid beta-oxidation, and microsomal TG transfer protein, an important factor for lipoprotein secretion due to the CLA diet. We previously reported that the severe hyperinsulinemia in control Zucker rats was attenuated in CLA-fed rats due to an enhanced level of plasma adiponectin, which improves insulin sensitivity. In the present study, the adiponectin concentration was increased and the mRNA expression of tumor necrosis factor-alpha, an inflammatory cytokine, was markedly suppressed in the liver of CLA-fed Zucker rats. We speculate that the enhanced level of liver adiponectin may prevent the development and progression of NAFLD in CLA-fed Zucker rats.     

Lupin protein influences the expression of hepatic genes involved in fatty acid synthesis and triacylglycerol hydrolysis of adult rats

To assess the effect of lupin protein on concentrations of lipids in plasma lipoproteins and liver and hepatic mRNA concentrations of genes involved in lipid metabolism, adult rats were fed egg albumin-based diets containing either lupin protein from Lupinus albus or casein (50 g/kg) supplemented (hypercholesterolaemic) or not (normolipaemic) with a cholesterol-cholate mixture for 20 d. Lupin protein compared with casein lowered the concentrations of TAG in liver (P < 0.01) and circulating VLDL + chylomicrons (P < 0.05) of hypercholesterolaemic rats, but not of normolipaemic rats. Hepatic mRNA concentrations of genes involved in fatty acid synthesis such as sterol regulatory element-binding protein-1c, glucose-6-phosphate dehydrogenase, fatty acid synthase, stearoyl-CoA desaturase-1 and acyl-CoA:glycerol-3-phosphate acyltransferase were lower and mRNA concentrations of lipoprotein lipase, hepatic lipase and apoA5 involved in TAG hydrolysis were higher in rats fed lupin protein than in rats fed casein. These effects were stronger in hypercholesterolaemic rats than in normolipaemic rats. Hypercholesterolaemic rats fed the lupin protein had higher liver cholesterol concentrations (P < 0.01) and lower levels of LDL-cholesterol (P < 0.05) than rats fed casein. No effect of lupin protein was observed on cholesterol concentration in VLDL + chylomicrons and HDL and hepatic mRNA concentrations of genes involved in cholesterol and bile acid metabolism. In conclusion, the present study shows that lupin protein has hypotriacylglycerolaemic action possibly via down regulation of fatty acid synthesis genes and up regulation of genes involved in TAG hydrolysis. Alterations in cholesterol metabolism could not be explained on the basis of mRNA data.     

Combined effects of dietary conjugated linoleic acid and sesamin triacylglycerol and ketone body production in rat liver

The effects of a combination of dietary conjugated linoleic acid (CLA) supplemented with sesamin on hepatic ketogenesis and triacylglycerol secretion were compared using the livers of rats fed diets containing 1% CLA or linoleic acid (LA) in combination with 0.2% sesamin for 14 d, respectively. The feeding of CLA, as compared to LA, caused a significant reduction in the weight of perirenal adipose tissue but not that of epididymal adipose tissue, and affected neither growth parameters nor hepatic lipid concentration. Hepatic production of ketone bodies was consistently higher in rats fed CLA than in those fed LA, while triacylglycerol secretion was reversed. No significant difference was noted in the hepatic secretion of cholesterol among the groups. Although there was no effect of the dietary combination of CLA with sesamin on adipose tissue weight, hepatic lipid parameters and ketone body production were observed: i.e., triacylglycerol secretion tended to be reduced. These results suggest that the dietary combination of CLA with sesamin may be an effective approach for lowering serum triacylglycerol levels. The decreased hepatic secretion of triacylglycerol is, in part, due to enhanced fatty acid oxidation in the liver.     

Dietary sea cucumber cerebroside alleviates orotic acid-induced excess hepatic adipopexis in rats

ABSTRACT: BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a prevalent chronic liver disease in industrialized countries. The present study was undertaken to explore the preventive effect of dietary sea cucumber cerebroside (SCC) extracted from Acaudina molpadioides in fatty liver rats. METHODS: Male Wistar rats were randomly divided into four groups including normal control group, NAFLD model group, and two SCC-treated groups with SCC at 0.006% and 0.03% respectively. The fatty liver model was established by administration of 1% orotic acid (OA) to the rats. After 10d, serum and hepatic lipid levels were detected. And the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were also determined. Besides, to gain the potential mechanism, the changes of key enzymes and gene expressions related to the hepatic lipid metabolism were measured. RESULTS: Dietary SCC at the level of 0.006% and 0.03% ameliorated the hepatic lipid accumulation in fatty liver rats. SCC administration elevated the serum triglyceride (TG) level and the ALT, AST activities in OA-fed rats. The activities of hepatic lipogenic enzymes including fatty acid synthase (FAS), malic enzyme (ME) and glucose-6-phosphatedehydrogenase (G6PDH) were inhibited by SCC treatment. And the gene expressions of FAS, ME, G6PDH and sterol-regulatory element binding protein (SREBP-1c) were also reduced in rats fed SCC. However, dietary SCC didn't affect the activity and mRNA expression of carnitine palmitoyltransferase (CPT) in liver. Besides, suppression of microsomal triglyceride transfer protein (MTP) activity was observed in SCC-feeding rats. CONCLUSIONS: These results suggested that dietary SCC could attenuate hepatic steatosis due to its inhibition of hepatic lipogenic gene expression and enzyme activity and the enhancement of TG secretion from liver.     

Comparison of native and capric acid-enriched mustard oil effects on oxidative stress and antioxidant protection in rats

The present study evaluated the effect of mustard oil enriched in capric acid, a medium-chain fatty acid, on antioxidant enzyme activities in liver and brain and on the levels of malondialdehyde (MDA) in liver, brain and plasma in rats; the effect of adding cholesterol to the diet was also investigated. Charles Foster male albino rats weighing 80-100 g were fed one of four diets for 30 d (six rats per group). In the absence of added dietary cholesterol, the addition of capric acid to the diet resulted in lower plasma total cholesterol, non-HDL-cholesterol and TAG concentrations, higher HDL-cholesterol concentrations, higher antioxidant enzyme activities in liver and brain and lower MDA concentrations in liver, brain and plasma. Adding cholesterol to the diet increased plasma total cholesterol, non-HDL-cholesterol and TAG concentrations, decreased HDL-cholesterol concentration, decreased the activities of antioxidant enzymes and increased tissue and plasma MDA concentrations. Including capric acid in the diet of rats receiving cholesterol at least partly prevented the effects of the increased cholesterol. It is concluded that compared with native mustard oil, capric acid-enriched mustard oil improves blood lipids, enhances antioxidant protection and reduces lipid peroxidation.     

Effect of high vitamin A or tocopherol intake on hepatic lipid metabolism and intestinal absorption and secretion of lipids and bile acids in the chick

The effect of high dietary vitamin A or tocopherol, or both, on lipid absorption and secretion in the gastrointestinal tract and on serum and hepatic lipids was determined in the chick. High dietary vitamin A increased secretion of cholesterol, bile acids, phospholipids and fatty acids to the duodenum, and tocopherol enhanced cholesterol and bile acid secretion to the duodenum. No differences in over-all absorption were observed. Serum cholesterol was depressed by vitamin A and hepatic lipids were enhanced, except phosphatidyl choline which was depressed. Tocopherol increased hepatic triglycerides and cholesterol. In vitro fatty acid synthesis from lactate by liver homogenates was enhanced by vitamin E and cholesterogenesis enhanced by both vitamin A and tocopherol. delta 9 Desaturation was also enhanced by vitamin E. It is concluded that both vitamin A and tocopherol affect the hepatic synthesis and catabolism of cholesterol and that vitamin E also influences fatty acid metabolism.     

The contrasting effect of dietary phosphatidylethanolamine and phosphatidylcholine on serum lipoproteins and liver lipids in rats

The effect of dietary phosphatidylethanolamine (PE) and phosphatidylcholine (PC) added to cholesterol-free semipurified diet on serum lipoprotein and hepatic and fecal lipids was compared to the effect on rats fed soybean oil (controls). The dietary PE, but not PC, caused a decrease in serum cholesterol, phospholipid, apolipoprotein A-I (apoA-I) and apoE and an increase in high molecular weight apoB. The simultaneous addition of PC and ethanolamine also decreased serum apoA-I and cholesterol. The distribution patterns of phospholipid subclasses in the liver and fatty acid composition of hepatic and plasma phospholipids were also altered by dietary PE. Both PE and PC increased to a similar extent the excretion of fecal neutral steroids and hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity compared to the controls. The present study, therefore, demonstrated for the first time that the PE in the soybean phospholipid preparation is responsible for the alterations of profiles of serum lipids and apoproteins in rats.     

Suppression of rat liver fatty acid synthesis by eicosa-5,8,11,14-tetraynoic acid without a reduction in lipogenic enzymes

In meal-fed rats supplementation of safflower oil (5 g per 100 g diet) to a fat-free basal diet resulted in the characteristic suppression of liver fatty acid synthetase and acetyl-CoA carboxylase activities, which was accompanied by a 60% decrease in the rate of hepatic fatty acid synthesis. The decline in activity of these lipogenic enzymes was completely prevented by adding 0.05% eicosa-5,8,11,14-tetraynoic acid (TYA) to the safflower oil diet. Fatty acid analysis of the livers indicated that TYA significantly impaired the conversion of linoleate to arachidonate. Apparently the selective suppression of lipogenic enzymes by dietary linoleate is not caused by linoleate per se but requires its conversion to longer-chain fatty acids and/or protaglandins. In spite of high activities of fatty acid synthetase and acetyl-CoA carboxylase, liver fatty acid synthesis continued to be inhibited by the safflower oil + TYA dietary regimen. This continued inhibition of lipogenesis was due to the TYA, because addition of TYA to the fat-free diet precipitated a significant decline in liver fatty acid synthesis without a drop in lipogenic enzymes. Inhibition of fatty acid synthesis by TYA could not be attributed to a decrease in liver glucose utilization based on hepatic glycogen concentration, nor was it due to a reduction in the fraction of catalytically active polymeric acetyl-CoA carboxylase based on sensitivity of the enzyme activity to avidin.     

The position of rumenic acid on triacylglycerols alters its bioavailability in rats

The metabolic fate of rumenic acid (9cis,11trans-octadecenoic acid) related to its position on the glycerol moiety has not yet been studied. In the present work, synthetic triacylglycerols (TAG) esterified with oleic and rumenic acids were prepared. Rats were force-fed synthetic dioleyl monorumenyl glycerol with (14)C labeled rumenic acid in the internal (sn-2) or in the external position (sn-1 or sn-3). Rats were then placed in metabolic cages for 16 h. At the end of the experiment, the radioactivity in tissues, carcass and expired CO(2) was measured. Rumenic acid that was esterified at the external positions on the TAG was better absorbed and oxidized to a greater extent than when esterified at the internal position. The fatty acid from the 2-TAG form was also better incorporated into the rat carcass. In the liver, rumenic acid appeared mainly in TAG (50%) and to a lesser extent in phospholipids (33%) whatever its dietary form. Moreover, analyses of lipids from Camembert cheese and butter revealed that rumenic acid was located mainly on the sn-1 or sn-3 positions (74%). Taken together, these data suggest that rumenic acid from dairy fat may be well absorbed and used extensively for energy production.