Fatty liver caused by chronic alcohol ingestion is prevented by dietary supplementation with pyruvate or glycerol

Earlier studies showed that the fatty liver, caused by feeding rats the Lieber-DeCarli alcohol diet for four weeks, was prevented if the diet was supplemented with dihydroxyacetone (22 g/l), pyruvate (22 g/l) and riboflavin (2.2 g/l). In the present study, we observed that fatty liver was prevented if the alcohol diet was supplemented with glycerol and lactate (22 g/l each) and riboflavin (2.2 g/l). Hence, the prevention of alcoholic fatty liver by the dietary supplementation with dihydroxyacetone and pyruvate may not be related to their capacity to serve as hydrogen acceptors and to oxidize NADH produced during ethanol metabolism. When rats were fed the alcohol diet supplemented with either glycerol or pyruvate, the hepatic triglyceride (TG) levels were similar to those in rats pair-fed a Lieber-DeCarli control diet in which alcohol was replaced with an isocaloric amount of dextrins. Therefore, the prevention of fatty liver does not require the simultaneous presence of several supplements. Dietary dihydroxyacetone or riboflavin did not reduce alcoholic fatty liver. Supplementation of the ethanol diet with isocaloric amounts of lactate or glucose, instead of pyruvate, did not abolish the development of fatty liver but caused a marked reduction in the hepatic TG levels. Animals fed the alcohol diet consumed only small amounts of carbohydrate for long periods of time. Since the inclusion of glucose or its metabolites in the alcohol diet fed to rats caused a marked decrease in the liver TG content, it is likely that the production or prevention of fatty liver is related to carbohydrate metabolism.     

Dietary arachidonic acid reduces fatty liver,increases diet consumption and weight gain in ethanol-fed rats

We fed young male Sprague-Dawley rats for 4 wk ad libitum liquid diets containing 34% of the calories as ethanol and 35% as fat with (AA+) and without (AA−) arachidonic acid (20∶4). Additional rats in the control groups were fed similar diets made isocaloric with dextrose with (CA+) and without (CA−) 20∶4. The liver triglyceride (TG) content of rats in the AA+ group was reduced ca. 3-fold over that of rats in the AA-group. The diet consumption and body wts of rats in the AA+ group were significantly greater than those of rats fed alcohol without the 20∶4 supplement (AA−). Also livers from rats in the AA+ group were as large as those from rats in control groups (CA+, CA−) and ca. twice as large as those from rats in the AA-group. The fatty acid composition of liver TG in rats fed the alcohol diet was similar to that of dietary fat. Levels of 20∶4 and docosatetraenoic acid (22∶4) in liver TG fatty acids from rats fed diets without arachidonate (AA−, CA−) were low (trace to 1.6%). After ingestion of arachidonic acid, 20∶4 increased to ca. 10% and 22∶4 to ca. 5%. The content of liver phospholipids was higher in livers of rats fed ethanol (AA−) than in those of controls (CA−). Presented at the ISF/AOCS World Congress, April 27-May 1, 1980, New York City.     

Hepatic origin of triglycerides in fatty livers produced by the continuous intragastric infusion of an ethanol diet

Male Wistar rats were maintained for 30 days on an independent and continuous intragastric infusion of ethanol and nutritionally defined liquid diet containing only a small amount of corn oil (CO-4.9% calories). Ethanol intake was progressively increased from 32% to 40.4% of the total calories to maintain a high degree of intoxication during this period. Rats in the control group were infused with an isocaloric diet in which alcohol was replaced by dextrose. The liver triglyceride (TG) content of rats given alcohol (61.5±16.4 mg/g) was ca. 10-fold greater than that of controls (5.9±2.1 mg/g) and similar to that observed previously in rats fed an ethanol diet containing high levels of fat (35% and 43% calories). In TG of fatty liver, the level of 18∶2 was small (3%), even though CO in the diet contained a high level of this acid. Furthermore, 16∶1 and 16∶0 contents were markedly elevated (16% and 40%, respectively) despite the fact that CO did not contain 16∶1 and had only a small amount of 16∶0. Liver TG having a fatty acid (FA) composition markedly different from that of CO and the presence of high levels of 16∶1 and 16∶0 indicate that the TG accumulated in the fatty liver originated from hepatic lipogenesis rather than from dietary fat.     

Kidney lipids: Changes caused by dietary 9-Trans, 12-Trans-octadecadienoate

Trans, trans-linoleate at 50 and 100% of dietary fat decreased kidney size and altered its composition.Trans, trans-linoleate as the sole source of dietary fat imparied growth and caused more severe symptoms of essential fatty acid deficiency than was observed with hydrogenated coconut oil (HCO). The concentration of renal cholesterol, phospholipids (PL), triglycerides (TG) and cholesteryl esters (CE) were also decreased. Linoleic (18∶2), homo-γ-linolenic acid (20∶3n6) and arachidonic acid (20∶4n6) were significantly depressed in lipid classes, especially in PL and CE, by dietarytrans, trans-linoleate. The increase in eicosatrienoate (20∶3n9), especially in PL and CE of kidneys of rats fed HCO (essential fatty acid deficient), was slight in rats fed 100%trans, trans-linoleate, indicating that thetrans, trans acid probably inhibited acyl elongation and desaturation.     

Divergent incorporation of dietary trans fatty acids in different serum lipid fractions

Trans fatty acids may be involved in atherosclerotic vascular diseases. We investigated the incorporation of dietary trans fatty acids and oleic acid into the serum triglycerides (TG), cholesterol esters (CE), and phospholipids (PL). Fourteen healthy female volunteers, aged 23.2±3.1 yr (mean±SD), body mass index 20.8±2.1 kg/m² participated in this study. All subjects consumed both a trans fatty acid-enriched diet (TRANS diet) and an oleic acid-enriched diet (OLEIC diet) for 4 wk according to a randomized crossover design. Both experimental diet periods were preceded by consumption of a baseline diet for 2 wk which supplied 37% of total energy (E%) as fat: 18 E% from saturated fatty acids (SFA), 12 E% from monounsaturated fatty acids, and 6 E% from polyunsaturated fatty acids. Five E% of the SFA in the baseline diet was replaced by trans fatty acids (18∶1 t and 18∶2 c,t+18∶2t,t, where c is cis and t is trans) in the TRANS diet and by oleic acid (18∶1n-9) in the OLEIC diet. After the TRANS diet, the proportions of 18∶1t and 18∶2t increased (P <0.001) in all serum lipid fractions analyzed. The increase of 18∶1 t in TG and PL (1.80±0.28 vs. 5.26±1.40; 1.07±0.34 vs. 3.39±0.76 mol% of total fatty acids, respectively) was markedly higher than that in CE (0.44±0.07 vs. 0.92±0.26), whereas that of 18∶2t was nearly the same in all three fractions. The proportions of palmitic, stearic, arachidonic, and eicosapentaenoic acids in TG, CE, and PL and that of oleic acid in TG and CE were decreased when compared with the baseline value. In contrast, the proportion of palmitoleic acid in TG and PL and that of linoleic acid in PL increased on the TRANS diet. After consumption of the OLEIC diet, the proportion of oleic acid increased in all three lipid fractions analyzed, and the percentage increase was nearly the same in all fractions. In contrast, the proportions of 18∶1 t in TG and PL and 18∶2 t in TG and CE decreased when compared with the baseline value. In conclusion, a moderate increase in dietary trans fatty acids resulted in a marked incorporation into serum lipids and decreased the conversion of linoleic acid to its more unsaturated long-chain metabolites. Analysis of 18∶1 t from serum TG and PL seems to reflect reliably the dietary intake of this fatty acid.     

Influence of dietary fat on metabolism of (14-14C)erucic acid in the perfused rat liver. Distribution of metabolites in lipid classes

Two groups of rats were fed diets containing 20% by weight of either partially hydrogenated marine oil supplemented with sunflower seed oil (PHMO) or palm oil (PO) for 8 wk. Using a liver perfusion system, the effect of dietary long chain monoenoic fatty acids on the uptake and metabolism of [14-¹⁴C]erucic acid was studied. The perfusion times were 15 and 60 min, respectively. The two groups showed equal ability for erucic acid uptake in the liver but differed in the channeling of the fatty acids into various metabolic pathways. A higher metabolic turnover of 22∶1 in the PHMO livers relative to the PO livers was demonstrated by an increased recovery of total [¹⁴C]labeling in the triglyceride (TG) and phospholipid (PL) fractions, already evident after 15 min of perfusion. The chainshortening capacity was highest in the PHMO group, reflected by a higher [¹⁴C]18∶1 incorporation in both TG and PL, and increasing from 15 to 60 min of perfusion. The amount of [¹⁴C]18∶1 found in PL and TG after 60 min of perfusion of livers from rats fed PO corresponded to that shown for the PHMO group after 15 min. The PL demonstrated a discrimination against 22∶1 compared to TG, and, when available, 18∶1 was highly preferred for PL-synthesis. The total fatty acid distribution in the TG, as determined by gas liquid chromatography (GLC), reflected the composition of the dietary fats. In the total liver PL, 22∶1 and 20∶1 were present in negligible amounts, although the PHMO diet contained 12–13% of both 22∶1 and 20∶1. In the free fatty acid fraction (FFA), the major part of the radioactivity (≈80%) was [14-¹⁴C]erucic acid, and only small amounts of [¹⁴C]18∶1(<2%) were presents, even after 60 min of perfusion. The shortened-chain 18∶1 was readily removed from the FFA pool and preferentially used for lipid esterification.     

Severe fatty liver in rats fed a fat-free ethanol diet,and its prevention by small amounts of dietary arachidonate

Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16∶1/16∶0 and 18∶1/18∶0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet. Presented at the XII International Congress of Nutrition, San Diego, CA, August 1981. Abbreviations: Diets are indicated as fat-free with ethanol (AF), fat-free without ethanol (CF), or similar diets with 0.9% of the calories as arachidonic acid with (AA) or without (CA) ethanol. The composition of these diets is discribed in the text and Table 1.     

Diabetes-induced and age-related changes in fatty acid proportions of plasma lipids in rats

Diabetes-induced and age-related proportional changes in plasma fatty acids of triglycerides (TG), phospholipids (PL), and cholesteryl esters (CE) were investigated using streptozotocin-induced diabetic and control rats. Among n-6 fatty acids from diabetic rat plasma, increased proportions of 18∶2n-6 and 20∶3n-6 in all three lipid classes and of 18∶3n-6 in PL at 1–3 months old and in TG at 3–5 months old were observed. The proportions of 20∶4n-6 decreased in both PL and CE, but were unchanged in diabetic TG. Among the n-3 fatty acids, in the early stage, diabetes caused increases in the proportions of 18∶3n-3 in PL and CE and of 20∶5n-3 and 22∶6n-3 in TG, while 22∶5n-3 was decreased later in the disease course. These results suggest reduced Δ5-desaturase activities on 20∶3n-6 but not on 20∶4n-3, while Δ6-desaturase activity on 18∶2n-6 was essentially unaffected. Furthermore, the reduction in Δ9-desaturase activity in diabetic rats may well explain the decreases in the proportions of 16∶1n-7 and 18∶1n-7. However, the proportion of 18∶1n-9, another product of Δ9-desaturase, was significantly increased in CE and PL as compared to the controls. Thus, there was a discrepancy between our results and those of earlier studies with respect to the n-9, n-6, and n-3 fatty acid proportions of plasma lipids in diabetic rats. We also investigated age-related changes in the proportions of plasma fatty acids. Although rather small, age-related changes were evident in both diabetic and control rats.     

Major clofibrate effects on liver and plasma lipids are independent of changes in polyunsaturated fatty acid composition induced by dietary fat

The effects of clofibrate on the content and composition of liver and plasma lipids were studied in mice fed for 4 wk on diets enriched in n−6 or n−3 polyunsaturated fatty acids (PUFA) from sunflower oil (SO) or fish oil (FO), respectively; both oils were fed at 9% of the diet (dry weight basis). Only FO was hypolipidemic. Both oil regimes led to slightly increased concentrations of phospholipids (PL) and triacylglycerols (TG) in liver as compared with a standard chow diet containing 2% fat. Clofibrate promoted hypolipidemia only in animals fed SO. Its main effect was to enlarge the liver, such growth increasing the amounts of major glycerophospholipids while depleting the TG. SO and FO consumption changed the proportion of n−6 or n−3 PUFA in liver and plasma lipids in opposite ways. After clofibrate action, the PUFA of liver PL were preserved better than in the absence of oil supplementation. However, most of the drug-induced changes (e.g., increased 18∶1n−9 and 20∶3n−6, decreased 22∶6/20∶5 ratios) occurred inrrespective of lipids being rich in n−6 or n−3 PUFA. The concentration of sphingomyelin (SM), a minor liver lipid that virtually lacks PUFA, increased with the dietary oils, decreased with clofibrate, and changed its fatty acid composition in both situations. Thus. oil-increased SM had more 22∶0 and 24∶0 than clofibrate-decreased SM, which was significantly richer in 22∶1 and 24∶1.     

Comparison of the thin layer chromatography/flame ionization detection system with other methods for the quantitative analysis of liver lipid contents in alcohol-fed rats and controls

In this study, we have examined the feasibility of using the Thin Layer Chromatography/Flame Ionization Detection (TLC/FID) system to evaluate the lipid content of alcohol-induced fatty liver by comparing the results with those from other methods. Various amounts of standards (tripalmitin, phosphatidylcholine and cholesterol) were spotted on Chromarods and scanned either with or without development in a solvent system. The detector responses were significantly greater when the spots were not developed. From the results with developed rods, conversion factors (amount/area) were calculated. These were used for the quantitative analysis of the liver lipids from rats fed a Lieber-DeCarli ethanol diet or a control diet for four weeks. The triglyceride (TG), phospholipid (PL), cholesterol (CH) and cholesterol ester (CE) contents (65.9, 25.4, 2.9 and 6.8 mg/g, respectively) obtained by the TLC/FID system were similar to those observed by other methods (67.9, 27.6, 3.0 and 8.3 mg/g, respectively). The liver lipid content in control rats also was similar to that obtained by other methods (TG, 19.0 vs 20.6; PL, 24.2 vs 21.8, CH, 2.1 vs 2.1 and CE, 1.8 vs 2.6 mg/g). Thus, the magnitude of changes in liver lipid levels due to chronic alcohol ingestion obtained by alternate methods also was found with TLC/FID. The TLC/FID system provides a convenient method for rapid analysis of the extent of fatty liver in alcohol-fed animals.     

Prostaglandin synthesis and fatty acid composition of phospholipids and triglycerides in skeletal muscle of chicks fed combinations of flaxseed oil and animal tallow

Chicks were fed isocaloric and isonitrogenous diets containing 6% (w/w) added fat consisting of various proportions of animal tallow and flaxseed oil (FSO). No differences among treatments were seen in growth rate, muscular deposition of protein and lipids nor in the muscle phospholipid (PL) and triglyceride (TG) contents. Prostaglandin (PG)E₂ synthesis in isolated skeletal muscle was depressed significantly by feeding FSO or by treatment with naproxen (6-methoxy-α-methyl-2-napthaleneacetic acid), an inhibitor of PG synthesis. The changes associated with diet may be related to differences in the fatty acid composition of muscle lipids. Levels of saturated fatty acids in muscle PL and TG were relatively insensitive to dietary treatments. Monounsaturated fatty acid levels were significantly lower in the FSO-fed groups. FSO diets caused significant depression in muscle PL 20∶4ω6 and almost completely inhibited 22∶5ω6 incorporation. FSO diets decreased ratios of ω6/ω3 fatty acids and increased the unsaturation index of muscle PL. Muscles of chicks fed FSO showed increased levels of 18∶3ω3, and of its derivatives 20∶4ω3 and 22∶5ω3. These results suggest that FSO inhibits PG synthesis and modifies the fatty acids of PL and TG of chick muscle. These changes may have implications for PG-dependent and/or membrane-dependent processes in muscle metabolism.     

A relationship between essential fatty acid and vitamin E deficiency

To test whether vitamin E deficiency might influence the course of essential fatty acid (EFA) deficiency, Long Evans rats were fed diets containing a marginal amount (1.5% of calories) of 18∶2ω6 or 18∶3ω3 fatty acid with complete absence of the other and with or without vitamin E. Vitamin E contents decreased continuously in serum and liver in all rats fed the E-free diets but in the brains of only the rats fed the marginal 18∶3ω3, E-free diet. It is considered that the vitamin E is cooxidized in the liver with 22∶6ω3, since this fatty acid is very low in livers of the rats fed the marginal 18∶2ω6 diet but much higher in livers of the rats fed the marginal 18∶3ω3 diet. Brain 22∶6ω3 values are comparable for both groups. The source of 22∶6ω3 is evidently in the mother's milk, since following weaning there is a precipitous drop in 22∶6ω3 in serum, liver and carcass of rats on the 18∶2ω6-containing diet. No significant signs of EFA deficiency were seen in the E-deficient rats. Operated for the U.S. Department of Energy by the University of California under contract no. DE-AC03-76-SF00012.     

Relationship between mouse liver Δ9 desaturase activity and plasma lipids

This study was undertaken to investigate the total plasma fatty acid composition and the relationship between plasma triacylglycerol (TG) levels and liver Δ9 desaturase activity in mice fed n−3 and/or n−6 fatty acid or hydrogenated coconut oil (HCO) (maximum 25 mg/g) supplemented diets. Generally, plasma TG levels and Δ9 desaturase activity were inversely correlated with the ratio of the sum of long chain n−3 fatty acids to 18∶2n−6 and to the ratio of the sum of long chain n−3 fatty acids to 18∶n−3, but they were positively correlated with the ratio of products and substrates (18∶1/18∶0) of the enzyme in plasma total lipids. The n−3 fatty acid (mainly 20∶5n−3) enriched diet, when compared to the HCO diet at 21 d, caused a significant reduction in plasma TG levels but not in Δ9 desaturase activity. However, a marked reduction in plasma TG content (50–60%) and Δ9 desaturase activity (55–70%) was observed when both 20∶5n−3 and 18∶3n−6 were supplemented in the diet. The plasma TG levels and Δ9 desaturase activity rose again when the animals were fed the HCO diet or chow. The results suggest that low dose supplementation of a mixture of n−3 (mainly 20∶5n−3) and n−6 (18∶3n−6) fatty acids modified both plasma TG content and liver Δ9 desaturase activity, in parallel.     

Effect of marine oil and rapessee oil on composition of fatty acids in lipoprotein triacylglycerols from rat blood plasma and liver perfusate

The fatty acid patterns of triacylglycerols (TG) from very low density lipoprotein (VLDL) in blood plasma and liver-perfusate from rats fed partially hydrogenated marine oil or rapeseed oil were determined. In the plasma from rats fed rapeseed oil for three days and three weeks, there was a small but significant decrease in the percentage of 22∶1 fatty acid from 17.2 to 11.2% with length of feeding. In liver-perfusate, the comparable decrease with dietary rapeseed oil was from 18.5 to 5.2%, and with dietary marine oil from 13.4 to 8.0%. In contrast to the liver-perfusate, the remaining liver had only a very low 22∶1 composition (ca 2%) independent of feeding period or diet. The results indicated that the liver exported the very long chain fatty acids and that an adaptation took place after three days feeding with rapeseed oil or marine oil. This adaptation in the liver could possibly explain why TG accumulation in hearts, which appears after three days' feeding with rapeseed oil or marine oil, disappears after an extended feeding period.     

Specific inhibition of hepatic fatty acid synthesis exerted by dietary linoleate and linolenate in essential fatty acid adequate rats

Dietary linoleate and linolenate were investigated for their ability to specifically inhibit liver and adipose tissue lipogenesis in meal-fed (access to food 900-1,200 hr), essential fatty acid (EFA) adequate rats. Supplementing a high carbohydrate diet containing 2.5% safflower oil with 3% palmitate 16∶0, oleate 18∶1, or linoleate 18∶2 did not affect in vivo liver or adipose tissue fatty acid synthesis. However, 18∶2 addition to the basal diet did result in a significant (P<0.05) decline of liver fatty acid synthetase (FAS) and glucose-6-phosphate dehydrogenase (G6PD) activities. When the safflower oil content of the basal diet was reduced to 1%, the addition of 3% 18∶2 or linolenate 18∶3 significantly (P<0.05) depressed hepatic FAS, G6PD, and in vivo fatty acid synthesis by 50%. Addition of 18∶1 caused no depression in hepatic FAS activity but did result in a significant (P<0.05) decline in liver G6PD activity and fatty acid synthesis which was intermediate between basal and basal +18∶2-or+18∶3-fed animals. Adipose tissue rates of lipogenesis were completely unaffected by dietary fatty acid supplementation. Similarly, the addition of 3 or 5% 18∶3 to a basal diet for only one meal resulted in no change in lipogenesis relative to that in animals fed the basal diet. The data indicate that, like rats fed EFA-deficient diets, dietary 18∶2 and 18∶3 exert a specific capacity to depress rat liver FAS and G6PD activities and rate of fatty acid synthesis. Michigan Agricultural Experiment station Journal Article No. 7581. D.R. Romsos is the recipient of Career Development Award K04 AM 00112     

Reduction of essential fatty acid deficiency in rats fed a low iron fat free diet

Young male rats were fed ad libitum for 8 weeks a low iron fat-free (FF-Fe) diet or a fat-free diet supplemented with iron (FF+Fe). The relative levels of 16∶1 to 16∶0 and 18∶1 to 18∶0 in the total fatty acids of liver and other tissues (plasma, erythrocytes and intestinal mucosa) were considerably decreased because of a lack of dietary iron. In rats fed the FF-Fe diet, the levels of essential fatty acids (18∶2ω6+20∶4ω6) in tissues were 2-to 3-fold greater than in the corresponding tissues of rats fed the FF+Fe diet. Eicosatrienoic acid (20∶3ω9) levels in tissue lipids from rats fed the FF+Fe diet were high (8–16%), whereas they were low (2–5%) in the case of animals fed the FF-Fe diet. The proportion of 20∶4 in total fatty acids of tissues was 2-to 3-fold greater in rats fed the FF-Fe diet than when they were fed the FF+Fe diet. Therefore, the relative levels of 20∶3ω9/20∶4ω6 varied from 1-2.9 in tissue lipids of rats fed the FF+Fe diet, while it varied only from 0.2–0.3 in animals fed the FF-Fe diet. These results suggest that a lack of dietary iron may reduce the synthesis of 16∶1, 18∶1, 20∶3 and 20∶4 and the metabolism of 20∶4.     

Dietary cod liver oil decreases arachidonic acid in rat gastric mucosa and increases stress-induced gastric erosions

The purpose of this study was to examine the influence of long-term feeding of dietary fat rich in either n−3 or n−6 fatty acids on the availability of arachidonic acid (20∶4n−6) in major phospholipids of gastric mucosa in rats. Three groups of male Wistar rats were fed either a standard diet, a cod liver oil-enriched diet (10% by weight), or a corn oil-enriched diet (10% by weight) for 8 mon. Dietary cod liver oil significantly reduced the level of 20∶4n−6 in phosphatidylcholine (PC) and in phosphatidylethanolamine (PE) of gastric mucosa. The loss of 20∶4n−6 was compensated for by eicosapentaenoic acid (20∶5n−3) in PC, whereas the decrease in 20∶4n−6 in PE corresponded to the increase in three n−3 fatty acids: 20∶5n−3, docosapentaenoic acid (22∶5n−3), and docosahexaenoic acid (22∶6n−3). The level of 20∶5n−3 was higher than the level of 22∶6n−3 both in PC and PE of mucosa in rats fed cod liver oil. Diets supplemented with corn oil increased the level of 18∶2n−6 but decreased the monoene fatty acids 16∶1 and 18∶1n−7 in PC but not in PE of gastric mucosa. The 20∶4n−6 levels of both PC and PE were markedly reduced by dietary cod liver oil, to about one-third of control levels. Similar changes were also observed in the stomach wall. Gastric erosions were observed in all rats exposed to restriction stress, but this form of stress induced twice the number of erosions in rats fed fish oil compared to control rats or rats fed corn oil. We conclude that a diet rich in fish oil altered the balance between n−6 and n−3 fatty acids in major gastric mucosal phospholipids, markedly reduced the availability of 20∶4n−6, and increased the incidence of gastric erosions induced by restriction or emotional stress.     

Effects of dietary triolein and sunflower oil on insulin release and lipid metabolism in zucker rats

Obese and lean male Zucker rats were fed ad libitum on diets containing either 50 (L) or 200 (H) g/kg diet of either triolein (T) or sunflowerseed oil (S). The specific activity of the hepatic microsomal Δ9 desaturase enzyme was depressed in both lean and obese rats fed the HS diet compared with the other three diets. The fatty acid composition of liver and subcutaneous white adipose tissue lipids were consistent with a lower Δ9 desaturation activity in rats fed the H diets, particularly for the HS diet. In both genotypes, microsomal Δ9 desaturase activity and the ratio of 16∶1/(16∶0+16∶1) fatty acids in liver lipids were inversely related to the proportion of 18∶2 in liver lipid. Plasma insulin concentrations and rates of glucose-stimulated insulin release in vivo were higher in obese rats compared with lean rats, and plasma insulin levels were higher in rats fed S compared with T. There was no relationship between Δ9 desaturase activity and either plasma insulin concentration or rates of insulin release in vitro. These findings suggest that hepatic Δ9 desaturase activity of Zucker rats is responsive to changes in the proportion of 18∶2 in liver lipids but is not affected by changes in insulin secretion.     

Effect of dietary lipids on the lipid composition and phospholipid deacylating enzyme activities of rat heart

Rats were fed lard-enriched (17%) or corn oil-enriched (17%) diets and were compared with rats fed a low fat (4.5%) diet. Cardiac protein, DNA, phospholipid (PL) and fatty acid (FA) compositions were analyzed. Neutral phospholipase A, lysophospholipase and creatine kinase activities in the membrane and cytosolic compartments were also investigated. No significant modification of cardiac protein, DNA nor PL was observed among the three groups. Some alterations appeared in the FA composition. A lard-enriched diet induced a significant increase of 22∶5n−3 and 22∶6n−3 in heart phosphatidylcholine (PC) and phosphatidylethanolamine (PE), whereas a linoleic acid-rich diet induced a specific increase of 22∶4n−6 and 22∶5n−6 in these two major PL. Compared to rats fed the low fat diet, membrane-associated phospholipase A activity, measured by endogenous hydrolysis of membrane PC and PE, showed a significant increase (+45%) for both PL in rats fed corn oil. However, the activity of membrane-associated phospholipases, measured with exogenous [1-¹⁴C]dioleoyl PC, was not different among the three groups of rats. Cytoplasmic activity was decreased in rats fed corn oil, and lysophospholipase and creatine phosphate kinase activities were not significantly affected by diet. FA modification of the long chain n−6 FA induced by corn oil may be responsible for the observed increase in phospholipase activity. Physiological implications are suggested in terms of membrane degradation and prostaglandin production. Presented in part at the International Symposium on Lipid Metabolism in the Normoxic and Ischemic Heart, Rotterdam, The Netherlands, September 1986.     

Metabolism of erucic acid in perfused rat liver: Increased chain shortening after feeding partially hydrogenated marine oil and rapeseed oil

The metabolism of [14-¹⁴C] erucic acid was studied in perfused livers from rats fed on diets containing partially hydrogenated marine oil or rapeseed oil for three days or three weeks. Control rats were given groundnut oil. Chain-shortening of erucic acid, mainly to 18∶1, was found in all dietary groups. In the marine oil and rapeseed oil groups, the percentage of chain-shortened fatty acids in very low density lipoproteins-triacylglycerols (VLDL-TG) exported from the liver increased after prolonged feeding. A similar increase was found in liver TG only with partially hydrogenated marine oil. This oil, rich intrans fatty acids, thus seemed to be more effective in promoting chain-shortening. The fatty acid composition of the secreted and stored TG differed both with respect to total fatty acids and radioactively labeled fatty acids, indicating that at least 2 different pools of TG exist in the liver. The lack of lipidosis in livers from rats fed dietary oils rich in 22∶1 fatty acids is discussed in relation to these findings. In conclusion, a discussion is presented expressing the view that the reversal of the acute lipidosis in the hearts of rats fed rapeseed oil or partially hydrogenated marine oils is, to a large extent, derived from the increased chain-shortening capacity of erucic acid in liver.