Dietary fats and energy levels differently affect tissue lipogenic enzyme activity in finishing pigs

The aim of the present study was to determine the relationship between high and low digestible energy levels (9.5 vs. 15.4 MJ ME/kg) and either tallow or soy oil supplementation (5%rpar; on lipogenic activities and fatty acid profile of the backfat tissue outer layer and liver tissue in finishing pigs. Twenty Large White pigs averaging 30 (initial) to 106 kg (final) live weight were allocated into four dietary groups and fed the diets ad libitum. The lipid content and fatty acid composition of the tissues were determined and glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme (ME), and fatty acid synthase (FAS) activity were measured. Growth performance and carcass measurements were affected by the dietary energy levels but not by the fat sources. Lipid deposition rate of animals fed the low energy diets was lowered regardless whether tallow or soy oil was supplemented. Unlike lipid deposition, fatty acid profile was influenced by both dietary factors. Pigs fed the low energy diet supplemented with soy oil exhibited the lowest level of saturated (P<0.001), monounsaturated (P<0.001), and the highest level of polyenic fatty acids in the backfat, the opposite was the case for the pigs fed the high energy diet supplemented with beef tallow. The fatty acid profile of the adipose tissue of animals fed the other two diets were intermediate, but clear distinction of the profile due to diets was visible. Independent of dietary treatments, lipogenic activities were up to 10 times higher in the backfat than in the liver. G6PDH activity was higher (P<0.05) due to high energy diet, whereas the activities of ME and FAS were not affected. Animals fed the high energy diet either supplemented with tallow or soy oil exhibited higher ME activity lpar;P<0.05) in the backfat, without any effects on G6PDH activity. In contrast, dietary fat sources affected the FAS activity, with lower activity lpar;P<0.05) exhibited in the backfat of animals fed the soy oil diets. The present results indicate that dietary manipulation, which change the flux through the pathway of lipogenesis and pentose-phosphate must affect differently the activities of the involved enzymes. The effect of the dietary energy level was stronger and overwhelmed the inducing effect of the PUFA on the activities of the collateral enzymes. In contrast the immediately involved lipogenic enzyme FAS responded more to dietary PUFA stimulation than to the energy supply.     

Oryzanol decreases cholesterol absorption and aortic fatty streaks in hamsters

Oryzanol is a class of nonsaponifiable lipids of rice bran oil (RBO). More specifically, oryzanol is a group of ferulic acid esters of triterpene alcohol and plant sterols. In experiment 1, the mechanisms of the cholesterol-lowering action of oryzanol were investigated in 32 hamsters made hypercholesterolemic by feeding chow-based diets containing 5% coconut oil and 0.1% cholesterol with or without 1% oryzanol for 7 wk. Relative to the control animals, oryzanol treatment resulted in a significant reduction in plasma total cholesterol (TC) (28%, P<0.01) and the sum of IDL-C, LDL-C, and VLDL-C (NON-HDL-C) (34%, P<0.01). In addition, the oryzanol-treated animals also exhibited a 25% reduction in percent cholesterol absorption vs. control animals. Endogenous cholesterol synthesis, as measured by the liver and intestinal HMG-CoA reductase activities, showed no difference between the two groups. To determine whether a lower dose of oryzanol was also efficacious and to measure aortic fatty streaks, 19 hamsters in experiment 2 were divided into two groups and fed for 10 wk chow-based diets containing 0.05% cholesterol and 10% coconut oil (w/w) (control) and the control diet plus 0.5% oryzanol (oryzanol). Relative to the control, oryzanol-treated hamsters had reduced plasma TC (44%, P<0.001), NON-HDL-C (57%, P<0.01), and triglyceride (TG) (46%, P<0.05) concentrations. Despite a 12% decrease in high density lipoprotein cholesterol (HDL-C) (P<0.01), the oryzanol-treated animals maintained a more optimum NON-HDL-C/HDL-C profile (1.1±0.4) than the contorl (2.5±1.4; P<0.0075). Aortic fatty streak formation, so defined by the degree of accumulation of Oil Red O-stained macrophage-derived foam cells, was reduced 67% (P<0.01) in the oryzanol-treated animals. From these studies, it is concluded that a constituent of the nonsaponifiable lipids of RBO, oryzanol, is at least partially responsible for the cholesterol-lowering action of RBO. In addition, the cholesterol-lowering action of oryzanol was associated with significant reductions in aortic fatty streak formation.     

Modulation of renal injury in pcy mice by dietary fat containing n−3 fatty acids depends on the level and type of fat

Low-fat diets and diets containing n−3 fatty acids (FA) slow the progression of renal injury in the male Han:Sprague-Dawley (SPRD)-cy rat model of polycystic kidney disease. To determine whether these dietary fat effects are similar in females and in another model of renal cystic disease, in this study we used both male and female pcy mice to examine the effects of fat level and type on disease progression. Adult pcy mice were fed 4, 10, or 20 g soybean oil/100 g diet for 130 d in study 1. In study 2, weanling pcy mice were fed high or low levels of fat rich in 18∶2n−6 (corn oil, CO) 18∶3n−3 (flaxseed oil/CO 4∶1 g/g, FO), or 22∶6n−3 (algal oil/CO 4∶1 g/g, DO) for 8 wk. In adult pcy mice, low-compared with high-fat diets lowered kidney weights (2.4±0.2 vs. 3.1±0.2 g/100 g body weight, P=0.006) and serum urea nitrogen (SUN) (9.6±0.6 vs. 11.9±0.6 mmol/L, P=0.009), whereas in young pcy mice it reduced renal fibrosis volumes (0.44±0.04 vs. 0.62±0.04 mL/kg body weight, P<0.0001). FO feeding in young pcy mice mitigated the detrimental effects of high fat on fibrosis while not altering kidney size, function, and oxidative damage when compared with the CO-fed mice. In contrast, DO-compared with CO-fed mice had higher kidney weights (2.64±0.07 vs. 2.24±0.08 g/100 g body weight, P=0.005), SUN (9.4±0.57 vs. 7.0±0.62 nmol/L, P<0.0001), and cyst volumes (7.9±0.28 vs. 6.2±0.30 mL/kg body weight, P<0.0001) and similar levels of oxidative damage and fibrosis. The FA compositions of the diets were reflected in the kidneys: 18∶2n−6, 18∶3n−3, and 22∶6n−3 were the highest in the CO, FO, and DO diets, respectively. Dietary effects on kidney disease progression were similar in males and females. A low-fat diet slows progression of renal injury in male and female pcy mice, consistent with findings in the male Han:SPRD-cy rat. Dietary fat type also influenced renal injury, with flaxseed oil diets rich in 18∶3n−3 slowing early fibrosis progression compared with diets rich in 18∶2n−6 or in 22∶6n−3.     

Docosahexaenoic acid does not affect aggression of normal volunteers under nonstressful conditions. A randomized, placebo-controlled, double-blind study

We previously found that docosahexaenoic acid (DHA) intake prevents aggression enhancement at times of mental stress. In the present study we investigated changes in aggression under nonstressful conditions. Forty-six students of two universities took either DHA-rich fish oil capsules containing 1.5 g DHA (DHA group: 13 males and 9 females) or control oil capsules containing 97% soybean oil plus 3% of another fish oil (control group: 11 males and 13 females) for 3 mon in a double-blind fashion. At the start and end of the study they took an aggression-estimating test (P-F Study) without a stressor component. DHA (5.9 to 8.5%, P<0.001) and eicosapentaenoic acid (0.7 to 1.5%, P<0.001) increased in red blood cell phospholipids in the DHA group, while linoleic acid increased slightly (8.3 to 9.1%, P<0.002) in the soybean oil control group. In the control group, measured aggression levels decreased from 34.8 to 29.4% (P<0.005), whereas they remained stable in the DHA group (33.5 to 33.8%). The intergroup differences (−5.4 vs. 0.3%) were marginally significant (P≤0.05). Aggression levels were stable in the DHA group whether there was stressor (as previously shown) or not. This effect of DHA appears to be interesting, considering the reported association between a low intake of n-3 fatty acids and depression.     

Replacement of dietary fish oil with increasing levels of linseed oil: Modification of flesh fatty acid compositions in Atlantic salmon (<Emphasis Type="Italic">Salmo salar</Emphasis>) using a fish oil finishing diet

Five groups of salmon, of initial mean weight 127±3 g, were fed increasing levels of dietary linseed oil (LO) in a regression design. The control diet contained capelin oil (FO) only, and the same oil was blended with LO to provide the experimental diets. After an initial period of 40 wk, all groups were switched to a finishing diet containing only FO for a further 24 wk. Growth and flesh lipid contents were not affected by dietary treatment. The FA compositions of flesh total lipids were linearly correlated with dietary FA compositions (r ²=0.88–1.00, P<0.0001). LO included at 50% of added dietary lipids reduced flesh DHA and EPA (20∶5n−3) concentrations to 65 and 58%, respectively, of the concentrations in fish fed FO. Feeding 100% LO reduced flesh DHA and EPA concentrations to 38 and 30%, respectively, of the values in fish fed FO. Differences between diet and flesh FA concentrations showed that 16∶0, 18∶1n−9, and especially DHA were preferentially retained in flesh, whereas 18∶2n−6, 18∶3n−3, and 22∶1n−11 were selected against and presumably utilized for energy. In fish previously fed 50 and 100% LO, feeding a finishing diet containing FO for 16 wk restored flesh DHA and EPA concentrations, to ≈80% of the values in fish fed FO throughout. Flesh DHA and EPA concentrations in fish fed up to 50% LO were above recommended intake values for humans for these EFA. This study suggests that LO can be used as a substitute for FO in seawater salmon feeds and that any reductions in DHA and EPA can be largely overcome with a finishing diethigh in FO before harvest.     

Effect of dietary fish oil on blood levels of free fatty acids,ketone bodies and triacylglycerol in humans

Although the reduction of serum triacylglycerol concentrations by dietary fish oil is a well-known effect, the exact mechanism of this effect has not been previously studied in human subjects. Therefore, the aim of this study was (i) to examine the effect of short-term fish oil supplementation on blood concentrations of ketone bodies, free fatty acids and triacylglycerol in healthy humans and (ii) to verify whether the observed relationships between these variables would be consistent with reduced lipolysis and/or enhanced hepatic fatty acid oxidation after fish oil supplementation. Twenty subjects (21–23 years, normal liver function tests) were randomly divided into two groups to supplement their usual diet with either 30 g/d of fish oil (n=11) or olive oil (n=9). Venous blood samples were drawn after an overnight fast, before and after 1, 3 and 7 d of fish oil/olive oil supplementation. Blood concentrations of triacylglycerol and free fatty acids decreased consistently after fish oil supplementation; the reduction was already significant after one day of fish oil (P<0.001 for triacylglycerol andP=0.01 for free fatty acids). In contrast, neither of these blood values changed after olive oil supplementation (P>0.10). No significant changes in glucose, insulin or ketone body levels were observed in either group after supplementation. After fish oil, but not after olive oil supplementation, the ratio of blood ketone body levels to free fatty acid levels increased significantly (P<0.05). Furthermore, after fish oil supplementation only, free fatty acid levels were significantly correlated with levels of ketone bodies (day 7 of supplementation: r=0.90,P<0.001) and triacylglycerol (maximum value on day 3: r=0.77,P<0.01). These findings suggest that reduced lipolysis and increased hepatic β-oxidation/ketogenesis may contribute to reduced triacylglycerol levels after ω3 fatty acid supplementation in humans. Turnover studies are needed in order to further quantitate these processes.     

Regulation of very low density lipoprotein apo B metabolism by dietary fat saturation and chain length in the guinea pig

Studies investigated the effects of dietary fatty acid composition and saturation on the regulation of very low density lipoprotein (VLDL) apo B flux, clearance, and conversion to low density lipoprotein (LDL) in guinea pigs fed semipurified diets containing 15% (w/w) corn oil (CO), lard (LA), or palm kernel oil (PK). Plasma cholesterol levels were highest with dietary PK (3.1±1.0 mmol/L) followed by LA (2.4±0.4 mmol/L) and CO (1.6±0.4 mmol/L) intake. VLDL particles were larger (P<0.05) in the LA (78±7 nm) and PK (69±10 nm) groups compared to animals fed CO (49±5 nm). VLDL-apo B fractional catabolic rates (FCR) were highest in guinea pigs fed the LA diet (P<0.05) and VLDL apo B flux, estimated from VLDL ¹²⁵I-apo B turnover kinetics, were higher in LA compared to PK or CO fed guinea pigs. In the case of PK consumption, the kinetic estimates of VLDL apo B flux significantly underestimated rates compared to direct VLDL apo B secretion measurements and LDL turnover analyses. These data demonstrate that differences in the composition and amount of saturated fatty acids have differential effects on VLDL apo B flux, catabolism, and conversion to LDL which, together with changes in LDL receptor-mediated catabolism, determine plasma LDL cholesterol levels in guinea pigs. The data also indicate that kinetic analysis of VLDL metabolism in PK fed animals is inaccurate possibly due to the presence of a small, nonequilibrating pool of newly synthesized VLDL which is rapidly converted to LDL.     

Gender and dietary fat affect α-tocopherol status in F344/N rats

For four weeks, groups of eight male and eight female F344/N rats were fed diets containing 15.5, 20, 30 or 40% of energy (en%) as fat. The fat was composed of corn oil and beef tallow with 9 en% from linoleate in all diets. Females had greater mean hepatic α-tocopherol levels, whereas males had greater plasma α-tocopherol and cholesterol concentrations. In males, the plasma ratio of α-tocopherol/cholesterol was significantly greater than in females (P<0.05). Plasma α-tocopherol increased with increasing en% fat (r=0.51,P<0.001) in both sexes, but dietary fat did not alter hepatic α-tocopherol levels. These results suggest that plasma α-tocopherol may serve as a biomarker of total dietary fat intake and that in F344/N rats gender differences affect α-tocopherol and cholesterol status.     

γ-tocotrienol as a hypocholesterolemic and antioxidant agent in rats fed atherogenic diets

This study was designed to determine whether incorporation of γ-tocotrienol or α-tocopherol in an atherogenic diet would reduce the concentration of plasma cholesterol, triglycerides and fatty acid peroxides, and attenuate platelet aggregability in rats. For six weeks, male Wistar rats (n=90) were fed AIN76A semisynthetic test diets containing cholesterol (2% by weight), providing fat as partially hydrogenated soybean oil (20% by weight), menhaden oil (20%) or corn oil (2%). Feeding the ration with menhaden oil resulted in the highest concentrations of plasma cholesterol, low and very low density lipoprotein cholesterol, triglycerides, thiobarbituric acid reactive substances and fatty acid hydroperoxides. Consumption of the ration containing γ-tocotrienol (50 μ/kg) and α-tocopherol (500 mg/kg) for six weeks led to decreased plasma lipid concentrations. Plasma cholesterol, low and very low density lipoprotein cholesterol, and triglycerides each decreased significantly (P<0.001). Plasma thiobarbituric acid reactive substances decreased significantly (P<0.01), as did the fatty acid hydroperoxides (P<0.05), when the diet contained both chromanols. Supplementation with γ-tocotrienol resulted in similar, though quantitatively smaller, decrements in these plasma values. Plasma α-tocopherol concentrations were lowest in rats fed menhaden oil without either chromanol. Though plasma α-tocopherol did not rise with γ-tocotrienol supplementation at 50 mg/kg, γ-tocotrienol at 100 mg/kg of ration spared plasma α-tocopherol, which rose from 0.60±0.2 to 1.34±0.4 mg/dL (P<0.05). The highest concentration of α-tocopherol was measured in plasma of animals fed a ration supplemented with α-tocopherol at 500 mg/kg. In response to added collagen, the partially hydrogenated soybean oil diet without supplementary cholesterol led to reduced platelet aggregation as compared with the cholesterol-supplemented diet. However, γ-tocotrienol at a level of 50 mg/kg in the cholesterol-supplemented diet did not significantly reduce platelet aggregation. Platelets from animals fed the menhaden oil diet released less adenosine triphosphate than the ones from any other diet group. The data suggest that the combination of γ-tocotrienol and α-tocopherol, as present in palm oil distillates, deserves further evaluation as a potential hypolipemic agent in hyperlipemic humans at atherogenic risk.     

Dietary n‐3 fatty acids reduce the delayed hypersensitivity reaction and antibody production more than n‐6 fatty acids in broiler birds

The splenocyte fatty acid profile and immune response of broiler chickens were investigated. One hundred and twenty day‐old broiler chicks were fed diets containing conjugated linoleic acid (CLA) (Diet I), sunflower oil (Diet II), flaxseed oil (Diet III) or fish oil (Diet IV). The total lipid content of the diets was 3.5%. Body weight and feed intake was higher (P <0.05) in Diet IV compared to Diets I, II and III. Birds fed Diet III and IV had a higher content of n‐3 fatty acids in splenocytes than those fed Diets I and II. Serum anti‐BSA immunoglobulin content was higher (P <0.05) in birds fed Diets III and IV, compared to those fed Diets I and II. Delayed type hypersensitivity response, measured as the wing web skin swelling reaction (thickness) to Mycobacterium butyricum injection (s.c.), increased (P <0.05) from 0.71 and 0.98 mm in Diets IV and III, respectively, to 1.19 and 1.41 mm in Diets I and II, respectively. The number of CD4⁺ and CD8⁺ blood lymphocytes and CD4⁺, CD8⁺ and IgM⁺ splenocytes did not differ (P >0.05) between treatment groups. N‐3 fatty acids increased production performances and antibody mediated responses, while n‐6 fatty acids and conjugated linoleic acid increased cell mediated responses in broiler birds.     

Fasting and postprandial lipid response to the consumption of modified milk fats by guinea pigs

The objective of the present study was to investigate the effect of three modified milk fats with different melting profiles on fasting and postprandial lipid responses and on fecal fat content in guinea pigs. We hypothesized that the consumption of modified milk fat with a high m.p. results in reduced fasting and postprandial lipid responses compared with that of modified milk fat fractions with lower m.p. To test this hypothesis, male Hartley guinea pigs were fed isoenergetic diets containing 110 g of fat/kg, either from one of the three modified milk fats with high (HMF), medium (MMF), or low melting profiles (LMF), or from one of the two reference fats as whole mil fat (MF) or a fat blend similar to that of nonhydrogenated soft margarine (MA) for 28 d. Food intake (P<0.05) and body weight gain (P<0.05) were reduced in the animals fed the HMF diet compared with the other groups. In the fasting state, plasma LDL cholesterol was highest in animals fed the LMF diet, intermediary in those fed the MMF and MF diets, and lowest in those fed the HMF and MA diets (P<0.05). Postprandially, the areas under the 0- to 3-h curves for the changes in plasma TG were lower in the HMF group than in the MA- and LMF-fed guinea pigs (P<0.05). The fecal fat content was higher (P<0.05) in the HMF group compared to the other milk fat groups. The present results suggest that modified milk fats can impact food intake, body weight gain, fasting cholesterolemia, and postprandial triglyceridemia, and these changes may be attributed to an altered fat absorption.     

The urinary excretion of thiobarbituric acid reactive substances and malondialdehyde by normal adult males after consuming a diet containing salmon

In this study we investigated the output of thiobarbituric acid reactive substances (TBARS) and malondialdehyde (MDA), as thiobarbituric acid (TBA)-MDA adduct, in the urine from subjects eating a diet in which the only source of n−3 long-chain, polyunsaturated fatty acids was fresh salmon. Nine healthy men, ages 30–65, were confined in the United States Department of Agriculture Western Human Nutrition Research Center, San Francisco, CA, for 100 d; food intake and exercise levels were controlled. All subjects were placed on a stabilization diet (StD) for 20 d, then six were fed the salmon diet for 40 d. The others remained on the StD. The groups switched diets for the last 40 d. Both diets were isocaloric (16% protein, 54% CHO and 30% fat by energy %). The salmon diet contained 7.5% of calories from n−6 fatty acids (FAs) and 2% from n−3 FAs, primarily eicosapentaenoic acid and docosahexaenoic acid in a 50∶60 ratio, while the StD contained 7.5% from n−6 FAs and <0.3% n−3 FAs (with presumably no significant amounts of C₂₀ or C₂₂ n−3 FAs). Twenty-four hour urinary output was collected, and 2% 3−d pool samples prepared for analysis of urinary TBARS and the TBA-MDA adduct. The total urinary output of each individual varied considerably, and on a daily basis the concentration of autoxidation products in an individual's urine varied also. However, the mean daily output (in μmoles TBA-MDA equivalents/day) at the end of the salmon diet feeding period was significantly greater (7.05±1.33 TBARS,P<0.05; and 7.07±1.73 TBA-MDA adduct,P<0.01) compared to when the subjects were eating the StD (5.65±1.09 TBARS and 4.65±0.76 TBA-MDA adduct). When the TBARS and TBA-MDA adduct values were normalized relative to creatinine output (in nmoles TBA-MDA equivalents/μmole creatinine), the data achieved even greater statistical significance. The mean output of the group eating the salmon diet was 0.478±0.076 for TBARS (P<0.01) and 0.476±0.082 for the TBA-MDA adduct (P<0.001)vs. 0.345±0.059 for TBARS and 0.283±0.041 for the TBA-MDA adduct when the subjects were consuming the StD. Thus, the consumption of cooked fish may increase one's exposure to MDA and other autoxidation products, compounds that may be carcinogenic or mutagenic.     

Blood pressure,serum lipids,and fatty acids in populations on a lake-fish diet or on a vegetarian diet in Tanzania

Major risk factors for coronary heart disease were assessed in two populations of Tanzania, one on a fish diet (FD) living along the coast of Lake Nyasa, and the other, mainly on a vegetarian diet (VD), living in a farming area. Lower blood pressure values were found in the FD subjects (n=618) vs. VD (n=618) (systolic blood pressure, SBP, 120±15 vs. 135±20,P<0.01; diastolic blood pressure, DBP, 70±9 vs. 78±11,P<0.01, respectively). In an FD subgroup (n=61), total cholesterol (TC) (122 vs. 136 mg/dL,P<0.01); triglycerides (TG) (82 vs. 105 mg/dL,P<0.01); and lipoprotein (a) [Lp(a)] (19.9±18.4 vs. 32.3±22.4,P<0.001) were lower than in a VD subgroup (n=55). Serum fatty acids (FA) in the FD subgroup were as follows: eicosapentaenoic acid (EPA) (20∶5) 2.48 vs. 0.72%, docosahexaenoic acid (DHA) (22∶6) 5.93 vs. 1.49%, vs. the VD, respectively. Arachidonic acid (AA) (20∶4n-6) also was higher in the FD vs. the VD group (9.85 vs. 8.30%,P<0.05), whereas 18∶2n-6 was about double (23.97 and 14.85%) in VD vs. FD. The peculiar serum FA pattern in FD reflected the FA of dietary fish. In fact, in four main species of lake fish, DHA was 8–19%, higher than EPA (1.8–4.2%), in contrast with the situation in cold-water fish, and AA was 5.8–8%, higher than in cold-water fish. The data, obtained in populations strictly on natural, unprocessed, low-fat diets, show that a diet based on freshwater fish results in lower BP, serum TC, TG, and Lp(a), and suggests that serum AA is not reduced when the major dietary n-3 is DHA rather than EPA.     

Fish oil supplementation of lactating mothers affects cytokine production in 2 1/2-year-old children

n−3 PUFA influence immune functioning and may affect the cytokine phenotype during development. To examine whether maternal fish oil supplementation during lactation could modify later immune responses in children, 122 lactating Danish mothers with a fish intake below the population median were randomized to groups supplemented for the first 4 mon of lactation with 4.5 g/d of fish oil (equivalent to 1.5 g/d of n−3 long-chain PUFA) or olive oil. Fifty-three mothers with a fish intake in the highest quartile of the population were also included. The FA composition of erythrocyte membranes was measured at 4 mon and at 2 1/2 yr. Plasma immunoglobulin E (IgE) levels and cytokine production in lipopolysaccharide-stimulated whole-blood cultures were determined at 2 1/2 yr. Erythrocyte n−3 PUFA at 4 mon were higher in infants from the fish oil group compared with the olive oil group (P<0.001) but were no longer different at 2 1/2 yr. The median production of lipopolysaccharide-induced interferon γ(IFN-γ) in the fish oil group was fourfold higher than that in the olive oil group (P=0.034), whereas interleukin-10 (IL-10) production was similar. The IFN-γ/IL-10 ratio was twofold higher in the fish oil group (P=0.019) and was positively correlated with 20∶5n−3/20∶4n−6 in erythrocytes at 4 mon (P=0.050). The percentages of atopic children and plasma IgE were not different in the two groups, but the study was not designed to look at atopy. Cytokine responses and erythrocyte FA composition in children of mothers with a high fish intake were intermediate in comparison with those in the randomized groups. Fish oil supplementation during lactation resulted in increased in vitro IFN-γ production in the children 2 yr after the supplementation was given, which may reflect a faster maturation of the immune system.     

Evidence that leptin contributes to intestinal cholesterol absorption in obese (ob/ob) mice and wild-type mice

In the present study, the effect of leptin on intestinal cholesterol absorption was investigated in C57 BL/6 OlaHsd Lep^ob/Lep^ob obese (ob/ob) mice and lean C57 BL/6 (wild-type) mice. Animals were treated either with or without recombinant leptin for 2 wk. Cholesterol absorption was measured by the constant isotope feeding method and indirectly by the ratio of campesterol to cholesterol in serum. In ob/ob mice, cholesterol absorption was significantly higher compared to wild-type mice [83.4±2.3% (SD) vs. 77.6±1.5%, P<0.01]. Treatment with leptin significantly reduced cholesterol absorption in both ob/ob and wild-type mice by 8.5 (P<0.001) and 5.2% (P<0.05), respectively. Serum concentrations of campesterol and the ratio of campesterol to cholesterol in ob/ob mice were significantly higher compared to wild-type mice (2.2±0.3 mg/dL vs. 1.2±0.3 mg/dL, P<0.001; and 36.8±2.8 μg/mg vs. 28.0±3.3 μg/mg, P<0.001). After treatment of ob/ob mice with leptin, concentrations of campesterol and its ratio to cholesterol were significantly lower (2.2±0.3 mg/dL vs. 1.0±0.2 μg/mg, P<0.001; and 36.8±2.8 μg/mg vs. 13.2±2.2 μg/mg, P<0.001, respectively). In wild-type mice, the ratio of campesterol to cholesterol in serum was also significantly lower after treatment with leptin (28.0±3.3 μg/mg vs. 22.6±5.0 μg/mg, P<0.05). A significant positive correlation (r=0.701, P<0.01) between cholesterol absorption and the ratio of campesterol to cholesterol, in serum was found. It is concluded that leptin contributes to intestinal cholesterol absorption in ob/ob mice and lean wild-type mice.     

Dietary lipid modification of myocardial eicosanoids following ischemia and reperfusion in the rat

Several different edible oils were compared for their ability to modify eicosanoid biosynthesis following experimentally-induced myocardial ischemia and reperfusion in the rat. Two types of palm oil [neutralized, bleached, and deodorized (NBDPO) and refined, bleached, and deodorized (RBDPO)] and partially hydrogenated soybean oil (SBO) were tested against a diet supplemented with sunflower seed oil (SSO) rich in n−6 polyunsaturated fatty acids (PUFA). Fish oil (FO) rich in n−3 PUFA, with its known cardioprotective actions, served as an internal reference point for the study. Test oils were fed as a 12% (w/w) supplement for nine months before the induction of myocardial ischemia and reperfusion. Palm oil diets exerted effects indistinguishable from the SBO group against cardiac arrhythmia, which occurred following alterations to coronary blood flow. Arrhythmic potentials, as expressed by a hierarchical scale (0–9) of arrhythmia score, were: SSO, 1.5±0.5; FO, 0.9±0.4; SBO; 3.1±0.5^*; NBDPO, 3.2±0.5^*; RBDPO, 3.3±0.6^*,^* P<0.05 vs. SSO. Following ischemia and reperfusion, both SSO and RBDPO groups tended to show an increase in myocardial prostacyclin, with the effect being more prominent in the RBDPO group (SSO, 10%; RBDPO, 25%). Thromboxane production was reduced in the FO group. Interestingly, cardiac muscle from both FO and palm oil groups displayed a reduced capacity to produce 12-hydroxyeicosatetraenoic acid SSO, 591.9±95.8; SBO, 375.5±48.9; NBDPO, 287.2±64.7^*; RBDPO, 230.9±80.2^**; FO, 203.7±81.4^** (ng/g dry wt,^* P<0.05,^** P<0.01). No clear relationship was seen between the availability of 20∶4n−6 in myocardial phospholipids and eicosanoid profile. Data suggests that fatty acid composition of edible oils is not the only determinant of arrhythmic vulnerability and eicosanoid production. Based on a paper presented at the PORIM International Palm Oil Congress, Kuala Lumpur, Malaysia, September 1993.     

Camelina sativa Oil,Fatty Fish,and Lean Fish Do Not Markedly Affect Urinary Prostanoids in Subjects with Impaired Glucose Metabolism

Dietary fatty acids are suggested to affect oxidative stress; however, results from interventions have been inconclusive. The aim was to examine if fatty fish, lean fish, and Camelina sativa oil (CSO) affect the urinary prostanoid levels in subjects with impaired glucose metabolism. Altogether 79 participants aged 43–72 years completed a randomized controlled study lasting 12 weeks. There were four parallel groups, fatty fish, lean fish (four fish meals/week in both), CSO providing 10 g/day alpha-linolenic acid (ALA), and control diet with limited fish and ALA containing oil consumption. Urinary prostanoids (prostaglandin F_2α, 5-F_2t-isoprostanes and 15-F_2t-isoprostane metabolites, isofuran, 8-F_3t-isoprostanes, and 4 - (RS)-4-F_4t-neuroprostane) of 72 participants (age: mean (±SD) 58.9 ± 6.5 years; body mass index: 29.3 ± 2.5 kg/m²) collected over 12-h were measured using liquid chromatography tandem-mass spectrometry. Plasma phospholipid fatty acids were determined using gas chromatography. Our study showed that the proportion of ALA in plasma phospholipids increased in the CSO group (overall difference among the groups p-value <0.001). In the fatty fish group, proportions of eicosapentaenoic and docosahexaenoic acids increased (overall p-value <0.001 for both). Prostaglandin F_2α was higher in the CSO group than in the control group (p < 0.05), however, there were no other significant changes in urinary excretion of other prostanoids among the study groups. At baseline, arachidonic acid in plasma phospholipids was positively (r = 0.247, p < 0.05) and ALA negatively (r = −0.326, p < 0.05) associated with urinary total isoprostanes. In conclusion, CSO, fatty fish, and lean fish consumption do not cause major changes in oxidative stress markers in subjects with impaired glucose tolerance.     

Maternal fish oil supplementation in lactation: Effect on visual acuity and n−3 fatty acid content of infant erythrocytes

Studies on formula-fed infants indicate a beneficial effect of dietary DHA on visual acuity. Cross-sectional studies have shown an association between breast-milk DHA levels and visual acuity in breast-fed infants. The objective in this study was to evaluate the biochemical and functional effects of fish oil (FO) supplements in lactating mothers. In this double-blinded randomized trial, Danish mothers with habitual fish intake below the 50th percentile of the Danish National Birth Cohort were randomized to microencapsulated FO [1.3 g/d long-chain n−3 FA (n−3 LCPUFA)] or olive oil (OO). The intervention started within a week after delivery and lasted 4 mon. Mothers with habitual high fish intake and their infants were included as a reference group. Ninety-seven infants completed the trial (44 OO-group, 53 FO-group) and 47 reference infants were followed up. The primary outcome measures were: DHA content of milk samples (0, 2, and 4 mon postnatal) and of infant red blood cell (RBC) membranes (4 mon postnatal), and infant visual acuity (measured by swept visual evoked potential at 2 and 4 mon of age). FO supplementation gave rise to a threefold increase in the DHA content of the 4-mon milk samples (P<0.001). DHA in infant RBC reflected milk contents (r=0.564, P<0.001) and was increased by almost 50% (P<0.001). Infant visual acuity was not significantly different in the randomized groups but was positively associated at 4 mon with infant RBC-DHA (P=0.004, multiple regression). We concluded that maternal FO supplementation during lactation did not enhance visual acuity of the infants who completed the intervention. However, the results showed that infants with higher RBC levels of n−3 LCPUFA had a better visual acuity at 4 mon of age, suggesting that n−3 LCPUFA may influence visual maturation.     

Effect of n−3 fatty acid-rich fish oil supplementation on the oxidation of low density lipoproteins

This study was aimed at determining the effect of fish oil supplementation on copper-catalyzed oxidation of low density lipoproteins (LDL) from nine hypertriglyceridemic human subjects. A rapid headspace gas chromatographic method was used to measure the volatile oxidation products from LDL. Propanal and hexanal were the major volatile products formed in the oxidation of n−3 and n−6 polyunsaturated fatty acids (PUFA), respectively. Fish oil supplementation resulted in a significant increase in propanal formation from 3.7 to 13.4 nmol/mL LDL (P<0.01); it also resulted in small decreases in pentanal formation from 14.7 to 11.4 nmol/mL LDL and in hexanal formation from 138 to 108 nmol/mL LDL (P<0.05). The changes in peroxidation products paralleled the changes in LDL composition, which showed a significant increase in n−3 PUFA from 3.2 to 14.6% (P<0.01) and a decrease in n−6 PUFA from 43.7 to 35.0% (P<0.05). Propanal formation was highly and significantly correlated with n−3 PUFA content (r=0.950,P<0.001). Since total volatiles remained unchanged, this indicated that the two groups of LDL samples did not differ in overall oxidative susceptibility. Although fish oil intake did not alter the oxidative susceptibility of LDL, the chemically modified LDL particles generated a distinct pattern of volatile oxidation products that reflected changes in their fatty acid composition.     

The Effectiveness of Fish Oil Supplementation in Asthmatic Rats is Limited by an Inefficient Action on ASM Function

Episodes of acute exacerbation are the major clinical feature of asthma and therefore represent an important focus for developing novel therapies for this disease. There are many reports that the n-3 fatty acids found in fish oil exert anti-inflammatory effects, but there are few studies of the action of fish oil on airway smooth muscle (ASM) function. In the present investigation, we evaluated the effect of fish oil supplementation on smooth muscle force of contraction in ovalbumin-induced asthmatic Wistar rats, and its consequences on static lung compliance, mucus production, leukocyte chemotaxis and production of proinflammatory cytokines. Fish oil supplementation suppressed the infiltration of inflammatory cells into the lung in asthmatic animals (2.04 ± 0.19 × 10⁶ cells vs. 3.33 ± 0.43 × 10⁶ cells in the control asthmatic group; P < 0.05). Static lung compliance increased with fish oil supplementation in asthmatic rats (0.640 ± 0.053 mL/cm H₂O vs. 0.399 ± 0.043 mL/cm H₂O; P < 0.05). However, fish oil did not prevent asthma-associated lung eosinophilia and did not affect the concentrations of tumor necrosis factor-α and interleukin-1β in lung tissue or the proportion of the airways obliterated with mucus. Fish oil had no effect on the force of contraction in asthmatic rats in response to acetylcholine (3.026 ± 0.274 mN vs. 2.813 ± 0.364 mN in the control asthmatic group). In conclusion, although fish oil exerts some benefits in this model of asthma, its effectiveness appears to be limited by an inefficient action on airway smooth muscle function.