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PubMed2005

Greater enrichment of triacylglycerol-rich lipoproteins with apolipoproteins E and C-III after meals rich in saturated fatty acids than after meals rich in unsaturated fatty acids.

BACKGROUND: Although there is considerable interest in the postprandial events involved in the absorption of dietary fats and the subsequent metabolism of diet-derived triacylglycerol-rich lipoproteins, little is known about the effects of meal fatty acids on the composition of these particles. OBJECTIVE: We examined the effect of meal fatty acids on the lipid and apolipoprotein contents of triacylglycerol-rich lipoproteins. DESIGN: Ten normolipidemic men received in random order a mixed meal containing 50 g of a mixture of palm oil and cocoa butter [rich in saturated fatty acids (SFAs)], safflower oil [n-6 polyunsaturated fatty acids (PUFAs)], or olive oil [monounsaturated fatty acids (MUFAs)] on 3 occasions. Fasting and postprandial apolipoproteins B-48, B-100, E, C-II, and C-III and lipids (triacylglycerol and cholesterol) were measured in plasma fractions with Svedberg flotation rates (S(f)) >400, S(f) 60-400, and S(f) 20-60. RESULTS: Calculation of the composition of the triacylglycerol-rich lipoproteins (expressed per mole of apolipoprotein B) showed notable differences in the lipid and apolipoprotein contents of the SFA-enriched particles in the S(f) > 400 and S(f) 60-400 fractions. After the SFA meal, triacylglycerol-rich lipoproteins in these fractions showed significantly greater amounts of triacylglycerol and of apolipoproteins C-II (S(f) 60-400 fraction only), C-III, and E than were found after the MUFA meal (P < 0.02) and more cholesterol, apolipoprotein C-III (S(f) > 400 fraction only), and apolipoprotein E than after the PUFA meal (P < 0.02). CONCLUSIONS: Differences in the composition of S(f) > 400 and S(f) 60-400 triacylglycerol-rich lipoproteins formed after saturated compared with unsaturated fatty acid-rich meals may explain differences in the metabolic handling of dietary fats.

Apolipoproteins C↗
PubMed1978

Fatty acid composition of submandibular salivary gland lipids in essential fatty acid deficient rats.

Essential fatty acid (EFA) deficiency was induced in young weanling rats by feeding a fat-free diet or a diet containing 7% Hydrogenated coconut oil (HCO). At intervals of 4, 8, and 16 weeks, rats from the deficient and the control groups were killed and their Submandibular Salivary Glands (SMSG) were dissected out and extracted for lipids. The fatty acid composition of total lipids, triglycerides (TG), free fatty acids (FFA), phosphatidyl choline (PC), and phosphatidyl ethanola-mine (PE) fractions was determined. The levels of 16:1 and 18:1 were increased whereas those of 18:2 and 20:4 were decreased in the EFA-deficient groups as compared to the controls. 5,8,11-eicosatrienoic acid (20:3 omega9) accumulated in the total lipids as well as other lipid fractions of the SMSG from the deficient rats. The levels of this fatty acid increased as the EFA-deficiency progressed. Changes in fatty acid composition of SMSG lipids of EFA-deficient rats were associated with a reduction in flow rate of whole saliva. Protein concentration and amylase activity of saliva was the same in the two groups.

Animals↗
PubMedDate not supplied

Dietary (n-3) fatty acids from menhaden fish oil alter plasma fatty acids and leukotriene B synthesis in healthy horses.

The study objective was to determine the effect of feeding corn oil or fish oil to horses on plasma fatty acid profiles and leukotriene B (LTB) synthesis by stimulated peripheral blood neutrophils. Two groups of horses (n = 5) were randomly assigned to diets supplemented with either 3.0% (by weight) corn oil or fish oil for a period of 14 weeks. The ratio of (n-6) to (n-3) fatty acids in oil supplements was 68.1:1 for corn oil and 0.12:1 for fish oil. Production of LTB4 and LTB, by peripheral blood neutrophils stimulated with calcium ionophore A23187 and plasma cholesterol, triacylglycerol, and alpha-tocopherol concentrations were measured. At 12 weeks, horses fed fish oil had increased plasma concentrations of eicosapentaenoic acid (27-fold; 8.5 versus 0.3 g/100 g fatty acids; P < .0001), docosahexaenoic acid (34-fold; 5.1 versus 0.1 g/100 g fatty acids; P < .0001), and arachidonic acid (8.3-fold; 4.1 versus 0.5 g/100 g fatty acids; P < .0001) compared with horses fed corn oil. Neutrophils from horses fed fish oil produced 78-fold (P = .01) more LTB5 and 9.5-fold (P = .003) more LTB4 compared with predietary levels, and 17.6-fold (P = .01) and 3.3-fold (P = .02), respectively, more than horses fed corn oil, and the ratio of LTB5 to LTB4 concentrations was 4.0-fold (P = .002) higher in horses fed fish oil. This study suggests that dietary polyunsaturated fatty acids modulate the leukotriene inflammatory response of horses. If the ratio of LTB5 to LTB4 concentrations is important in determining how inflammatory processes are mediated, then fish oil supplementation may have value in treatment of equine inflammatory diseases.

Animals↗
PubMed1990

Effects of prenatal ethanol and long-chain n-3 fatty acid supplementation on development in mice. 2. Fatty acid composition of brain membrane phospholipids.

Pregnant mice were fed equivalent daily amounts of a liquid diet containing 25% (kcal) ethanol, or with maltose dextrin substituted isocalorically for ethanol. The diet also contained 20% oil; this was either of two mixtures, one comprised of predominantly n-6 (18:2n-6) fatty acids, and the other containing an equivalent amount of n-6, but supplemented with a source of long chain n-3 (20:5n-3, 22:6n-3) fatty acids. An additional control group was fed lab chow ad libitum. The treatment was implemented from day 7 to 17 of gestation, whereafter all groups were fed lab chow. Birth occurred on day 19, and the fatty acid composition of the brain membrane phospholipids was determined in the pups 3 days after birth (day 22 postconception) and again, 10 days later (day 32 postconception). On day 22 the polyunsaturated fatty acid (PUFA) composition of the brain phospholipids reflected dietary availability, with the n-3/n-6 ratio higher in the n-3 groups; this was decreased by ethanol in the phosphatidylcholine (PC) fraction. The dietary effect was still apparent on day 32; again ethanol reduced this in both the PC and phosphatidylethanolamine (PE) fractions. The n-3 oil, but not ethanol, increased the 20:3n-6/20:4n-6 ratio, indicative of an inhibition of the activity of delta-5 desaturase. With respect to the 22:C compounds, the n-3 oil decreased the levels of 22:5n-6, while increasing those of 22:6n-3, but generally the sum of these two fatty acids remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Splanchnic exchange of glucose, amino acids and free fatty acids in patients with chronic inflammatory bowel disease.

In order to study arterial concentrations and splanchnic exchange of substrates and hormones in patients with chronic inflammatory bowel disease three patients with Crohn's disease and four with ulcerative colitis were studied using the hepatic venous catheter technique. Systemic turnover and regional exchange of free fatty acid were evaluated using intravenous infusion of 14C-labelled oleic acid. All measurements were made in the postabsorptive, overnight fasted state. Arterial glucose concentrations were 10% lower in the patients but net splanchnic glucose output was similar in patients and controls. Glucose precursor uptake (lactate, pyruvate, and glycerol), however, was increased two to five fold in the patients. Arterial amino acid concentrations were generally reduced but net splanchnic amino acid uptake was the same in patients and controls. Arterial concentrations of free fatty acid and oleic acid as well as systemic and fractional turnover were similar in patients and controls. The patients' splanchnic uptake of oleic acid was increased more than three fold in comparison with controls. Splanchnic release of oleic acid was also augmented in the patients. Both arterial concentrations and splanchnic production of ketone bodies were raised in the patients. The proportion of splanchnic free fatty acid uptake which could be accounted for by ketone body production was significantly greater in the patients (37 +/- 4%) than the controls (20 +/- 5%, p less than 0.025). Estimated hepatic blood flow was 55% greater (p less than 0.01) in the patients as compared with the controls (1930 +/- 150 vs 1240 +/- 70 ml/min), while splanchnic oxygen uptake was similar in the two groups. From these findings it is concluded that patients with chronic inflammatory bowel disease show (1) markedly increased hepatic blood flow, reflecting an inflammatory hyperaemia in the splanchnic region, (2) a normal net splanchnic glucose output, (3) accelerated hepatic gluconeogenesis as well as ketogenesis, probably as a consequence of the altered hormonal milieau, and (4) low concentrations of most amino acids possibly because of protein malabsorption. These findings underscore the importance of adequate protein and carbohydrate administration to this patient group.

Adult↗
PubMed2001

Effects of fatty acids and growth hormone on liver fatty acid binding protein and PPARalpha in rat liver.

The aim of this study was to investigate the interaction between long-chain fatty acids (LCFA) and growth hormone (GH) in the regulation of liver fatty acid binding protein (LFABP) and peroxisome proliferator-activated receptor-alpha (PPARalpha). Cultured rat hepatocytes were given oleic acid (OA; 500 microM) and GH (100 ng/ml) for 3 days. LFABP mRNA increased 3.6-fold by GH and 5.7-fold by OA, and combined incubation with GH and OA increased LFABP mRNA 17.6-fold. PPARalpha mRNA was decreased 50% by GH, but OA had no effect. Hypophysectomized (Hx) female rats were treated with L-thyroxine, cortisol, GH, and dietary fat for 7 days. PPARalpha mRNA levels were three- to fourfold higher in Hx than in normal female rats. GH decreased PPARalpha mRNA 50% in Hx rats. Dietary triglycerides (10% corn oil) increased LFABP mRNA and cytosolic LFABP about twofold but had no effect on PPARalpha mRNA in Hx rats. GH and dietary triglycerides had an additive effect on LFABP expression. Dietary triglycerides increased mitochondrial hydroxymethylglutaryl-CoA synthase mRNA only in the presence of GH. The diet increased serum triglycerides in Hx rats, and GH treatment prevented this increase. Addition of cholesterol to the diet did not influence LFABP levels but mitigated increased hepatic triglyceride content. In summary, these studies show that GH regulates LFABP expression independently of PPARalpha. Moreover, GH has different effects on PPARalpha-responsive genes and does not counteract the effect of LCFA on the expression of these gene products.

Animals↗
PubMed1990

Enzymes for biosynthesis de novo and elongation of fatty acids in mycobacteria grown in host cells: is Mycobacterium leprae competent in fatty acid biosynthesis?

Fatty acid synthetase activity in extracts of Mycobacterium leprae was equivalent to 1.7 pmol malonyl-CoA incorporated into fatty acid min-1 (mg protein)-1. This activity--if representative of living M. leprae organisms--is insufficient to enable them to synthesize their lipid requirements rapidly enough to support growth. The major activity for scavenging fatty acids in extracts of Mycobacterium microti and Mycobacterium avium, as well as in extracts of M. leprae, was acetyl-CoA-dependent fatty acyl-CoA 'elongase'. This activity was about four times higher in M. avium and M. microti grown in a medium which contained lipids, or when grown in mice, than in medium without added lipids. In contrast, the de novo fatty acid synthetase activity was repressed in M. avium and M. microti when grown in medium that contained lipids, or when grown in mice. These results are consistent with the hypothesis that mycobacteria grown in vivo preferentially scavenge lipids from the host cells, and suggest that a source of lipid should be included in media for attempted axenic isolation of M. leprae.

Acetyltransferases↗
PubMed2001

Growth reduction in glioma cells after treatment with tetradecylthioacetic acid: changes in fatty acid metabolism and oxidative status.

During aerobic metabolism, a small amount of partially reduced oxygen is produced, yielding reactive oxygen species (ROS). Peroxisomes and mitochondria are major contributors to cellular ROS production, which is normally balanced by consumption by antioxidants. The fatty acid analogue tetradecylthioacetic acid (TTA) promotes mitochondrial and peroxisomal proliferation, and may induce oxidative stress and change the growth potential of cancer cells. In the present study, we found that TTA reduced [(3)H]thymidine incorporation in the glioma cell lines BT4Cn (rat), D54Mg (human), and GaMg (human) in a dose- and time-dependent manner. The 50% inhibitory TTA doses were approximately 125 microM for BT4Cn and D54Mg cells and 40 microM for GaMg cells after 4 days. alpha-Tochopherol counteracted this inhibition in GaMg cells. TTA enhanced the oxidation of [1-(14)C]palmitic acid, which could be explained by stimulation of enzymes involved in peroxisomal (fatty acyl-CoA oxidase) and/or mitochondrial (carnitine palmitoyltransferase) fatty acid oxidation. The glutathione content and the activities of glutathione peroxidase, glutathione reductase, and glutathione S-transferase were differentially affected. Increased malondialdehyde (MDA) production was seen in TTA-treated GaMg and D54Mg cells, but not in BT4Cn cells, in vitro. In BT4Cn tumor tissue from TTA-treated rats, MDA was increased while the alpha-tocopherol content tended to decrease. TTA increased the level of cytosolic cytochrome c in BT4Cn cells, which suggests induction of apoptotic cascades. Although several mechanisms are likely to be involved in the TTA-mediated effects on growth, we propose that modulation of cellular redox conditions caused by changes in fatty acid metabolism may be of vital importance.

Animals↗
PubMed2004

A novel function for fatty acid translocase (FAT)/CD36: involvement in long chain fatty acid transfer into the mitochondria.

Fatty acid translocase (FAT)/CD36 is a long chain fatty acid transporter present at the plasma membrane, as well as in intracellular pools of skeletal muscle. In this study, we assessed the unexpected presence of FAT/CD36 in both subsarcolemmal and intermyofibril fractions of highly purified mitochondria. Functional assessments demonstrated that the mitochondria could bind (14)C-labeled palmitate, but could only oxidize it in the presence of carnitine. However, the addition of sulfo-N-succinimidyl oleate, a known inhibitor of FAT/CD36, resulted in an 87 and 85% reduction of palmitate oxidation in subsarcolemmal and intermyofibril fractions, respectively. Further studies revealed that maximal carnitine palmitoyltransferase I (CPTI) activity in vitro was inhibited by succinimidyl oleate (42 and 48% reduction). Interestingly, CPTI immunoprecipitated with FAT/CD36, indicating a physical pairing. Tissue differences in mitochondrial FAT/CD36 protein follow the same pattern as the capacity for fatty acid oxidation (heart >> red muscle > white muscle). Additionally, chronic stimulation of hindlimb muscles (7 days) increased FAT/CD36 expression and also resulted in a concomitant increase in mitochondrial FAT/CD36 content (46 and 47% increase). Interestingly, with acute electrical stimulation of hindlimb muscles (30 min), FAT/CD36 expression was not altered, but there was an increase in the mitochondrial content of FAT/CD36 compared with the non-stimulated control limb (35 and 37% increase). Together, these data suggest a role for FAT/CD36 in mitochondrial long chain fatty acid uptake and demonstrate system flexibility to match FAT/CD36 mitochondrial content with an increased capacity for fatty acid oxidation, possibly involving translocation of FAT/CD36 to the mitochondria.

Animals↗
PubMed1987

Possible involvement of acetyl coenzyme A carboxylase as well as fatty acid synthetase in the temperature-controlled synthesis of fatty acids in Saccharomyces cerevisiae.

Fatty acid synthetase (FAS) preparations from Saccharomyces cerevisiae cells grown at either 35 or 10 degrees C produced the same products at different temperatures and showed quite similar temperature-dependencies in Arrhenius plots, with break points at 25 degrees C. This break point does not appear to reflect a phase transition of phospholipids present in the purified FAS preparations but rather is associated with protein conformational changes. S. cerevisiae cells grown at 35 degrees C and then shifted to 10 degrees C produced fatty acids with a shorter average chain length than those fatty acids synthesized at 10 degrees C by cells already adapted to 10 degrees C (hyper response). Acetyl-CoA carboxylase activity was relatively higher in the cells grown at 35 degrees C than in the cells grown at 10 degrees C; moreover, fatty acids with longer average chain lengths were synthesized in vitro at higher malonyl-CoA concentrations, which was consistent with the difference in the average chain lengths of newly synthesized fatty acids in cells grown at 35 and 10 degrees C. However, the activity levels of acetyl-CoA carboxylase and fatty acid synthetase alone did not account for the hyper response phenomena.

Acetyl-CoA Carboxylase↗
PubMed1976

Studies on the formation by rat brain preparations of CDP-diglyceride from CTP and phosphatidic acids of varying fatty acid compositions.

The enzyme, CTP:phosphatidate cytidylyltransferase (EC2.7.7.41) which catalyses formation of CDP-diglyceride from CTP and phosphatidic acid has been studied in rat brain preparations and other tissues. Improvement, as judged by the higher tissue activities obtained, in the assay method for this enzyme was achieved through use of phosphatidic acids sonicated in buffer-detergent solution saturated with ether and containing bovine serum albumin and use of short incubation times which essentially provided a measure of initial rates. The enzyme of rat brain microsomes yielded with 1,2-dioleolphosphatidic acid as substrate a pH optimum of 6.8 with maleate buffer and optimal concentrations of 60mM for MG2+, 6MM for CTP and 250 mug per 0.8 ml for phosphatidic acid. Enzyme activity was mainly located in the 90,000 X g fraction (microsomal) with small but significant activity in the 12,000 X g fraction. Comparison of activities (nanomoles CTP incorporated per milligram protein per minute) amongst tissues showed the following order: brain, 1.87; liver, 1.32; lung, 1.19; small intestine, 1.00; kidney, 0.69; heart, 0.41; diaphragm, 0.07; skeletal muscle, 0.02. Examination of the effect of varying the fatty acid composition in the phosphatidic acids added exogenously gave the following order (activities in parentheses); 1-stearoyl-2-oleoyl- (5.58), 1-oleoyl-2-stearoyl- (5.37), 1,2-dioleoyl- (4.49) 1-palmitoyl-2-oleoyl-(3.85), 1-stearoyl-2-arachidonoyl-(3.31), 1-arachidonoyl-2-stearoyl-(3.16), 1,2-diarachidonoyl-(0.72), 1,2-dicaproyl-(0.67), 1,2-dipalmitoyl-(0.67) and 1,2-distearoyl-(0.18). The single bis- and lysophosphatidic acids tested were inactive as substrates. Apart from a possible preference for one or more unsaturated fatty acids the transferase enzyme showed no selectivity in respect to the fatty acid distribution of phosphatidic acids.

Animals↗
PubMed1990

Protein and carbohydrate selection respond to changes in dietary saturated fatty acids but not to changes in essential fatty acids.

We previously reported differences in protein and carbohydrate selection patterns in post-weanling rats fed beef tallow or soybean oil-based diets. Two experiments were designed to determine the characteristic of the dietary fat which mediates the selection behavior. For each experiment, dietary fat was 20% (w/w) of diets and fatty acid profiles were obtained by blending fat sources. Rats were randomly assigned to diets (24% protein, 40% carbohydrate) which varied only in fatty acid composition. After 2 weeks, rats selected from 2 diets with the fat composition previously fed, but varying in their protein and carbohydrate composition (55% protein, 4% carbohydrate and 5% protein, 61% carbohydrate). Experiment 1 was designed to test the effect of relative (omega 6: omega 3 ratios of 1 and 20) and absolute (15% or 4% omega 6, 0.7% or 0.2% omega 3) differences in essential fatty acids on macronutrient selection patterns. Differences in dietary essential fatty acids had no effect on energy intake or the proportion of energy consumed as protein and carbohydrate. Experiment 2 examined the effect of differences in the level of saturated fat (3-10% diet (w/w] on protein and carbohydrate selection. Animals selecting from diets with higher levels of saturated fat consumed more energy as protein and less as carbohydrate than rats selecting from diets with lower levels of saturated fat (p less than 0.0001). Regression analysis was used to examine the relationship between percent protein or carbohydrate energy and classes of dietary fat. The strongest relationship existed between percent dietary saturated fat and percent protein or carbohydrate energy (p less than 0.0001). Polyunsaturated:saturated fat ratio was also weakly associated with percent protein and carbohydrate energy (p less than 0.05). Polyunsaturated, monounsaturated, omega 6 and omega 3 fatty acids were not significantly related to percent protein or carbohydrate energy. These results indicated that protein and carbohydrate selection patterns are altered in response to qualitatively different dietary fatty acids, and that the amount of saturated fat in the diet is the important characteristic of dietary fat mediating the behavioral alteration.

Analysis of Variance↗
PubMed1985

Effect of dietary alpha- and gamma-linolenic acid on tissue fatty acids in guinea pigs.

Guinea pigs were fed regular chow diets supplemented with 5% (by weight) safflower oil, evening primrose oil, or linseed oil for 6 weeks. The unsaturated fatty acid content of these oils was 78.9% of 18:2n6, 74.1% of 18:2n6, and 9.2% of 18:3n6, or 21.5% of 18:2n6 and 46.9% of 18:3n3, respectively. In comparison with 18:2n6, dietary supplementation with 18:3n6 significantly increased the tissue levels of 18:3n6 and 20:3n6, whereas dietary 18:3n3 significantly elevated the levels of 18:3n3 in plasma and liver lipids. Dietary 18:3n3 also significantly increased 22:5n3 and 22:6n3 in total phospholipids. The tissue levels of 20:4n6, on the other hand, were not affected by either treatment. These data suggest that both delta 6- and delta 5 desaturation of n-6 fatty acids in guinea pigs are low, and that the metabolism of n-3 and n-6 fatty acids may be regulated by two different enzyme systems.

Animals↗
PubMed1974

Saturated fatty acid mutant of Saccharomyces cerevisiae with an intact fatty acid synthetase.

A Saccharomyces cerevisiae conditional mutant, LK 181, is described which grows at 37 C only when supplemented with a saturated fatty acid of 12 to 14 carbon atoms chain length. At 22 C, however, no fatty acid supplementation is required for growth. The fatty acid concentration required for optimal growth at 37 C is about four times lower for LK 181 than for fatty acid synthetase-deficient mutants. In contrast to all fatty acid synthetase mutants so far examined, mutant LK 181 cannot grow with palmitic acid. The addition of palmitic, palmitoleic, or oleic acid to the culture medium prevents LK 181 growth at temperatures between 22 and 37 C. In vivo as well as in vitro, cellular de novo fatty acid biosynthesis from acetate is unimpaired in this mutant. It is suggested that endogenously synthesized fatty acids, due to their chain lengths of 16 and more carbon atoms, cannot supplement the mutant LK 181. It is concluded that the exogeneously supplied fatty acids act as allosteric effectors for a mutationally altered cellular protein to restore its biological function at elevated temperatures, rather than as a substitute for endogenously synthesized long-chain fatty acids.

Acetates↗
PubMed1998

Conversion of palmitate to unsaturated fatty acids differs in a Neurospora crassa mutant with impaired fatty acid synthase activity.

The Neurospora crassa cel (fatty acid chain elongation) mutant has impaired fatty acid synthase activity. The cel mutant requires exogenous 16:0 for growth and converts 16:0 to other fatty acids. In contrast to wild-type N. crassa, which converted only 42% of the exogenous [7,7,8,8-(2)H4]16:0 that was incorporated into cell lipids to unsaturated fatty acids, cel converted 72%. In addition, cel contains higher levels of 18:3(delta 9,12,15) than wild-type, and synthesizes two fatty acids, 20:2(delta 11,14 and 20:3(delta 11,14,17, found at only trace levels in wild-type. Thus, the delta 15-desaturase activity and elongation activity on 18-carbon polyunsaturated fatty acids are higher for cel than wild-type. This altered metabolism of exogenous 16:0 may be directly due to impaired flux through the endogenous fatty acid biosynthetic pathway, or may result from altered regulation of the synthesis of unsaturated fatty acids in the mutant.

Fatty Acid Desaturases↗
PubMed1999

Conjugated linoleic acids alter milk fatty acid composition and inhibit milk fat secretion in dairy cows.

Conjugated linoleic acids (CLA) have positive health effects in experimental models. Our objective was to determine the effect of CLA supplementation on milk of dairy cows. A commercial source of CLA was infused abomasally to by-pass rumen fermentation. The supplement contained 61.2% CLA; the major CLA isomers were cis/trans 8,10, cis/trans 9,11, cis/trans 10,12 and cis/trans 11,13. Four Holstein cows were used in a 4 x 4 Latin square design. Treatments were 5-d infusions of 0, 50, 100 and 150 g/d of CLA supplement. Infusion increased milk fat content of CLA from 6.8 mg/g fat (zero dose) to 63.6 mg/g fat (highest dose). All of the major CLA isomers in the supplement were transferred to milk fat in a dose-dependent manner. Apparent efficiency of transfer to milk fat was 22.5, 22.5, 10.2 and 26.3% for cis/trans 8,10, cis/trans 9,11, cis/trans 10,12 and cis/trans 11,13, respectively. CLA infusion had no effect on milk protein and little effect on milk yield (21.5, 20.4, 20.9 and 18.3 kg/d for 0, 50, 100 and 150 g/d CLA supplement, respectively). However, CLA infusion dramatically reduced milk fat. On average, the content and yield of milk fat were reduced by 52 and 55%, respectively. The role of specific CLA isomers and mechanism(s) for the reduction in milk fat have not been established, although the pattern of milk fatty acids demonstrated effects were most pronounced on de novo fatty acid synthesis and the desaturation process. Overall, dietary supplemention of CLA increased milk fat content of CLA, altered milk fatty acid composition and markedly reduced the content and yield of milk fat.

Animals↗