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PubMed1978

Effects of dihydroxy bile acids and hydroxy fatty acids on the absorption of oleic acid in the human jejunum.

Perfusion studies of the normal human jejunum were performed to test whether dihydroxy bile acids and hydroxy fatty acids inhibit the absorption of oleic acid, since previous reports documented their inhibitory effects on the absorption of several other organic solutes. 3 mM deoxycholate and 7 mM glycodeoxycholate inhibited the absorption of 3 mM oleic acid in isotonic micellar solutions while inducing net fluid secretion. Similarly, fractional absorption of oleic acid decreased in the presence of hydroxy fatty acids. However, only the changes induced by 2 mM ricinoleic acid could be distinguished from changes induced by an increase in total fatty acid concentration. Under all experimental conditions, close linear relationships existed between net water movement and fractional absorption of glucose, xylose, and fatty acids, as well as between the absorption rates of these solutes. In contrast, net fluid secretion induced by hypertonic D-mannitol (450 mosmol/liter) had no effect on solute absorption. Our data and observations in the literature do not allow formulation of a hypothesis which would adequately define all effects of dihydroxy bile acids and fatty acids on intestinal transport processes. The observations help explain the malabsorption of fat and other nutrients in patients with the blind loop syndrome.

Adult↗
PubMed1980

Extrauterine fatty acid accretion in infant brain: implications for fatty acid requirements.

Total fatty acid content of infant brain was determined to assess minimal fatty acid requirements for synthesis of structural lipids in brain tissue during the first 13 weeks of life. Fatty acid accretion rates were determined by regression analysis of tissue fat components at varying postnatal ages. Quantitative fatty acid analysis indicated that postnatal accretion of long-chain polyenoic fatty acids in cerebellum, frontal and occipital brain lobes initially appeared to lag behind the rate of increase in brain weight and brain fat content. After a 4-week period total long-chain fatty acids increased at a rate similar to the increase in brain weight. Accretion of individual fatty acids in cerebellum also reflected changes in tissue total fatty acid content. These developmental changes in fatty acid components of whole brain and cerebellum are quantitatively relevant to estimation of the minimal extrauterine fatty acid requirements of the human neonate.

Brain↗
PubMed1977

Fatty acid synthesis in aorta. Isolation of fatty acid synthetase from chicken aorta.

Fatty acid synthesis by subcellular fractions of human aorta was studied by measuring the incorporation of either radioactive acetyl-CoA or malonyl-CoA into long chain fatty acids. The high speed supernatant fraction contained fatty acid synthetase and was capable of de novo fatty acid synthesis. The fatty acid synthetase from chicken aorta was purified 800-fold from the high speed supernatant and was judged to be 10% pure at this level. Its molecular weight was estimated to be 450,000 on the basis of agarose gel filtration chromatography, while under dissociating conditions a molecular weight of 220,000 was obtained on sodium dodecyl sulphate disc gel electrophoresis. Fatty acid synthesis was dependent on acetyl-CoA, malonyl-CoA and NADPH. The major product was free palmitic acid. In enzymatic and physical characteristics the chicken aorta fatty acid synthetase strongly resembles the synthetase isolated from chicken liver. The two enzymes cross-react immuno-chemically and this homology provides the possibility of studying the synthesis and degradation of the aorta synthetase during the development of atherosclerosis.

Acetyl Coenzyme A↗
PubMed1998

Hypothesis: are fatty acid patterns characteristic of essential fatty acid deficiency indicative of oxidative stress?

Several unrelated diseases show plasma and tissue fatty acid patterns characteristic of those seen in Essential Fatty Acid Deficiency Disease (EFADD). A common feature occurring in all these diseases is oxidative stress. We hypothesize that reactive oxygen species or products of oxidative damage, particularly those derived from lipids, act as signal molecules to alter desaturase enzymes and induce the fatty acid patterns characteristic of EFADD.

Animals↗
PubMed1996

Glucose and insulin-induced inhibition of fatty acid oxidation: the glucose-fatty acid cycle reversed.

In this study we have investigated a hypothesis that proposes the reverse of the so-called "glucose-fatty acid cycle, " i.e., that accelerated carbohydrate metabolism directly inhibits fatty acid oxidation. We studied normal volunteers in the basal state and during a hyperinsulinemic, hyperglycemic clamp (plasma insulin = 1,789 +/- 119 pmol/l, plasma glucose = 7.7 +/- 0.2 mmol/l). We quantified fat oxidation using indirect calorimetry and stable isotopes ([1-13C]oleate). Plasma oleate enrichment and free fatty acid (FFA) concentration were kept constant by means of infusion of lipids and heparin. Glucose oxidation increased from basal 6.2 +/- 0.8 to 22.3 +/- 1.4 mumol.kg-1.min-1 during the clamp (P < 0.01). Total (indirect calorimetry) and plasma fatty acid oxidation (isotopic determination) decreased from 2.6 +/- 0.2 to 0.4 +/- 0.3 (P < 0.01) and 2.2 +/- 0.2 to 1.4 +/- 0.1 mumol.kg-1.min-1 (P <0.05), respectively. We conclude that under the conditions of the present experiment, glucose and/or insulin directly inhibits fatty acid oxidation. Our findings suggest that, contrary to the prediction of the glucose-fatty acid cycle, the intracellular availability of glucose (rather than FFA) determines the nature of substrate oxidation in human subjects.

Adult↗
PubMed1984

Fatty acid composition of lizard tissue lipids and the effects of estradiol on serum free fatty acids.

Fatty acid analyses of lipids from lizard fat bodies, carcass, and blood serum were performed by GLC. Principal fatty acids from all three tissues were palmitate (16:0), stearate (18:0), oleate (18:1), and linoleate (18:2). Administration of estradiol to vitellogenic or non-vitellogenic lizards increased serum levels of non-esterified fatty acids, but had no effect on the fat body wet weights. Lizards receiving estradiol had a higher proportion of arachidonate and a lower proportion of oleate in their serum non-esterified fatty acids.

Acclimatization↗
PubMed1988

Dietary linoleic acid and the fatty acid profiles in rats fed partially hydrogenated marine oils.

The influence of the linoleic acid levels of diets containing partially hydrogenated marine oils (HMO) rich in isomeric 16:1, 18:1, 20:1 and 22:1 fatty acids on the fatty acid profiles of lipids from rat liver, heart and adipose tissue was examined. Five groups of rats were fed diets containing 20 wt % fat--16% HMO + 4% vegetable oils. In these diets, the linoleic acid contents varied between 1.9% and 14.5% of the dietary fatty acids, whereas the contents of trans fatty acids were 33% in all groups. A sixth group was fed a partially hydrogenated soybean oil (HSOY) diet containing 8% linoleic acid plus 32% trans fatty acids, mainly 18:1, and a seventh group, 20% palm oil (PALM), with 10% linoleic acid and no trans fatty acids. As the level of linoleic acid in the HMO diets increased from 1.9% to 8.2%, the contents of (n-6) polyunsaturated fatty acids (PUFA) in the phospholipids increased correspondingly. At this dietary level of linoleic acid, a plateau in (n-6) PUFA was reached that was not affected by further increase in dietary 18:2 (n-6) up to 14.5%. Compared with the HSOY- or PALM-fed rats, the plateau values of 20:4(n-6) were considerably lower and the contents of 18:2(n-6) higher in liver phosphatidylcholines (PC) and heart PC. Heart phosphatidylethanolamines (PE) on the contrary, had elevated contents of 20:4(n-6), but decreased 22:5(n-6) compared with the PALM group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed2004

Prolonged feeding of mice with conjugated linoleic acid increases hepatic fatty acid synthesis relative to oxidation.

Feeding mice conjugated linoleic acid (9 cis,11 trans/9 trans,11 cis-and 10 trans,12 cis-CLA in equal amounts) resulted in triacylglycerol accumulation in the liver. The objective of this study was to examine whether this steatosis is associated with changes in hepatic fatty acid synthesis and oxidation. Therefore, we measured the activities of key enzymes of fatty acid synthesis, i.e., acetyl-CoA carboxylase and fatty acid synthase and of fatty acid oxidation, i.e., 3-hydroxy-acyl-CoA dehydrogenase and citrate synthase in livers of mice fed a diet with 0.5% (w/w) CLA. CLA (a 1:1 mixture of the 10 trans, 12 cis and 9 cis, 11 trans isomers of octadecadenoic acid) was administered for 3 and 12 weeks with high-oleic sunflower oil fed as control. The proportion of body fat was significantly lower on the CLA than on the control diet and this effect was already significant after 3 weeks. The specific activites of 3-hydroxy-acyl-CoA dehydrogenase and citrate synthase were unaffected by CLA both after 3 and 12 weeks. The specific activity of fatty acid synthase was nonsignificantly raised (by 12%) after 3 weeks on the CLA diet but had increased significantly (by 34%) after 12 weeks of feeding. The specific activity of acetyl-CoA carboxylase had also increased both after 3 weeks (by 53%) and 12 weeks (by 23%) on the CLA diet, but this effect did not reach statistical significance. Due to CLA-induced hepatomegaly, the overall capacity for both fatty acid oxidation and synthesis-as evidenced by the total hepatic activities of 3-hydroxy-acyl-CoA dehydrogenase, citrate synthase, acetyl-CoA carboxylase, and fatty acid synthase-was significantly greater in the CLA-fed group after 12 weeks, although the overall capacity for fatty acid synthesis had increased more than that for fatty acid oxidation. Thus, this study indicates that prolonged, but not short-term, feeding mice with CLA increased hepatic fatty acid synthesis relative to oxidation, despite the decrease in body fat and the increase in liver weight seen earlier. It is concluded that the observed CLA-induced changes in hepatic fatty acid synthesis and oxidation are the result, rather than the cause, of the lowering of body fat.

Animals↗
PubMed1999

Effects of dietary polyunsaturated fatty acids and nucleotides on tissue fatty acid profiles of rats with carbon tetrachloride-induced liver damage.

The deficiency of polyunsaturated fatty acids (PUFA) that occurs in plasma of patients with liver cirrhosis has been assessed in rats with severe steatosis and mild liver necrosis induced by repeated administration of low doses of carbon tetrachloride (CCl(4)). The contribution of both dietary (n-3) long-chain PUFA and nucleotides to the recovery of the altered fatty acid profiles of tissue lipids of these rats has also been studied. Two groups of rats were used. The first was intraperitoneally injected 0.15 ml of a 10% (v/v) CCl(4)solution in paraffin per 100 g of body weight, three times a week for 9 weeks; the second received paraffin alone. After the treatment, six rats of each group were killed. Afterwards, the remaining controls were fed a semipurified diet (SPD) for 3 weeks, and the remaining rats in the CCl(4)group were divided into three new groups: the first was fed the SP diet; the second was fed the SP diet supplemented with 1% (n-3) polyunsaturated fatty acids (PUFA diet); and the third was fed the SP diet supplemented with 250 mg nucleotides per 100 g diet (NT diet). Fatty acids of plasma, erythrocyte membranes and liver microsomes were analyzed. Decreases in linoleic and arachidonic acids in both total plasma lipids and liver microsomal phospholipids were the main findings due to CCl(4)treatment. The rats that received CCl(4)and the PUFA diet showed the lowest levels of (n-6) PUFA and the highest levels of (n-3) PUFA in liver microsomal phospholipids, as well as a significant increase of (n-3) PUFAs in total plasma lipids. The animals that received the NT diet showed no signs of fatty infiltration and exhibited the highest levels of (n-6) PUFAs in liver microsomal phospholipids. These results show that CCl(4)affects fatty acid metabolism which is accordingly reflected in altered tissue fatty acid profiles, and that balanced diets containing PUFA and nucleotides are important for the recovery of the damaged liver in rats.

Animals↗
PubMedDate not supplied

[Effect of estrogens on the free fatty acid content and fatty acid-binding protein fractions in rabbit intestinal mucosa].

A study was made of the effect of ovariectomy and administration of estradiol-dipropionate on the level of estrogen receptors, low molecular protein fractions, incorporating fatty acid binding proteins (FABP), and free fatty acids (FFA) in the protein fractions of the cytosol of the intestinal mucosa of mature and immature female rabbits. The female rabbit upper intestinal mucosa was shown to possess cytoplasmic estrogen receptors and to have low metabolic activity of estradiol dehydrogenase (not being target tissue). Ovariectomy caused a decrease in the level of estrogen receptors, protein fractions, incorporating FABP, and FFA in them in enterocyte mucosa cytosol as compared to respective parameters in female rabbits in the pubertal and mature periods of their development. Estrogens were involved in the regulation of the level of intestinal fatty acid binding protein fractions and in ensuring physiological concentrations of absorbed fatty acids.

Animals↗
PubMed2000

Influence of dietary fish oil on conjugated linoleic acid and other fatty acids in milk fat from lactating dairy cows.

Lactating cows were fed menhaden fish oil to elevate concentrations of conjugated linoleic acid, transvaccenic acid, and n-3 fatty acids in milk. Twelve multiparous Holstein cows at 48+/-11 DIM were assigned randomly to a replicated 4 x 4 Latin square. Each treatment period was 35 d in length, with data collected d 15 to 35 of each period. On a dry matter (DM) basis, diets contained 25% corn silage, 25% alfalfa hay, and 50% of the respective concentrate mix. Fish oil was supplemented at 0, 1, 2, and 3% of ration DM. Linear decreases were observed for DM intake (28.8, 28.5, 23.4, and 20.4 kg/d) and milk fat (2.99, 2.79, 2.37, and 2.30%) for 0 to 3% dietary fish oil, respectively. Milk yield (31.7, 34.2, 32.3, and 27.4 kg/d) increased as dietary fish oil increased from 0 to 1% but decreased linearly from 1 to 3% dietary fish oil. Milk protein percentages (3.17, 3.19, 3.21, and 3.17) were similar for all treatments. When the 2% fish oil diet was fed, concentrations of conjugated linoleic acid and transvaccenic acid in milk fat increased to 356% (to 2.2 g/ 100 g of total fatty acids) and 502% (to 6.1 g/100 g), respectively, of amounts when 0% fish oil was fed. There were no additional increases in these fatty acids when cows were fed 3% fish oil. The n-3 fatty acids increased from a trace to over 1 g/100 g of milk fatty acids, when the 3% fish oil diet was fed. Fish oil supplementation to diets of dairy cows increased the conjugated linoleic acid, transvaccenic acid, and n-3 fatty acids in milk.

Animal Feed↗