A randomised controlled study of the effect of long chain polyunsaturated fatty acid supplementation on stool hardness during formula feeding.
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BACKGROUND: The passage of hard stools is significantly more common in formula fed infants than breast fed infants and this might be the result of differences in fat absorption between breast and formula fed infants. Experimental studies indicate that long chain polyunsaturated fatty acids (LCPUFAs) might influence fat hydrolysis and absorption. AIM: To investigate the relation of LCPUFA supplementation to stool frequency and consistency during the first 4 months of life. DESIGN: Double blind, randomised, controlled study of 88 healthy infants. RESULTS: 1905 stools (858 from LCPUFA supplemented infants, 1047 non-supplemented infants) were examined. The mean (SEM) number of stools passed for each three day study period was significantly less in the LCPUFA group (5.5 (0.3) v 6.2 (0.2); p < 0.05). In both groups, there was a significant reduction in the number of stools passed with age (p < 0.001). During the first 3 months, the mean (SEM) percentage of hard stools passed by infants in the LCPUFA supplemented group was 7.7 (2.1) compared with 19.2 (2.8) for unsupplemented infants (p = 0.001). CONCLUSION: The prevalence of hard stools is significantly reduced in infants fed a formula that is supplemented with LCPUFAs. (+info)
10-Undecynoic acid, an inhibitor of cytochrome P450 4A1, inhibits ethanolamine-specific phospholipid base exchange reaction in rat liver microsomes.
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1,12-Dodecanedioic acid, the end-product of omega-hydroxylation of lauric acid, stimulates in a concentration dependent manner, phosphatidylethanolamine synthesis via ethanolamine-specific phospholipid base exchange reaction in rat liver endoplasmic reticulum. On the other hand, administration to rats of 10-undecynoic acid, a specific inhibitor of omega-hydroxylation reaction catalyzed by cytochrome P450 4A1, inhibits the ethanolamine-specific phospholipid base exchange activity by 30%. This is accompanied by a small but significant decrease in phosphatidylethanolamine content in the endoplasmic reticulum and inhibition of cytochrome P450 4A1. On the basis of these results it can be proposed that a functional relationship between cytochrome P450 4A1 and phosphatidylethanolamine synthesis exists in rat liver. Cytochrome P450 4A1 modulates the cellular level of lauric acid, an inhibitor of phospholipid synthesis. In turn, ethanolamine-specific phospholipid base exchange reaction provides molecular species of phospholipids, containing mainly long-chain polyunsaturated fatty acid moieties, required for the optimal activity of cytochrome P450 4A1. (+info)
Regular exercise modulates muscle membrane phospholipid profile in rats.
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We investigated the effect of regular exercise and changes in dietary fatty acid profile on skeletal muscle phospholipid fatty acid profile in rats. Rats were randomly divided into three groups and for 4 wk fed either a carbohydrate-rich diet (CHO, 10 percent of total energy (E%) fat, 20 E% protein, 70 E% CHO) or one of two fat-rich diets (65 E% fat, 20 E% protein, 15 E% CHO) containing predominantly either saturated or monounsaturated fatty acids. Each dietary group was randomly assigned to a trained (6 d/wk, progressive to 60 min, 28 m/min at a 10 degrees incline) or a sedentary group. The effect of training was apparent in the three hindlimb muscles analyzed: red quadriceps, white quadriceps and soleus. The unsaturation index was significantly lower in the trained than in the sedentary groups (206 +/- 2 vs. 215 +/- 2, P < 0. 01), which largely reflected a lower content of arachidonic acid [20:4(n-6): 14.5 +/- 0.5 vs. 16.6 +/- 0.4% of total fatty acids, P < 0.01] and docosahexaenoic acid [22:6(n-3): 11.1 +/- 0.2 vs. 11.7 +/- 0.3% of total fatty acids, P < 0.03] and a concomitant higher content of linoleic acid [18:2(n-6): 20.0 +/- 0.4 vs. 17.8 +/- 0.4% of total fatty acids, P < 0.01]. Training affected skeletal muscle membrane structural composition, and this occurred independently of dietary fatty acid changes. This change likely reflects an increased utilization of highly unsaturated fatty acids for energy, an effect which may have deleterious effects on insulin action. (+info)
Metabolism of cholesterol is altered in the liver of C3H mice fed fats enriched with different C-18 fatty acids.
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We examined whether the degree of saturation of C-18 fatty acids influenced hepatic cholesterol metabolism in C3H mice. The mice were fed diets containing 20 g/100 g fat, enriched in stearic (18:0), oleic (18:1) or linoleic acid (18:2) with or without 1 g/100 g cholesterol. Plasma total cholesterol concentration was lower in mice fed the 18:0 diet relative to those fed the 18:1- or 18:2-enriched diets (P < 0.05) regardless of dietary cholesterol supplementation. Dietary cholesterol significantly raised hepatic total cholesterol concentration (P < 0.05) in those fed the 18:1- and 18:2-enriched diets, but not in mice fed the 18:0-enriched diet. Dietary cholesterol raised biliary cholesterol concentration (P < 0. 05) in mice fed the 18:1- and 18:2-enriched diets, but not in mice fed the 18:0-enriched diet. The cholesterol saturation index was variably affected by the fat diets. Feeding diets containing cholesterol suppressed the hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity and induced acyl coenzyme A:cholesterol acyl transferase (ACAT) activity compared with feeding diets without cholesterol (P < 0.05), indicating that the liver was exposed to dietary cholesterol. Hepatic ACAT activity was lower in mice fed the 18:0-enriched diet compared with those fed the 18:1- or 18:2-enriched diets (P < 0.05). Addition of cholesterol to the 18:1 diet induced the largest increase of hepatic ACAT activity, and this was associated with the enrichment of VLDL with cholesterol. Varying the degree of saturation of C-18 fatty acids influences the metabolism and disposition of hepatic cholesterol. (+info)
Scintigraphic evidence for a specific long-chain fatty acid transporting system deficit and the genetic background in a patient with hypertrophic cardiomyopathy.
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The mechanism of cardiac uptake of long-chain free fatty acids has not been fully determined. We encountered a hypertrophic cardiomyopathy patient who showed a lack of cardiac uptake of 2 different types of long-chain fatty acid analogues on the scintigraphic images. Flow cytometric analysis revealed no platelet or monocyte CD36 molecule expression (type I CD36 deficiency) and his CD36 gene showed homozygous mutation for 478C to T substitution, leading to an abnormal CD36 amino acid sequence. These findings strongly suggest that a specific transporting system rather than a simple diffusion is commonly involved in the cardiac uptake of long-chain free fatty acids in humans, and that the CD36 protein is the most likely candidate for the specific transporter and to explain scintigraphic defects on fatty acid imaging. (+info)
trans Fatty acids in human milk are inversely associated with concentrations of essential all-cis n-6 and n-3 fatty acids and determine trans, but not n-6 and n-3, fatty acids in plasma lipids of breast-fed infants.
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BACKGROUND: Human milk fatty acids vary with maternal dietary fat composition. Hydrogenated dietary oils with trans fatty acids may displace cis n-6 and n-3 unsaturated fatty acids or have adverse effects on their metabolism. The effects of milk trans, n-6, and n-3 fatty acids in breast-fed infants are unclear, although n-6 and n-3 fatty acids are important in infant growth and development. OBJECTIVE: We sought to determine the relations between trans and cis unsaturated fatty acids in milk and plasma phospholipids and triacylglycerols of breast-fed infants, and to identify the major maternal dietary sources of trans fatty acids. DESIGN: We collected milk from 103 mothers with exclusively breast-fed 2-mo-old infants, blood from 62 infants, and 3-d dietary records from 21 mothers. RESULTS: Mean (+/-SEM) percentages of trans fatty acids were as follows: milk, 7.1 +/- 0.32%; infants' triacylglycerols, 6.5 +/- 0. 33%; and infants' phospholipids, 3.7 +/- 0.16%. Milk trans fatty acids, alpha-linolenic acid (18:3n-3), arachidonic acid (20:4n-6), docosahexaenoic acid (22:6n-3) (P < 0.001), and linoleic acid (18:2n-6) (P = 0.007) were each related to the same fatty acid in infant plasma phospholipids. Milk trans fatty acids were inversely related to milk 18:2n-6 and 18:3n-3, but not to milk or infant plasma 20:4n-6 or 22:6n-3. trans Fatty acids represented 7.7% of maternal total fat intake (2.5% of total energy); the major dietary sources were bakery products and breads (32%), snacks (14%), fast foods (11%), and margarines and shortenings (11%). CONCLUSIONS: There were comparable concentrations of trans fatty acids in the maternal diet, breast milk, and plasma triacylglycerols of breast-fed infants. Prepared foods were the major dietary source of trans fatty acids. (+info)
Essential fatty acid requirements of vegetarians in pregnancy, lactation, and infancy.
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Long-chain polyunsaturated fatty acids (LCPUFAs) derived from linoleic (18:2n-6) and alpha-linolenic (18:3n-3) acids are required for the normal development of the retina and central nervous system, but the extent to which they can be synthesized from the parent fatty acids is debated. Consuming LCPUFAs markedly increases their proportions in tissue lipids compared with their parent fatty acids. Thus, it has been argued that LCPUFAs must be supplied in the diet. LCPUFAs are generally absent from plant foods, thus it is important find out how essential fatty acid requirements are met by vegetarians. A developing fetus obtains LCPUFAs via selective uptake from its mother's plasma and LCPUFAs are present in the breast milk of vegetarians. There is no evidence that the capacity to synthesize LCPUFAs is limited in vegetarians. However, there are greater proportions of n-6 LCPUFAs and lower proportions of n-3 LCPUFAs in vegetarians compared with omnivores. This difference is probably a consequence of the selection of foods by vegetarians with high amounts of linoleic acid. Although lower concentrations of docosahexaenoic acid (22:6n-3; DHA) have been observed in blood and artery phospholipids of infants of vegetarians, it is uncertain whether their brain lipids contain lower proportions of DHA than do those of infants of omnivores. On the basis of experiments in primates that showed altered visual function with a high ratio of linoleic acid to alpha-linolenic acid, it would be prudent to recommend diets with a ratio between 4:1 and 10:1 in vegetarians and that excessive intakes of linoleic acid be avoided. (+info)
Essential fatty acids in health and chronic disease.
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Human beings evolved consuming a diet that contained about equal amounts of n-3 and n-6 essential fatty acids. Over the past 100-150 y there has been an enormous increase in the consumption of n-6 fatty acids due to the increased intake of vegetable oils from corn, sunflower seeds, safflower seeds, cottonseed, and soybeans. Today, in Western diets, the ratio of n-6 to n-3 fatty acids ranges from approximately 20-30:1 instead of the traditional range of 1-2:1. Studies indicate that a high intake of n-6 fatty acids shifts the physiologic state to one that is prothrombotic and proaggregatory, characterized by increases in blood viscosity, vasospasm, and vasoconstriction and decreases in bleeding time. n-3 Fatty acids, however, have antiinflammatory, antithrombotic, antiarrhythmic, hypolipidemic, and vasodilatory properties. These beneficial effects of n-3 fatty acids have been shown in the secondary prevention of coronary heart disease, hypertension, type 2 diabetes, and, in some patients with renal disease, rheumatoid arthritis, ulcerative colitis, Crohn disease, and chronic obstructive pulmonary disease. Most of the studies were carried out with fish oils [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)]. However, alpha-linolenic acid, found in green leafy vegetables, flaxseed, rapeseed, and walnuts, desaturates and elongates in the human body to EPA and DHA and by itself may have beneficial effects in health and in the control of chronic diseases. (+info)