Essential fatty acid status in patients.
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The aim of this study was to determine whether plasma and red cell fatty acid levels were associated with cardiovascular disease, and whether any association was independent of other major risk factors. Over 1100 subjects were examined in a random sample survey of the general population (the Edinburgh Artery Study). Fatty acids were measured in three plasma fractions (triglyceride, cholesteryl ester and phospholipid) and in red cell phospholipids. Fatty acid levels in groups with cardiovascular disease (myocardial infarction (MI), angina and lower limb disease) were compared with a no disease group. In the cholesteryl ester and phospholipid fractions there were significantly lower levels of eicosapentaenoic acid in the MI group on univariate analysis (p<0.05), but not when adjusted for age, sex, smoking and systolic blood pressure using logistic regression. In the red cell fraction, alpha-linolenic acid was significantly lower in those with stroke (p<0.01) and lower limb disease (p<0.05). Linoleic acid was significantly raised in the triglyceride fraction in those with MI, probably reflecting recent dietary changes. There were significant increases in dihomo-gamma-linolenic acid in the phospholipid and red cell fractions in those with MI, and in the phospholipid fraction in the stroke group. These results do not support the hypothesis that n-6 fatty acids are protective against cardiovascular disease, although there may be some beneficial effects of the n-3 fatty acid, alpha-linolenic acid. Results from cross-sectional surveys must, however, be interpreted with caution because the presence of disease may affect dietary intake.
The present report deals with a densitometric study of the ultrastructural images of the urothelial membrane of rats in the following experimental conditions: (1) EFA-deficient (EFAD) rats; (2) EFA-sufficient (EFAS) rats; and (3) EFAD rats that were fed the EFAD diet for 30 weeks and received an EFAS diet for the following 10 weeks (EFAD/S group). On electron micrographs of the transitional epithelium of ureters and urinary bladder of these rats, optical density (OD) profiles of the urothelial unit membrane were recorded and digitized using a computer-controlled microdensitometer with a solid-state self-scanned photodiode array sensor. A Gaussian curve was adopted as a model for the distribution of electron-dense material in each osmiophilic leaflet. Gaussian parameters were used to estimate the thickness of the urothelial membrane and of each osmiophilic leaflet, and the amount of electron-dense material and the maximal electron density present in each leaflet. In EFAS rats, the thick urothelial membrane was asymmetric like that of the normal, resulting from a greater thickness of the outer leaflet and a greater electron density of the cytoplasmic one. In EFAD rats, a loss of the characteristic ultrastructural asymmetry and a decrease of the total thickness of the unit membrane were detected. These changes were partially reversed in the EFAD/S rats.
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Pregnant zinc deficient and zinc adequate rats were injected subcutaneously with evening primrose oil throughout gestation and for 3 days post partum. The nursing pups were injected intragastrically with zinc-65 on day 3 of live and sacrifices 4 h later. The % of the total injected zinc recovered in the carcass (minus the gut and gut contents) was significantly increased in those pups nursed by mothers injected with evening primrose oil, regardless of their dietary zinc intake. The fatty acid composition of the total lipid extract of the gut and gut contents of the neonates with increased zinc-65 absorption indicated that these pups had higher proportions of arachidonic acid and other metabolites of linoleic acid than did those with lower zinc-65 absorption. In other 3-day-old rat pups, intragastric injection of linoleic, gamma-linolenic or dihomo-gamma-linolenic acids along with the dose of zinc-65 very significantly increased zinc-65 absorption in a dose-related manner. Arachidonic acid however had no significant effect on zinc-65 absorption. Prostaglandin E1 caused a significant increase in zinc-65 absorption but prostaglandin E2 had no consistent effect. Indomethacin caused a dose-related inhibition of zinc-65 absorption.
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Impaired conversion of linoleic acid to gamma-linolenic acid (GLA) has been demonstrated in animal diabetes and inferred from blood fatty acid profiles in human diabetes. This impairment could theoretically lead to defective nerve function because metabolites of GLA are known to be important in nerve membrane structure, nerve blood flow, and nerve conduction. Administration of GLA corrects the impaired nerve function in animal models of diabetes. Two multicenter, randomized, placebo-controlled trials in humans with diabetic neuropathy have shown significant benefits of GLA as compared with placebo in neurophysiological parameters, thermal thresholds, and clinical sensory evaluations. Further work is needed to define the place of this therapeutic approach and its interactions with other treatment modalities.
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Previous studies have shown that chronic administration of SR-3 (a 1:4 mixture of alpha-linolenic and linoleic acid) affects spatial learning, thermoregulation, pain threshold, and protection from seizures. The mode of action of SR-3 is unknown. One possible explanation is that SR-3 induces changes in the FA profile and in the cholesterol level in neuronal membranes. This study used 10 independent groups of rats (ni = 12) given 4 weeks of either saline, mineral oil (vehicle), alpha-tocopherol (antioxidant), alpha-linolenic acid, linoleic acid, or one of 5 different ratios of alpha-linolenic acid:linoleic acid (1:3, 1:4, 1:5, 1:6, 1:7) as free fatty acids. FA profile and cholesterol level were examined by GC method in synaptosomes obtained from the frontal cortex of the rats. The mineral oil treated group served as the control group. No difference was found in the FA profile or cholesterol level except for the SR-3 treated group. The ratio of 1:4 was found to have a significant influence on decreasing the cholesterol level and in inducing major changes in the FA profile, such as an increase in EFA. These effects of SR-3 may result in modification of the membrane fluidity, which may, in turn, enhance cognitive and neuropharmacological effects.
A study on how EFA deficiency affects lipid metabolism of rat skin, especially lipid on skin surface, was made. The total amount of lipid on skin surface of rat increased due to EFA deficiency, but not significantly. The sterol ester in skin surface lipid was maintained at a normal level in a EFA deficient rat, but the free sterol level was higher than that of the control rat. The glycerides decreased markedly due to EFA deficiency. It was recognized that branched fatty acids increased in each lipid fraction on skin surface. It was considered that such changes in skin surface lipid were characteristic to skin. It was not predictable whether these changes resulted directly from EFA deficiency or secondary from the occurrence of dermal symptoms.
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