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PubMed2005

Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status: a potential marker of fetal insulin resistance.

BACKGROUND: Pregestational maternal diabetes increases obesity and diabetes risks in the offspring. Both conditions are characterized by insulin resistance, and diabetes is associated with low membrane arachidonic (AA) and docosahexaenoic (DHA) acids. OBJECTIVE: We investigated whether type 1 and type 2 diabetes in pregnancy compromise maternal and fetal membrane essential fatty acids (FAs). DESIGN: We studied 39 nondiabetic (control subjects), 32 type 1 diabetic, and 17 type 2 diabetic pregnant women and the infants they delivered. Maternal and cord blood samples were obtained at midgestation and at delivery, respectively. Plasma triacylglycerols and choline phosphoglycerides and red blood cell (RBC) choline and ethanolamine phosphoglyceride FAs were assessed. RESULTS: The difference in maternal plasma triacylglycerol FAs between groups was not significant. However, the type 1 diabetes group had lower plasma choline phosphoglyceride DHA (3.7 +/- 0.9%; P < 0.01) than did the control group (5.2 +/- 1.6%). Likewise, RBC DHA was lower in the type 1 [choline: 3.4 +/- 1.5% (P < 0.01); ethanolamine: 5.9 +/- 2.5% (P < 0.05)] and type 2 [choline: 3.5 +/- 1.6% (P < 0.05)] diabetes groups than in the control group (choline: 5.5 +/- 2.2%; ethanolamine: 7.5 +/- 2.5%). Cord AA and DHA were lower in the plasma (type 1: P < 0.01) and RBC (type 2: P < 0.05) choline phosphoglycerides of the diabetics than of the control subjects, and cord RBC ethanolamine phosphoglycerides were lower in DHA (P < 0.05) in both diabetes groups than in the control group. CONCLUSIONS: Diabetes (either type) compromises maternal RBC DHA and cord plasma and RBC AA and DHA. The association of these 2 FAs with insulin sensitivity may mean that the current finding explains the higher incidence of insulin resistance and diabetes in the offspring of diabetic women.

Adult↗

PubMed1987

The role of essential fatty acids in alcohol dependence and tissue damage.

Evidence for the role of essential fatty acids in alcohol dependence is reviewed. If alcohol-induced tissue damage is associated with impaired fatty acid and phospholipid metabolism, supplements of essential fatty acids might be beneficial in the treatment of alcoholics. The evidence for this effect is examined.

Adult↗

PubMed2000

Oxidant stress and essential fatty acids in patients with risk and established ARDS.

Oxygen free radicals are important mediators of both physiological and pathological events. In acute lung injury, the activated lymphocytes stimulate tumor necrosis factor (TNF) and other cytokines. These lymphokines augment free radical generation by polymorphonuclear leukocytes (PMNLs), macrophages and other cells which may ultimately produce acute respiratory distress syndrome (ARDS). This is supported by our results presented here in that there is a significant increase in lipid peroxidation products in patients with established ARDS. The amount of lipid peroxidation was significantly higher in the established ARDS group compared to patients who are at risk for ARDS. Nitric oxide concentrations were significantly decreased in established ARDS compared to the control and those who are at risk for ARDS. Fatty acid analysis of the plasma phospholipid fraction revealed a significant decreased in linoleic acid, gamma-linolenic acid, dihomo-gamma-linolenic acid and arachidonic acid levels of n-6 series and alpha-linolenic acid, eicosapentaenoic acid, docosa-hexanenoic acid of n-3 series. Patients who are at risk for ARDS have decreased levels of gamma-linolenic acid of the n-6 series, alpha-linolenic acid and eicosapentaenoic acid of the n-3 series. These results suggest that lipid peroxides and alteration in essential fatty acid metabolism may have a role in the pathogenesis of ARDS.

Arachidonic Acid↗

PubMed1979

The concentrations of free fatty acids, triglycerides and phospholipids in submandibular salivary glands of rats in essential fatty acid deficiency.

EFA deficiency was created in young weanling rats by feeding for 16 weeks purified diets containing 0% fat or 7% hydrogenated coconut oil (HCO). Control rats were fed similar diets which contained 7% corn oil or 5% HCO + 2% corn oil. Submandibular salivary gland (SMSG) lipids were extracted and analyzed for the concentration of the free fatty acids (FFA), triglycerides (TG), total lipid P and the proportions of various phospholipids. In EFA-deficient SMSG, the concentrations of FFA and TG fractions were lower compared to those of the controls. Total lipid P was either unaffected or slightly increased; the proportion of phospholipids was not changed. Possible reasons for these changes in SMSG lipids are discussed.

Animals↗

PubMed1976

Specific inhibition of hepatic fatty acid synthesis exerted by dietary linoleate and linolenate in essential fatty acid adequate rats.

Dietary linoleate and linolenate were investigated for their ability to specifically inhibit liver and adipose tissue lipogenesis in meal-fed (access to food 900-1,200 hr), essential fatty acid (EFA) adequate rats. Supplementing a high carbohydrate diet containing 2.5% safflower oil with 3% palmitate 16:0, oleate 18:1, or linoleate 18:2 did not affect in vivo liver or adipose tissue fatty acid synthesis. However, 18:2 addition to the basal diet did result in a significant (P less than 0.05) decline of liver fatty acid synthetase (FAS) and glucose-6-phosphate dehydrogenase (G6PD) activities. When the safflower oil content of the basal diet was reduced to 1%, the addition of 3% 18:2 or linolenate 18:3 significantly (P less than 0.05) depressed hepatic FAS, G6PD, and in vivo fatty acid synthesis by 50%. Addition of 18:1 caused no depression in hepatic FAS activity but did result in a significant (P less than 0.05) decline in liver G6PD activity and fatty acid synthesis which was intermediate between basal and basal +18:2- or +18:3-fed animals. Adipose tissue rates of lipogenesis were completely unaffected by dietary fatty acid supplementation. Similarly, the addition of 3 or 5% 18:3 to a basal diet for only one meal resulted in no change in lipogenesis relative to that in animals fed the basal diet. The data indicate that, like rats fed EFA-deficient diets, dietary 18:2 and 18:3 exert a specific capacity to depress rat liver FAS and G6PD activities and rate of fatty acid synthesis.

Adipose Tissue↗

PubMed1998

Essential fatty acid metabolism in infants with cholestasis.

Long-chain polyunsaturated fatty acids are important for the growth and early development of the central nervous system. Cholestatic infants suffer from fat malabsorption and disturbed lipid metabolism and therefore may be at risk of developing polyunsaturated fatty acid depletion. The aims of this study were to determine essential fatty acid status in cholestatic infants and to study the relationship to disease severity, degree of undernutrition, antioxidant status and mode of feeding. Twenty-four-hour dietary records were obtained in 34 cholestatic infants, and measurements were taken of skin fold thicknesses, bilirubin levels, activities of serum alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, prothrombin time, serum concentrations of albumin, bile acids, total lipids, phospholipids, cholesterol, vitamins A and E, the fatty acid composition of plasma phospholipids and plasma lipid peroxides expressed as thiobarbiturate reactive substance (TBARS). Plasma phospholipid fatty acids and TBARS were also determined in 12 age-matched healthy control infants. The cholestatic patients had very low percentage values of phospholipid essential fatty acids, particularly linoleic acid ( 18:2omega-6, median 14.74% vs 20.76% in controls, p < 0.001) and its major metabolite arachidonic acid (20:4omega-6, 6.80 vs 7.87%, p=0.04). The patients' essential fatty acid depletion was reflected by increased levels of the non-essential fatty acids, Mead acid (20:3omega-9, 0.74 vs 0.21%, p < 0.001) and palmitoleic acid (16:1omega-7, 2.20 vs 0.43%, p < 0.001). Polyunsaturated fatty acid profiles did not differ between infants with biliary atresia (n=13) and those with intrahepatic cholestasis (n=21), or between 17 infants with severe malnutrition (all skin folds < 10th percentile) and mild malnutrition (at least two skin folds > 10th percentile). TBARS were significantly higher in cholestatic patients than in controls (2.74 vs 0.85 nmol ml(-1), p < 0.001) and correlated with direct (r=0.41, p=0.02) and total bilirubin. The daily dietary intake of linoleic acid (per 100 kcal) correlated with plasma phospholipid linoleic acid (r=0.38,p=0.037) and total omega-6 fatty acids (r=0.38,p=0.036). Breastfed cholestatic infants (n=6) had higher values of the omega-3 long-chain polyunsaturated fatty acids docosapentanoic acid (22:5omega-3, 0.47 vs 0.28%, p=0.0006) and docosahexanoic acid (22:6omega-3, 2.39 vs 1.73%, p=0.01) than formula-fed infants, while disease severity was similar in the two groups. In conclusion, cholestatic infants are at high risk of essential fatty acid depletion, which appears to be related to fat malabsorption, hepatic essential fatty metabolism, enhanced lipid peroxidation and dietary intake.

Body Height↗

PubMed1985

Abnormal essential fatty acid composition of tissue lipids in genetically diabetic mice is partially corrected by dietary linoleic and gamma-linolenic acids.

Genetically diabetic mice (db/db) and their non-diabetic litter-mates were maintained for 15 weeks on diets supplemented with safflower oil or evening primrose (Oenothera bienis) oil, both essential fatty acid (EFA)-rich sources, or hydrogenated coconut oil (devoid of EFA). Plasma glucose was higher in the diabetic mice supplemented with the oils than in the unsupplemented diabetic mice. In the oil-supplemented non-diabetic mice, plasma glucose did not differ compared with the unsupplemented non-diabetic mice. The proportional content of arachidonic acid in the phospholipids of the pancreas was significantly decreased in diabetic mice, an effect which was completely prevented by supplementation with safflower or evening primrose oil but not hydrogenated coconut oil. In the liver phospholipids of the diabetic mice, dihomo-gamma-linolenic acid was proportionally increased, an effect reduced by supplementation with safflower oil but not evening primrose or hydrogenated coconut oils. In the liver triglycerides of the diabetic mice, gamma-linolenic acid, dihomo-gamma-linolenic acid and arachidonic acid were all proportionally decreased, effects which were also prevented by safflower or evening primrose oil but not hydrogenated coconut oil. Alopecia and dry scaly skin were prominent in the diabetic mice but less extensive in the diabetic mice supplemented with EFA.

Animals↗

PubMed1983

The role of essential fatty acids and prostaglandins in the premenstrual syndrome.

Many of the features of the premenstrual syndrome are similar to the effects produced by the injection of prolactin. Some women with the premenstrual syndrome have elevated prolactin levels, but in most the prolactin concentrations are normal. It is possible that women with the syndrome are abnormally sensitive to normal amounts of prolactin. There is evidence that prostaglandin E1, derived from dietary essential fatty acids, is able to attenuate the biologic actions of prolactin and that in the absence of prostaglandin E1 prolactin has exaggerated effects. Attempts were made, therefore, to treat women who had the premenstrual syndrome with gamma-linolenic acid, an essential fatty acid precursor of prostaglandin E1. Gamma-linolenic acid is found in human, but not cows', milk and in evening primrose oil, the preparation used in these studies. Three double-blind, placebo-controlled studies, one large open study on women who had failed other kinds of therapy for the premenstrual syndrome and one large open study on new patients all demonstrated that evening primrose oil is a highly effective treatment for the depression and irritability, the breast pain and tenderness, and the fluid retention associated with the premenstrual syndrome. Nutrients known to increase the conversion of essential fatty acids to prostaglandin E1 include magnesium, pyridoxine, zinc, niacin and ascorbic acid. The clinical success obtained with some of these nutrients may in part relate to their effects on essential fatty acid metabolism.

Clinical Trials as Topic↗

PubMed1995

Essential fatty acid consumption and risk of breast cancer.

Animal and ecological studies of essential fatty acids suggest that omega-3 fatty acids found in fish oils and omega-6 fatty acids found in vegetable oils may be playing a role in the etiology of breast cancer. Essential fatty acids may modulate breast cancer risk by interacting with prostaglandins, which have immunosuppressive and platelet aggregative capabilities. The fatty acid composition of adipose tissue reflects the dietary consumption of essential fatty acids over a period of years. Biochemical techniques have been used in epidemiological studies to accurately estimate fatty acid consumption. However, analytical epidemiology studies that have used biochemical measurements of adipose tissue fatty acid composition, have not supported a relationship between consumption of these essential fatty acids and breast cancer risk.

Adipose Tissue↗

PubMed1998

Lipid content and fatty acid composition in foods commonly consumed by nursing Congolese women: incidences on their essential fatty acid intakes and breast milk fatty acids.

The fat content and fatty acid (FA) composition of nearly 40 foods, currently consumed by 102 nursing Congolese mothers living in Brazzaville, were determined to assess their impact on mothers' essential fatty acid (EFA) intakes and breast milk FA. Data on mothers' milk FA and dietary habits which allowed food selection were recently published (Rocquelin et al., 1998). Most foods were locally produced. Food samples were collected at local markets, bleached if necessary to avoid microbial degradation, and stored at +4 degrees C or -20 degrees C. They were lyophilized upon their arrival in the laboratory before lipid analyses. FA composition of food lipids was determined by capillary gas chromatography. Staple diets included low-fat, high-carbohydrate foods (processed cassava roots, wheat bread) and high-polyunsaturated fatty acid (PUFA) foods: soybean oil (high in 18 : 2 n-6 and alpha-18 : 3 n-3), bushbutter (dacryodes edulis), peanuts, avocado (high in fat and 18 : 2 n-6), freshwater and salt-water fish (high in LC n-3 and/or n-6 PUFA), and leafy green vegetables (low in fat but very high in alpha-18 : 3 n-3). Their frequent consumption by nursing mothers provided enough EFA to meet requirements due to lactation. It also explains why mothers' breast milk was rich in C8-C14 saturated FA (26% of total FA) and in n-6, n-3 PUFA (respectively 15.0% and 2.4% of total FA) highly profitable for breastfed infants' development. From this point of view, dietary habits of Congolese mothers have to be sustained for they are more adequate than most Western-type diets.

Animals↗

PubMed1975

[Effect of an essential fatty acids free diet on the lipidic composition of rat testicles (author's transl)].

The effect of a fat free diet on the fatty acid composition and histological changes of the testis of old rats was studied to investigate the possible function of docosa-4,7,10,13,16-pentaenoic acid in rat testicles. The lipidic composition, the fatty acid composition, the conversion of docosa-7,10,13,16-tetraenoic acid to arachidonic acid and the activity of the 6-desaturase were determined during the different periods in which the rats received a fat free diet. Comparatively, the changes in the fatty acid composition of the liver were also studied. Only the liver showed a change in the triglyceride content during the first month of treatment, and it regained its normal values afterwards. Both liver and testis changed the fatty acid composition. An increase of the acids of the oleic series and a decrease of the components of the linoleic series were shown. These changes were similar to the ones provoked by an essential fatty acid deficient diet on young animals. The amount of docosa-4,7,10,13,16-pentaenoic acid was very little changed. No significant change was shown either in the retroconversion of docosa-7,10,13,16-tetraenoic acid to arachidonic acid. However, the 6-desaturase activity of the testis was enhanced by the fat deficient diet. The possibility that arachidonic acid in the adult rat is mainly supplied by linoleic acid and not by the retroconversion of docosa-4,7,10,13,16-pentaenoic acid is discussed.

Animals↗

PubMed1988

Increased vascular reactivity induced by essential fatty acid deficiency in rat autoperfused hindquarters.

The effects of essential fatty acid deficiency (EFAD) on vascular reactivity to vasoconstrictor stimuli were studied in rat autoperfused hindquarters. Weanling male Sprague-Dawley rats (aged 21 days) were fed diets containing 8% (weight/weight) of stearax plus 2% safflower oil (control diet) or 10% stearax (EFAD diet) for 8 weeks. There was no difference in systemic blood pressure or body weight between the two groups. Basal production of immunoreactive 6-keto-PGF1 alpha by aortic segments was much less in EFAD aortae than in control aortae. In contrast, immunoreactive 6-keto-PGF1 alpha produced by incubating aortic segments with exogenous arachidonic acid (12 mumol/l) was much greater in EFAD aortae than in control aortae. Moreover, conversion of [14C]-arachidonate to [14C]-6-keto-PGF1 alpha was more pronounced in EFAD aortae than in control aortae. Vasoconstrictor responses to noradrenaline (0.01-1.0 mumol/l) and angiotensin II (0.001-1.0 mumol/l) infused into the blood perfused hindquarters were then examined. The rats on the EFAD diet were more sensitive to both noradrenaline and angiotensin II than rats on the control diet (P less than 0.05, two-way ANOVA). Thus, a deficiency of essential fatty acids can lead to increased vascular sensitivity to vasoconstrictor stimuli. Deficiency of arachidonic acid in phospholipid stores is also accompanied by augmented cyclo-oxygenase activity in the vessel wall, similar to that observed previously in spontaneously hypertensive rats (SHR) and rats with one kidney renovascular hypertension.

6-Ketoprostaglandin F1 alpha↗

PubMed2002

A double-blind, randomized, placebo-controlled trial of essential fatty acid supplementation in the maintenance of remission of ulcerative colitis.

BACKGROUND: Essential fatty acid supplementation has been found to ameliorate certain chronic inflammatory diseases. This effect is thought to be mediated through the modulation of eicosanoid synthesis. Pro-inflammatory eicosanoids have been implicated in ulcerative colitis. AIM: To investigate the possible therapeutic benefit of essential fatty acids in quiescent ulcerative colitis to reduce the frequency of disease relapse. METHODS: A randomized, double-blind, placebo-controlled study was performed with a treatment duration of 12 months. Patients with quiescent disease received either trial medication (gamma-linolenic acid, 1.6 g, eicosapentaenoic acid, 270 mg, and docosahexaenoic acid, 45 mg, per day) or placebo (sunflower oil, 500 mg/day). The primary end-point was disease activity, assessed by a previously validated clinical index, sigmoidoscopic appearance and histology. RESULTS: Sixty-three patients were randomized, 31 to receive essential fatty acid treatment and 32 to receive placebo. Disease relapse rates were similar at 12 months (placebo, 38%; essential fatty acids, 55%), as were changes in sigmoidoscopic grade from baseline. CONCLUSIONS: The supplementation of the diet with this combination of essential fatty acids does not prolong the period of disease remission of ulcerative colitis.

Administration, Oral↗

PubMed1987

Rapid induction of essential fatty acid deficiency by intragastric infusion of triolein-supplemented total parenteral nutrition solutions: evidence of increased hepatic cholesterol esterification in the rat.

Rats were fed linoleic acid from a safflower oil emulsion or triolein-supplemented total parenteral nutrition solutions by continuous intragastric infusion for 7 and 14 d. Biochemical signs of essential fatty acid deficiency (EFAD) developed in rats supplemented with triolein compared with those receiving linoleic acid, and the relationship between hepatic cholesterol esterification and the distribution of free cholesterol in plasma lipoproteins was investigated in the EFAD and control animals. Results indicate that hepatic triglyceride (TG) and cholesterol ester content are greater and plasma levels of TG and cholesterol are lower in triolein-supplemented groups. Hepatic accumulation of cholesterol esters is associated with an increase in hepatic acyl-CoA:cholesterol acyltransferase activity and also with plasma very low density lipoprotein (VLDL) and high-density lipoprotein (HDL), which contain a greater proportion of cholesterol esters. These data suggest that EFAD can be rapidly induced with continuous intragastric feeding and that hepatic accumulation of cholesterol esters and enrichment of VLDL and HDL with cholesterol esters are early indicators of EFAD in the rat.

Acyl Coenzyme A↗

PubMed1977

Essential fatty acid deficiency induced by total parenteral nutrition and by medium-chain triglyceride feeding.

In hospitalized infants receiving either prolonged total parenteral nutrition without fat or a formula of medium-chain triglyceride, the fatty acid composition of platelet, red blood cell, and plasma lipids was determined. The results showed that the changes in the fatty acid composition occurred not only in plasma but also in platelets and red blood cells, and the decrease in linoleic and arachidonic acid and the concurrent increase in 5,8,11-eicosatrienoic acid were confirmed to be dramatic evidence of essential fatty acid deficiency. There was no effect of essential fatty acid deficiency upon the phospholipid distribution in red blood cells or plasma.

Animals↗

PubMed2003

Relationship between the niacin skin flush response and essential fatty acids in schizophrenia.

The skin flush response to niacin is selectively mediated by the release of vasodilatory prostaglandins from the skin. The normal skin flush response to niacin is attenuated in many individuals with schizophrenia (SCZ). This finding suggests abnormal prostaglandin signaling in SCZ. Since prostaglandins are derived from arachidonic acid (AA), the finding of an abnormal skin flush response is consistent with biochemical data suggesting relative depletion of AA, and other essential fatty acids (EFAs), in a substantial portion of people with SCZ. This paper will describe the mechanism of the skin flush response to niacin, and will review evidence that the response to niacin is abnormal in SCZ, that this abnormality is not related to psychotropic medications, and that it may be a marker of the EFA deficiency which has been documented to be present in many patients with SCZ.

Arachidonic Acid↗

PubMed1975

The effect of essential fatty acid deficiency upon fatty acid uptake by the brain.

Young adult rats, either control or essential fatty acid deficient, were administered either [3-H] oleic acid or [3-H] arachidonic acid by stomach tube. In addition, a group of control rats was given [3-H] palmitic acid. The rats were killed at various times therafter, and the radioactivity of the lipids of brain and plasma was examined. In confirmation of previous work, the blood lipid label was found to rise rapidly and then fall, wheras the activity of brain lipids increased slowly and did not show a decline through the 24-h period studied. Analysis of the brain uptake data according to first-order kinetics confirmed the impressions gained from visual inspection of the data. The initial rate of uptake of arachidonic acid was about 4.5 times that of oleic acid in control animals and in deficient animals. Essential fatty acid deficiency, however, did not induce an altered rate of uptake for either oleic acid or arachidonic acid. The rate of uptake of palmitic acid by control rats was not significantly different from that of oleic acid. Even though the initial rates of incorporation of oleic and arachidonic acids were not changed during essential fatty acid deficiency, the final levels of radioactivity obtained in brain lipids were higher in deficient rats with both fatty acids. The plateau value obtained with oleic acid was 1.5 times higher in deficient animals, while the plateau value for arachidonic acid was 1.7 times higher. An experiment in which deficient animals were allowed access to a control diet for 12 or 24 h prior to the labeling experiment suggested that the higher levels of radioactivity found in brain lipids of deficient animals was not due to an isotope dilution effect. Such animals still displayed the labeling pattern of deficient animals with arachidonic acid, while the results with oleic acid varied somewhat. Our results suggest that essential fatty acid deficiency does not alter the ability of the brain to take up the fatty acids studied. However, the fatty acids, especially arachidonic, are retained in the brain to a greater extent in the deficient animals.

Animals↗

PubMed2003

Essential fatty acids and the brain.

OBJECTIVE: To review the role of essential fatty acids in brain membrane function and in the genesis of psychiatric disease. METHOD: Medline databases were searched for published articles with links among the following key words: essential fatty acids, omega-3 fatty acids, docosahexanoic acid, eicosapentanoic acid, arachidonic acid, neurotransmission, phospholipase A2, depression, schizophrenia, mental performance, attention-deficit hyperactivity disorder, and Alzheimer's disease. Biochemistry textbooks were consulted on the role of fatty acids in membrane function, neurotransmission, and eicosanoid formation. The 3-dimensional structures of fatty acids were obtained from the Web site of the Biochemistry Department, University of Arizona (2001). RESULTS: The fatty acid composition of neuronal cell membrane phospholipids reflects their intake in the diet. The degree of a fatty acid's desaturation determines its 3-dimensional structure and, thus, membrane fluidity and function. The ratio between omega-3 and omega-6 polyunsaturated fatty acids (PUFAs), in particular, influences various aspects of serotoninergic and catecholaminergic neurotransmission, as shown by studies in animal models. Phospholipase A2 (PLA2) hydrolyzes fatty acids from membrane phospholipids: liberated omega-6 PUFAs are metabolized to prostaglandins with a higher inflammatory potential, compared with those generated from the omega-3 family. Thus the activity of PLA2 coupled with membrane fatty acid composition may play a central role in the development of neuronal dysfunction. Intervention trials in human subjects show that omega-3 fatty acids have possible positive effects in the treatment of various psychiatric disorders, but more data are needed to make conclusive directives in this regard. CONCLUSION: The ratio of membrane omega-3 to omega-6 PUFAs can be modulated by dietary intake. This ratio influences neurotransmission and prostaglandin formation, processes that are vital in the maintenance of normal brain function.

Aged↗