linoleic-acid and Syndrome

Chronic idiopathic pain syndromes are major causes of personal suffering, disability, and societal expense. Dietary n-6 linoleic acid has increased markedly in modern industrialized populations over the past century. These high amounts of linoleic acid could hypothetically predispose to physical pain by increasing the production of pro-nociceptive linoleic acid-derived lipid autacoids and by interfering with the production of anti-nociceptive lipid autacoids derived from n-3 fatty acids. Here, we used a rat model to determine the effect of increasing dietary linoleic acid as a controlled variable for 15 weeks on nociceptive lipid autacoids and their precursor n-6 and n-3 fatty acids in tissues associated with idiopathic pain syndromes.. Increasing dietary linoleic acid markedly increased the abundance of linoleic acid and its pro-nociceptive derivatives and reduced the abundance of n-3 eicosapentaenoic acid and docosahexaenoic acid and their anti-nociceptive monoepoxide derivatives. Diet-induced changes occurred in a tissue-specific manner, with marked alterations of nociceptive lipid autacoids in both peripheral and central tissues, and the most pronounced changes in their fatty acid precursors in peripheral tissues.. The present findings provide biochemical support for the hypothesis that the high linoleic acid content of modern industrialized diets may create a biochemical susceptibility to develop chronic pain. Dietary linoleic acid lowering should be further investigated as part of an integrative strategy for the prevention and management of idiopathic pain syndromes.

Topics: Animals; Autacoids; Dietary Fats; Fatty Acids, Omega-3; Linoleic Acid; Male; Nociception; Organ Specificity; Oxylipins; Pain; Rats, Inbred F344; Syndrome

The object of this study was to investigate whether the levels of cardiolipin in cultured skin fibroblasts of patients with Barth syndrome (BTHS) can be restored by addition of linoleic acid to growth media. To this end, fibroblasts from controls and BTHS patients were grown in the presence or absence of linoleic acid. High-performance liquid chromatography-electrospray ionization tandem mass spectrometry was used for quantitative and compositional analysis of cardiolipin. Incubation of cells from both BTHS and controls with different concentrations of linoleic acid led to a dose- and time-dependent increase of cardiolipin levels. The increased levels of cardiolipin in fibroblasts of BTHS patients after treatment with linoleic acid indicate that an increased amount of linoleic acid in the diet might be beneficial to BTHS patients.

Topics: Adolescent; Cardiolipins; Cells, Cultured; Child; Chromatography, High Pressure Liquid; Fibroblasts; Genetic Diseases, X-Linked; Humans; Infant; Linoleic Acid; Phosphatidylglycerols; Spectrometry, Mass, Electrospray Ionization; Syndrome

The potential effects of oil specimens related to cases of toxic oil syndrome (TOS) on the liver microsomal lipid composition from guinea pigs were investigated. For four weeks, animals were fed diets supplemented with either "case oil" (oil related to cases of TOS) or "control oil" (oil unrelated to cases of TOS), either previously heated or not. Results were compared with those from guinea pigs fed the same diet with no oil. The administration of case oil produced changes in liver microsomal lipid composition. Statistically significant differences were also found between heated case and heated control oils. The cholesterol/phospholipid molar ratios and the major phospholipid class distribution were unaffected under these diet conditions. However, increases in the relative contents of linoleic and arachidonic acids and, simultaneously, a reduction in palmitic and palmitoleic acid levels were observed by diet effects. Heated oil administration decreased the saturated/unsaturated ratios in all cases. Our data suggest that changes observed in the fatty acid composition are attributable to the free fatty acid contents of administered oils. The toxic constituents of case oil seem to be able to alter the liver microsomal lipid composition.

Topics: Aniline Compounds; Animals; Brassica; Dietary Fats, Unsaturated; Fatty Acids; Fatty Acids, Monounsaturated; Guinea Pigs; Linoleic Acid; Linoleic Acids; Lipid Metabolism; Male; Microsomes, Liver; Oils; Oleic Acid; Oleic Acids; Palmitic Acid; Palmitic Acids; Plant Oils; Rapeseed Oil; Stearic Acids; Syndrome

Phospholipid class, peak profile of each phospholipid class, loosely bound fatty acids, covalently (tightly) bound fatty acids of the erythrocyte membranes, and plasma fatty acids were investigated using high-performance liquid chromatography in six patients with chorea-acanthocytosis and 14 age- and sex-matched normal control subjects. Additionally, six patients with Huntington's disease were included as disease control subjects in the study of covalently bound fatty acids. Study of covalently (tightly) bound fatty acids in erythrocyte membrane proteins after alkaline hydrolysis, hitherto undescribed in chorea-acanthocytosis, revealed that palmitic acid (C16:0) was significantly increased and stearic acid (C18:0) was decreased in the patients with chorea-acanthocytosis. Analyses for total covalently bound fatty acids disclosed that palmitic and docosahexaenoic (C22:6) acids were increased and stearic acid was decreased in chorea-acanthocytosis. Phospholipid class (phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and phosphatidylserine) and peak profile of each phospholipid class from the erythrocyte membranes did not differ between the patients with chorea-acanthocytosis and the control subjects. Of the loosely bound fatty acids, linoleic acid (C18:2) was significantly decreased in those with chorea-acanthocytosis, which seemed to be nonspecific.

Topics: Acanthocytes; Adult; Chorea; Erythrocyte Membrane; Fatty Acids; Female; Humans; Huntington Disease; Linoleic Acid; Linoleic Acids; Male; Membrane Lipids; Membrane Proteins; Middle Aged; Palmitic Acid; Palmitic Acids; Phospholipids; Stearic Acids; Syndrome

The total and free fatty acid composition of plasma and lipid peroxide concentrations was studied in 32 cholestatic children with syndromatic paucity of interlobular bile ducts (Alagille's syndrome). The mean lipid peroxide value in these patients was 8.80 +/- 3.70 nmol/ml, nearly 4 times higher than the mean control value. Compared to the control group, the patients exhibited significant variations in total fatty acids, and in particular a relative decrease in linoleic acid (from 29.5 +/- 6.1% in the controls to 19.1 +/- 8.03% in the patients) compensated by an increase in saturated and monounsaturated fatty acids. The plasma lipid peroxide levels were inversely correlated with the unsaturated/saturated fatty acids ratio in total fatty acids, and with the vitamin E status (vitamin E/total lipids). Most of the total and free fatty acid variations observed were largest in patients with severe jaundice. Dietary fat malabsorption and the increase in lipid peroxidation partly explain these results. Furthermore, in free fatty acids, we observed a marked increase in arachidonic acid (from 1.43 +/- 0.85% in the controls to 4.27 +/- 2.24% in the patients), suggesting abnormal eicosanoid synthesis.

Topics: Adolescent; Bile Ducts; Bilirubin; Child; Child, Preschool; Cholestasis; Fatty Acids; Fatty Acids, Nonesterified; Fatty Acids, Unsaturated; Humans; Infant; Linoleic Acid; Linoleic Acids; Lipid Peroxidation; Lipid Peroxides; Syndrome; Vitamin E

At least two groups of schizophrenics will be described. One such group may have a mutant delta-6-desaturase which prefers the omega-6-series essential fatty acids over the omega-3 series essential fatty acids resulting in low cis-linoleic acid blood levels. This subgroup may be related to the low histamine type schizophrenia. In contrast, we describe the possible existence of another group of schizophrenic patients with elevated cis-linoleic acid blood levels, elevated fasting insulin levels, elevated EGOT and urinary kryptopyrolle termed "delta-6-pyroluria." The etiology of this group may be due to a block instead of a mutant delta-6-desaturase. The elevated fasting insulin level may be an attempt to overcome the malfunctioning pathway.

Topics: Alprostadil; Aspartate Aminotransferases; Fatty Acid Desaturases; Fatty Acids, Essential; Humans; Insulin; Linoleic Acid; Linoleic Acids; Linoleoyl-CoA Desaturase; Mutation; Prostaglandins; Pyrroles; Schizophrenia; Syndrome

Topics: Arachidonic Acid; Humans; Hypersensitivity; Immune System Diseases; Linoleic Acid; Liver Diseases; Syndrome

Topics: Arachidonic Acid; Humans; Hypersensitivity; Immune System Diseases; Linoleic Acid; Liver Diseases; Syndrome