Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Fatty Alcohols”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1986

[Immunohistochemical studies on the occurrence of HBs antigen in alcoholic fatty liver and alcoholic fatty liver hepatitis].

120 liver biopsies of alcoholic fatty liver, alcoholic hepatitis and cirrhosis were studied immunohistochemically with regard to the occurrence of HBs-antigen. In no instance HBs-antigen was detected. These findings suggest neither a major influence of hepatitis B-virus on the progression of alcoholic liver cell damage nor a defect in immunologic responsiveness to hepatitis B-virus component in the alcoholic.

Adult↗
PubMed1997

1-Alkenyl group of ethanolamine plasmalogen derives mainly from de novo-synthesized fatty alcohol within peroxisomes, but not extraperoxisomal fatty alcohol or fatty acid.

The origin of the 1-alkenyl group of ethanolamine plasmalogen was investigated. Three candidates were examined for the fatty alcohol forming the 1-alkenyl group. [1-(14)C]Hexadecanoic acid, [1-(14)C]hexadecanol, or [1-(14)C]lignoceric acid was administered to rats treated with 0.25% clofibrate-chow for 2 weeks. At 0.5, 1, 2, 3, and 4 h after administration of the radiolabeled compound, rats were killed and ethanolamine-containing phosphoglyceride (EPG)-rich fraction was isolated from the liver. The components of the 1-radyl group in EPG-rich fraction were separated and the radioactivity was determined. The radiolabel after administration of [1-(14)C]hexadecanoic acid or [1-(14)C]hexadecanol was almost wholly incorporated into diacyl-type glycerophosphoethanolamine (GPE), and was predominantly found in hexadecanoic acid fraction. Therefore, the long-chain fatty acid may be incorporated intact into the diacyl groups, and the long-chain fatty alcohol may be similarly incorporated after oxidation to the acid. In contrast, the radiolabel after the administration of [1-(14)C]lignoceric acid was found in the 1-alkenyl group of ethanolamine plasmalogen. After hydrolysis of the 1-alkenyl group by treatment of the plasmalogen with HCl vapor, the radiolabeled products were chiefly stearaldehyde and palmitaldehyde. The above data indicate that nascent fatty alcohol de novo synthesized from acetyl-CoA derived by peroxisomal beta-oxidation is almost exclusively used as the fatty alcohol forming the 1-alkenyl group of ethanolamine plasmalogen.

Aldehydes↗
PubMed1988

Interaction of amphiphiles with integral membrane proteins. I. Structural destabilization of the anion transport protein of the erythrocyte membrane by fatty acids, fatty alcohols, and fatty amines.

The effect of model amphiphiles on the structural stability of the anion exchange protein (band 3) of the human erythrocyte membrane was studied by differential scanning calorimetry. The concentration of membranes, as well as the concentration, head group, alkyl chain length, degree of unsaturation, and double bond configuration of a variety of alkane derivatives were all varied in a systematic way. The depression of the denaturation temperature of band 3 per unit membrane concentration of the amphiphile was then determined in order to quantitate the potency of each drug. Saturated fatty acids of chain length C8 to C24 displayed a monotonic decrease in potency up to C20, followed by a dramatic diminution in potency at C22 and C24. Unsaturation caused only minor increases in the abilities of fatty acids to perturb the anion exchanger, and surprisingly, there was neither a trend for the number of double bonds nor a significant cis-trans distinction. Arachidonic acid, as an exception, was much more effective than any other amphiphile in destabilizing band 3. Fatty acids were about three times more potent than fatty amines and fatty alcohols; however, the enhanced partitioning of the latter into the membrane compensated at certain membrane/buffer ratios for its reduced intrinsic potency. A quantitative model interpretation of the data is presented in an accompanying paper.

Amines↗
PubMed1984

[Alcoholic fatty liver, alcoholic hepatitis and alcoholic cirrhosis. Drinking behavior and incidence of clinical, clinico-chemical and histological findings in 282 patients].

Drinking pattern as well as clinical, biochemical and histological findings were recorded of 282 males with alcohol-induced liver disease (fatty liver in 103, hepatitis in 61, cirrhosis in 118). The proportion of persons under 50 years of age was significantly greater with alcoholic hepatitis (70%) than cirrhosis (46%). Mean daily alcohol consumption was clearly lower among those with fatty liver than hepatitis or cirrhosis (P less than 0.02). Duration of alcohol abuse was on average shorter in patients with fatty liver and hepatitis than with cirrhosis (excessive consumption of less than 15 years was 61% and 62%, respectively, in the former, 28% in the latter (P less than 0.02). Symptoms and clinical and biochemical findings did not help in differentiating between hepatitis without cirrhotic change and cirrhosis. The most marked differences between cirrhosis and hepatitis, on one hand, and fatty liver, on the other, related to the frequency of certain signs and symptoms: upper abdominal pain, hard consistency of the liver, generalized jaundice, bleeding from esophageal varices and ascites; among biochemical findings they were: elevation of serum-bilirubin concentration above 34 mumol/l (2 mg/dl), lowering of the Quick values and of albumin concentration. Mortality rate during hospital stay was lower among patients with hepatitis but no cirrhotic change (6.6%) than among those with cirrhotic change (31.4%). While the prognosis under abstinence was relatively more favourable in patients with mild or moderately severe hepatitis, nonicteric forms require closer attention than has been given them so far.

Adult↗
PubMed1988

Sjögren-Larsson syndrome. Impaired fatty alcohol oxidation in cultured fibroblasts due to deficient fatty alcohol:nicotinamide adenine dinucleotide oxidoreductase activity.

Lipid metabolism was studied in cultured skin fibroblasts from patients with the inherited disorder, Sjögren-Larsson syndrome (SLS). Intact SLS fibroblasts incubated in the presence of [1-14C]palmitate accumulated more radioactive hexadecanol than did normal cells, whereas incorporation of radioactivity into other cellular lipids was unaltered. The hexadecanol content of SLS fibroblasts was abnormally elevated. Hexadecanol accumulation was not due to increased fatty alcohol synthesis nor its deficient utilization for glycerol ether synthesis. The half-life of intracellular hexadecanol loaded into SLS fibroblasts was increased (70 min) compared with normal (15 min), and intact SLS fibroblasts showed impaired oxidation of [14C]-hexadecanol to fatty acid. Fatty alcohol:NAD+ oxidoreductase, the enzyme catalyzing this reaction, was deficient in SLS fibroblasts. Mean total activity in SLS fibroblasts (n = 5) was 13% of that in normal fibroblasts, and palmitoyl CoA-inhibitable activity was 1% of normal. Fibroblasts from two obligate SLS heterozygotes had enzyme activities intermediate between that in normal fibroblasts and individuals with SLS. These results suggest that the primary defect in SLS is deficiency of fatty alcohol:NAD+ oxidoreductase. SLS represents the first inherited disorder in man associated with an isolated abnormality in fatty alcohol metabolism.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1987

Fatty alcohol metabolism in cultured human fibroblasts. Evidence for a fatty alcohol cycle.

Intact cultured human fibroblasts reduced [1-14C]palmitate to radioactive hexadecanol in a concentration-dependent manner. In the presence of 30 microM radioactive palmitate, cellular levels of labeled hexadecanol increased over time and reached a steady state corresponding to at least 0.1% of cell-associated radioactive palmitate. These levels of [14C]hexadecanol were increased up to 10-fold when exogenous nonradioactive hexadecanol was present, suggesting that radioactive hexadecanol was actively metabolized. Cells incubated in fatty acid-free medium with [1-14C]hexadecanol rapidly oxidized it to palmitic acid; less than 2% of the hexadecanol taken up by the cells was incorporated into the ether linkage of phosphatidylethanolamine, and no incorporation into wax esters was detected. Double-label experiments involving incubation of intact fibroblast with [3H]palmitate and [14C]hexadecanol demonstrated simultaneous synthesis of hexadecanol from palmitate and oxidation of hexadecanol to palmitate. Addition of exogenous palmitate to the medium of intact cells inhibited the oxidation of hexadecanol to fatty acid in a concentration-dependent fashion. This was associated with an increase in the fibroblast content of hexadecanol and loss of hexadecanol into the medium. Activity of fatty alcohol:NAD+ oxidoreductase, which catalyzes the oxidation of hexadecanol to palmitic acid, was inhibited by palmitoyl-CoA and NADH, but not by palmitic acid. These results are consistent with the presence of a "fatty alcohol cycle" in which hexadecanol is synthesized from palmitate via acyl-CoA and simultaneously oxidized back to free fatty acid. Fatty acyl-CoA, which is the primary substrate for fatty alcohol synthesis, may also regulate the intracellular level of fatty alcohol by inhibiting its oxidation.

Acyl Coenzyme A↗
PubMed1979

Fatty alcohols in capelin, herring and mackerel oils and muscle lipids: I. Fatty alcohol details linking dietary copepod fat with certain fish depot fats.

It is shown that the shorter chain (C14-C18) minor fatty alcohols in copepods, fish body lipids, and commercial fish oils are all qualitatively present, and quantitatively similar in proportions to acids found in the depot fats of capelin and mackerel, and in some herring. Although these fatty acids can be formed de novo in fish, copepod alcohols offer an alternative dietary source. Monoethylenic fatty alcohol details, especially for the 22:1 isomers, are reviewed, and the latter are discussed as precursors of the 22:1 fatty acids of fish depot fats, specifically of the dominant 22:1 omega 11 isomer.

Animals↗
PubMed1998

Metadoxine accelerates fatty liver recovery in alcoholic patients: results of a randomized double-blind, placebo-control trial. Spanish Group for the Study of Alcoholic Fatty Liver.

BACKGROUND/AIMS: Our aim was to investigate the effectiveness of metadoxine (pyridoxol L, 2 pyrrolidone-5-carboxylate) in the treatment of alcoholic fatty liver. METHODS: A double-blind randomized multicenter trial involving 136 chronic active alcoholic patients diagnosed with fatty liver by clinical, biochemical and ultrasonographic criteria was performed. Patients were treated with 1500 mg/day of metadoxine (n = 69) or placebo (n = 67) for 3 months. Patients were clinically and biochemically evaluated every month. Ultrasonography was performed before and after treatment. RESULTS: At the end of the study there was a significant improvement in the liver function tests in both groups. However, the changes were more rapid and greater in patients treated with metadoxine, in whom significant changes in serum levels of bilirubin, aminotransferases and gammaglutamyl transpeptidase were already observed after 1 month of treatment, and normalization of these parameters was observed at the end. After treatment, the percentage of patients with ultrasonographic signs of steatosis was significantly lower in the metadoxine group (28% vs 70%, p < 0.01) and the degree of steatosis was also lower in this group. Sixteen patients treated with metadoxine and 15 with placebo continued drinking. Alcohol intake was lower than initially, and similar in both groups. In the metadoxine group, the biochemical changes were similar in both the abstinent and the nonabstinent patients. In contrast, in the placebo group the improvement in the liver function tests was significantly higher in abstinents. Among patients who continued drinking, the prevalence (45% vs 92%, p < 0.05) and the degree of steatosis were also significantly lower in patients treated with metadoxine. CONCLUSIONS: In patients with alcoholic fatty liver, metadoxine accelerates the normalization of liver function tests and the ultrasonographic changes, even in those who do not completely abstain from alcohol intake. Thus, metadoxine could be useful in the treatment of the early stages of alcoholic liver disease.

Adult↗
PubMed1995

Determinants of progression to cirrhosis or fibrosis in pure alcoholic fatty liver.

"Pure" alcoholic fatty liver has been widely assumed to be "benign" with very low risk of progression to cirrhosis. Studies thus far have included either patients with coexisting recognised precursor lesions of cirrhosis or have been restricted to short-term histological follow-up. We have followed 88 patients, first seen between 1978 and 1985, with a histological diagnosis of pure alcoholic fatty liver and no evidence of fibrosis or alcoholic hepatitis, for a median of 10.5 years, to determine any factors predictive of disease progression. Of the 88, at follow-up nine had developed cirrhosis and a further seven fibrosis. Eight of nine patients with cirrhosis had continuing alcohol consumption of more than 40 units per week at follow-up; in the other patients, consumption was unknown. Independent histological predictors of progression on index biopsy were: presence of mixed macro/microvesicular fat, and presence of giant mitochondria. We can no longer regard alcoholic fatty liver as benign. In the presence of continuing high alcohol consumption the above histological features identified those at high risk (47-61%) of disease progression. Therefore, patients with these features should be counselled intensively regarding their alcohol consumption.

Adult↗
PubMed1989

Sjögren-Larsson syndrome: inherited defect in the fatty alcohol cycle.

We investigated fatty alcohol metabolism in eight patients with Sjögren-Larsson syndrome, and in nine obligate heterozygotes. Fatty alcohol: nicotinamide-adenine dinucleotide oxidoreductase (FAO) activity was deficient in cultured skin fibroblasts (mean 18% of normal, n = 8) and peripheral blood leukocytes (mean 22% of normal, n = 3) from patients with Sjögren-Larsson syndrome. The palmitoyl coenzyme A-inhibitable component of FAO activity was decreased to 10% and 15% of normal in fibroblasts and leukocytes, respectively, of patients with Sjögren-Larsson syndrome. Most affected patients accumulated long-chain fatty alcohol in plasma, with a greater relative accumulation of octadecanol (mean threefold greater than normal) than hexadecanol (mean twofold greater than normal). Erythrocyte lipid alkyl ether linkages derived from hexadecanol were slightly increased in three of four patients. Fibroblasts and leukocytes from heterozygotes with Sjögren-Larsson syndrome showed mean FAO activities that were intermediate between those seen in homozygotes and in normal control subjects. The heterozygotes had normal fatty alcohol concentrations in plasma. These studies demonstrate FAO deficiency in patients with Sjögren-Larsson syndrome, and suggest that accumulation of fatty alcohol or its metabolic products may be important in the pathogenesis of this disorder.

Adolescent↗