Utilization of long chain fatty acids by rat liver: Studies of the role of fatty acid binding protein

Burnett, David; Lysenko, N.; Manning, Joan A.; Ockner, Robert K.

doi:10.1016/0016-5085(79)90272-5

Cited by 118 publications

(35 citation statements)

References 31 publications

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“…There is evidence that L-FABP, stimulates fatty acid esterifying activities of the microsomes (35,36). The relationship between the changes in cytosolic fatty acid-binding and the accumulation of the major fatty acid esters, found in the present study, is consistent with this possibility.…”

Section: Discussionsupporting

confidence: 89%

Gender Differences in the Response of Hepatic Fatty Acids and Cytosolic Fatty Acid-Binding Capacity to Alcohol Consumption in Rats

Shevchuk

Baraona

et al. 1991

Experimental Biology and Medicine

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To investigate possible gender differences in the response of hepatic fatty acids and cytosolic fatty acid-binding capacity to ethanol consumption, both female and male rats (41 days of age) were pair fed liquid diets (with a littermate of the same sex) for 28 days. The diets contained 36% of energy either as ethanol or as additional carbohydrate. After ethanol feeding, the hepatic concentration of fatty acids increased 155% in females (P less than 0.01), whereas there was only a trend for an increase (22%) in males. This was associated with a much smaller increase of cytosolic fatty acid-binding capacity in females (58%) than in males (161%). Whereas the ethanol-induced increase in fatty acid-binding capacity provided an ample excess of binding sites for the fatty acids in males, the increase in females was barely sufficient for the binding of the large increase of fatty acids produced by ethanol in the females. The cytosolic protein responsible for this binding, the liver fatty acid-binding protein of the cytosol (L-FABPc), also promotes esterification of the fatty acids. In keeping with the postulated role of this protein, the ethanol-induced increases in hepatic triacylglycerols, phospholipids, and cholesterol esters were smaller in females than in males. The gender difference in cholesterol esters was associated with parallel changes in acyl-CoA transferase activity. A possible implication of the relatively small and most likely inadequate increase in liver fatty acid-binding capacity and fatty acid esterification during alcohol consumption in the females is that under these circumstances the risk for development of a potentially deleterious accumulation of fatty acids in the liver is increased, thereby contributing to the enhanced vulnerability of females to alcohol-induced hepatotoxicity.

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Section: Discussionsupporting

confidence: 89%

Gender Differences in the Response of Hepatic Fatty Acids and Cytosolic Fatty Acid-Binding Capacity to Alcohol Consumption in Rats

Shevchuk

Baraona

et al. 1991

Experimental Biology and Medicine

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“…On the other hand, an analysis of lipid droplets from rat livers showed no free fatty acids in the floating lipid layer (30). Other potentially mitigating factors are the binding of fatty acids to protein (31), and the presence of cholesterol (32).…”

Section: Discussionmentioning

confidence: 99%

Hepatic Free Fatty Acids in Alcoholic Liver Disease and Morbid Obesity

et al. 2007

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Alcoholic liver disease is characterized by the accumulation of fat and inflammatory changes in the liver. Because free fatty acids, the precursors of triglycerides, can damage biological membranes, accumulation of free fatty acids in the liver might be in part responsible for the functional and morphological changes seen in alcoholic liver disease. We, therefore, determined the hepatic lipid composition in biopsies from 31 patients with alcoholic liver disease, 18 patients with morbid obesity, and 5 patients without evidence of liver disease. Free fatty acids were found in all liver biopsies. Patients with morbid obesity or alcoholic liver disease had significantly higher fatty acid and triglyceride levels than did controls (p <, 0.01). Patients with alcoholic liver disease had significantly higher fatty acid levels than did patients with morbid obesity (p < 0.05), while there was no difference in the triglyceride concentrations between these two groups. The distribution of the fatty acids in the free fatty acid fraction differed significantly from that in the triglyceride fraction indicating a preferential incorporation of unsaturated fatty acids into triglycerides. This difference in the distribution pattern was lost in patients with the most severe forms of alcoholic liver disease. The data are consistent with the hypothesis that accumulation of free fatty acids in patients with alcoholic liver disease may be responsible for or contribute to the observed functional and morphological damages.

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“…This, in turn, results in enhanced microsomal -oxidation and peroxisomal ␤-oxidation of fatty acids and in a greater stimulatory effect of L-FABPc on microsomal acylglycerol synthesis [117].…”

Section: Physiological Role Of Cyp2e1 and Possible Therapeutic Intervmentioning

confidence: 99%

CYP2E1: from ASH to NASH

Lieber¹

2004

Hepatology Research

142

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Utilization of long chain fatty acids by rat liver: Studies of the role of fatty acid binding protein

Cited by 118 publications

References 31 publications

Gender Differences in the Response of Hepatic Fatty Acids and Cytosolic Fatty Acid-Binding Capacity to Alcohol Consumption in Rats

Gender Differences in the Response of Hepatic Fatty Acids and Cytosolic Fatty Acid-Binding Capacity to Alcohol Consumption in Rats

Hepatic Free Fatty Acids in Alcoholic Liver Disease and Morbid Obesity

CYP2E1: from ASH to NASH

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