Fatty acid in liver

Trans fatty acids in liver of rats Silica AgNOj argentation 15... 

High acetyl CoA levels from 3-oxidation of fatty acids in liver cells inhibit the pyruvate dehydrogenase complex and activate pyruvate carboxylase, which increases oxaloacetate synthesis. 

What is the biochemical basis for the differential handling of medium-chain versus long-chain fatty acids in liver ... 

Cabre, E., Periago, J.L., Gonzalez, J., Gonzalez-Huix, F., Abad-Lacruz, A., Gil, A., Sancbez-Medina, F., Esteve- Comas, M., Fernandez-Ban-ares, F., Planas, R., Gassull, M.A. Plasma polyunsaturated fatty acids in liver cirrhosis with or without chronic hepatic encephalopathy a preliminary study. X. Parenter. Enter. Nutr. 1992 16 359-363... 

Phospholipids and glycosphingolipids are amphipathic lipid constituents of membranes (Chapter 10). They play an essential role in the synthesis of plasma lipoproteins (Chapter 20) and eicosanoids (Chapter 18). They function in transduction of messages from cell surface receptors to second messengers that control cellular processes (Chapter 30) and as surfactants. Cholesterol is mainly of animal origin and is an essential constituent of biomembranes (Chapter 10). In plasma, cholesterol is associated with lipoproteins (Chapter 20). Cholesterol is a precursor of bile acids formed in the liver of steroid hormones secreted by adrenals, gonads, and placenta and 7-dehydrocholesterol of vitamin D formed in the skin. In tissues, cholesterol exists primarily in the unesterified form (e.g., brain and erythrocytes), although appreciable quantities are esterified with fatty acids in liver, skin, adrenal cortex, and plasma lipoproteins. 

Mortiaux, A. and Dawson A. M., Plasma free fatty acids in liver disease, Gut, 2, 304, 1961. 

Although hypoglycin causes hypoglycemia, it acts by inhibiting an acyl CoA dehydrogenase involved in (3-oxidation that has specificity for short- and medium-chain fatty acids. Because more glucose must be oxidized to compensate for the decreased ability of fatty acids to serve as fuel, blood glucose levels may fall to extremely low levels. Fatty acid levels, however, rise because of decreased (3-oxidation. As a result of the increased fatty acid levels, a-oxidation increases, and dicarboxylic acids are excreted in the urine. The diminished capacity to oxidize fatty acids in liver mitochondria results in decreased levels of acetyl CoA, the substrate for ketone body synthesis. 

Conjugated Fatty Acids in Liver Lipid Classes of Mice Fed 1 % CLA (% of total fatty acids)... 

Propylthiouracil-treated animals also showed a decrease in the percent of linoleic acid distribution in liver. In spite of the results obtained by different authors (Ellefson and Mason, 1964 Mitchel and Truchot, 1962 Kirkeby, 1972), the changes in the percent distribution of total fatty acids in plasma are small and unimportant (Table 3). The probable explanation for the low linoleic acid concentration in liver could be that the supply of essential fatty acids from the diet does not parallel the increase of lipid degradation (Kirkeby, 1972), thereby giving a relative linoleic acid deficiency despite the food intake. The changes on A6 and A9 desaturation activities are not apparently related with the modifications observed in the percent distribution of total fatty acids in liver. This fact could be explained considering that the composition of liver and plasma lipids is a result of a balance between dietary fat, lipid, and carbohydrate metabolism, lipolysis of tissue lipids, and endocrinological factors. 

The particulars of the condensation mechanism will be disregarded for the moment. The essential point here is that 2-carbon fragments are formed from fatty acids which may then condense to yield acetoacetate. The fact that little or no isotope is found in the a- and y-carbons of acetoacetate from carboxyl-labeled fatty acids in liver - - or from carboxyl-labeled acetate in kidney slices provides evidence that the orientation of the carbons of the 2-carbon fragment is not altered. 

Crozier, GL, Fleith, M, Traitler, H and Finot, PA (1989) Black currant seed oil feeding and fatty acids in liver lipid classes of guinea pigs. Lipids, 24, 460-466. 

Ould El Kebir, M., Barnathan, G., Gaydou, E.M., Siau, Y, and Miralles, J. (2007) Fatty acids in liver, muscle and gonad of three tropical rays including non-methylene-interrupted dienoic fatty acids. Lipids, 42, 525-535. 

During more acute episodes the excretion of 3-hydroxyisovaleric acid increases. This metabolite is also observed in urine from patients with 3-methyl-crotonylglycinuria and tends to characterize that disorder (Section 10.3.2), but its occurrence is due to different mechanisms in the different diseases. In isovaleric acidaemia, the supply of glycine is exceeded by the accumulation of isovaleryl-CoA during periods of increased leucine catabolism (for example, high protein intake, infections) the isovaleryl-CoA is hydrolysed to free isovaleric acid which accumulates in turn in the tissues and body fluids. The free isovaleric acid is then oxidized to 3-hydroxyisovaleric acid and is excreted into the urine. The accumulation of isovaleric acid during these periods exacerbates the severity of the disease and produces the acute episodes observed. The isovaleric acid is believed to be oxidized by an a>-l oxidation process (Tanaka et al, 1968), which occurs simultaneously with co-oxidation of fatty acids in liver (Den, 1965). This is supported to some extent by the finding of low concentrations of methylsuccinic acid in urine, which had been stored for several years, from a patient with isovaleric acidaemia (Baerlocher etal, 1973). 

---