Kidney fatty acid synthesis

MVA is now known to be metabolized by routes other than those which give rise to terpenoids and steroids. The breakdown occurs predominantly in the kidneys to give C2 units that can be utilized in fatty-acid synthesis. The sterol and the shunt pathways have been evaluated in nine different tissues of rat previous conclusions that the kidneys are the predominant site of both types of metabolism have been confirmed. MVA is known to accumulate, at a low level, in the blood, and these results suggest that impairment of renal clearance of serum MVA by either route may account for the hypercholesterolaemia associated with some kidney disorders. A study of the effects of possible antimetabolites of MVA (for example the 2,3-anhydro-compound) on the formation of cholesterol in cell-free systems from liver has been reported. ... 

Acetyl-CoA synthetase has been crystallized from heart mitochondria. In heart, kidney and skeletal muscle it is confined to the mitochondrial matrix but in adipose tissue and mammary gland it is also present in the cytosol. In liver, it is only found in the cytosol. Where tissues contain the extramitochondrial enzyme, it is because they require acetate to be activated as the first step in fatty acid synthesis (section 3.2.2). 

Mercury is known to exert an effect on the synthesis of membrane lipids. Mercuric chloride produces lipid alteration in pig kidney epithelial cells (LLC-PK, cells), with rapid accumulation of unesterified fatty acids (particularly arachidonic acid) and lysophospholipids and loss of cellular phospholipids... 

Fat synthesis in the liver (right). Fatty acids and fats are mainly synthesized in the liver and in adipose tissue, as well as in the kidneys, lungs, and mammary glands. Fatty acid biosynthesis occurs in the cytoplasm—in contrast to fatty acid degradation. The most important precursor is glucose, but certain amino acids can also be used. 

Carbon tetrachloride causes centrilobular liver necrosis and steatosis after acute exposure, and liver cirrhosis, liver tumors, and kidney damage after chronic administration. The mechanism underlying the acute toxicity to the liver involves metabolic activation by cytochrome P-450 to yield a free radical (trichloromethyl free radical). This reacts with unsaturated fatty acids in the membranes of organelles and leads to toxic products of lipid peroxidation including malondialdehyde and hydroxynonenal. This results in hepatocyte necrosis and inhibition of various metabolic processes including protein synthesis. The latter leads to steatosis as a result of inhibition of the synthesis of lipoproteins required for triglyceride export. 

Butyrate appears to have its most profound effects on neoplastic cells such as HeLa in addition to morphological and biochemical differentiation, the fatty acid inhibits cell growth (2). Previous studies have established a correlation between decreased ganglioside synthesis and malignant transformation (43-46). Transformed baby hamster kidney and newborn rat kidney cells exhibited a loss of GM3 and sialyl transferase activity (43,44). 

Biotin forms part of several enzyme systems and is necessary for normal growth and body function. Biotin functions as a cofactor for enzymes involved in carbon dioxide fixation and transfer. These reactions are important in the metaboHsm of carbohydrates, fats, and proteins, as well as promotion of the synthesis and formation of nicotinic acid, fatty acids, glycogen, and amino acids (5—7). Biotin is absorbed unchanged in the upper part of the small intestine and distributed to all tissues. Highest concentrations are found in the Hver and kidneys. Little information is available on the transport and storage of biotin in humans or animals. A biotin level in urine of approximately 160 nmol/24 h or 70 nmol/L, and a circulating level in blood, plasma, or serum of approximately 1500 pmol/L seems to indicate an adequate supply of biotin for humans. However, reported levels for biotin in the blood and urine vary widely and are not a reHable indicator of nutritional status. 

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