Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.4.1.2 (acetyl-CoA carboxylase)
 2,876 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An inhibitor and stimulator of in vitro hepatic fatty acid synthesis are present in renal microsomes. In addition, a stimulator of fatty acid synthesis is present in renal lysosomes. Renal microsomal inhibition of hepatic fatty acid synthesis is not due to the depletion of cofactors in the system. This inhibitor appears to be located exclusively in the kidney medullary microsomes. It is destroyed by Pronase and heat treatment suggesting it may be a protein. Its effects on fatty acid synthesis may be attributed in part to ATPase activity as well as a direct effect on the hepatic fatty acid synthesizing system. A stimulator of hepatic fatty acid synthesis is present in the buffer insoluble fraction of an acetone powder preparation of renal microsomes. This stimulator is relatively heat labile and does not appear to be a phospholipid. The lysosomal stimulator of hepatic fatty acid synthesis is associated with the contents of renal lysosomes and not with the lysosomal membranes. It acts at the acetyl-CoA carboxylase step and its activity is not affected by fasting or aminonucleoside induced nephrosis.
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PMID:Effect of renal microsomes and renal lysosomes on in vitro hepatic fatty acid synthesis. 113 13

Triamcinolone or triiodothyronine (T3) was administered to rats with nephrosis induced by aminonucleoside of puromycin and to control nontreated rats. Triamcinolone produced hyperglycemia, hyperinsulinemia and liver glycogen deposition in control rats and to a lesser extent in nephrotic rats. Triamcinolone treatment did not affect plasma protein and albumin levels but increased the level of plasma triglycerides and cholesterol in the very low density lipoprotein (VLDL) and LDL but not high density lipoprotein fractions. The exacerbation of hyperlipoproteinemia was attributed both to increase hepatic lipid synthesis and delayed removal, since it was associated with the induction of hepatic acetyl-CoA carboxylase, the regulatory enzyme of lipogenesis, as well as with marked suppression of adipose tissue lipoprotein lipase (LPL). The hepatic lipase activity was found to be elevated in nephrotic rats but was suppressed by triamcinolone treatment, indicating a reduced capacity of VLDL to LDL conversion. T3 treatment resulted in serum glucose and insulin increases similar to triamcinolone, but more moderate in nephrotic vs. control rats, and in marked reduction in liver glycogen content. Plasma protein levels were not affected, but contrary to control rats, T3 treatment produced an elevation in serum triglycerides and cholesterol in nephrotic rats. The activity of several hepatic lipogenic enzymes, including acetyl-CoA carboxylase, was markedly elevated, as was the activity of gluconeogenic enzymes. Thus, the hyperlipoproteinemia on T3 treatment appeared to be mainly due to predomination of lipid synthesis over removal, since the activities of enzymes responsible for plasma lipid disposal, adipose tissue LPL and hepatic lipase were enhanced both in control and nephrotic rats. It is remarkable that both T3 and triamcinolone induce the lipogenic enzymes and apolipoproteins in the liver of nephrotic rats, already pronouncedly stimulated to replace the excreted plasma proteins. Thus, the nephrotic liver is able to respond to hormonal stimulation with further specific protein and lipid synthesis. It is also pertinent that the recovery from immunosuppressive treatment of human nephrosis, developing on an immune background, may result in more impressive amelioration of proteinuria and hypoproteinemia than of hyperlipoproteinemia because of the lipidemic effect of glucocorticoids.
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PMID:Hyperlipoproteinemia of aminonucleoside-induced nephrotic syndrome--modulation by glucocorticoids and triiodothyronine. 868 44