Regulation of fatty acid synthesis via phosphorylation of acetyl-CoA carboxylase

1. The effect of nutritional status on fatty acid synthesis in brown adipose tissue was compared with the effect of cold-exposure. Fatty acid synthesis was measured in vivo by 3H2O incorporation into tissue lipids. The activities of acetyl-CoA carboxylase and fatty acid synthetase and the tissue concentrations of malonyl-CoA and citrate were assayed. 2. In brown adipose tissue of control mice, the tissue content of malonyl-CoA was 13 nmol/g wet wt., higher than values reported in other tissues. From the total tissue water content, the minimum possible concentration was estimated to be 30 microM 3. There were parallel changes in fatty acid synthesis, malonyl-CoA content and acetyl-CoA carboxylase activity in response to starvation and re-feeding. 4. There was no correlation between measured rates of fatty acid synthesis and malonyl-CoA content and acetyl-CoA carboxylase activity in acute cold-exposure. The results suggest there is simultaneous fatty acid synthesis and oxidation in brown adipose tissue of cold-exposed mice. This is probably effected not by decreases in the malonyl-CoA content, but by increases in the concentration of free long-chain fatty acyl-CoA or enhanced peroxisomal oxidation, allowing shorter-chain fatty acids to enter the mitochondria independent of carnitine acyltransferase (overt form) activity.

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Chronic ethanol administration depresses fatty acid synthesis in rat adipose tissue

Biochemical Journal ◽

10.1042/bj2510547 ◽

1988 ◽

Vol 251 (2) ◽

pp. 547-551 ◽

Cited By ~ 8

Author(s):

J S Wilson ◽

M A Korsten ◽

L P Donnelly ◽

P W Colley ◽

J B Somer ◽

...

Keyword(s):

Adipose Tissue ◽

Fatty Acid ◽

Fatty Acid Synthesis ◽

Fatty Acid Synthetase ◽

Acid Synthesis ◽

Chronic Ethanol ◽

Ethanol Administration ◽

Acetyl Coa Carboxylase ◽

Acetyl Coa ◽

Chronic Ethanol Administration

Administration of ethanol as part of a nutritionally adequate liquid diet to female Wistar rats was found to depress markedly incorporation of labelled glucose into adipose-tissue acylglycerol fatty acids. Similar results with labelled pyruvate and acetate suggested inhibition of the fatty-acid-synthesis pathway at, or distal to, the acetyl-CoA carboxylase step. Activities of acetyl-CoA carboxylase and fatty acid synthetase were markedly lower in ethanol-fed animals. The activity of another lipogenic enzyme, phosphatidate phosphohydrolase, was not affected by chronic ethanol feeding. These findings suggest that chronic ethanol administration has marked effects on adipose-tissue lipogenesis.

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Stimulation of hepatic lipogenesis and acetyl-coenzyme A carboxylase by vasopressin

Biochemical Journal ◽

10.1042/bj1980485 ◽

1981 ◽

Vol 198 (3) ◽

pp. 485-490 ◽

Cited By ~ 21

Author(s):

F Assimacopoulos-Jeannet ◽

R M Denton ◽

B Jeanrenaud

Keyword(s):

Fatty Acid ◽

Dose Response ◽

Fatty Acid Synthesis ◽

Response Curve ◽

Acid Synthesis ◽

Dose Response Curve ◽

Dependent Manner ◽

Hepatic Lipogenesis ◽

Acetyl Coa Carboxylase ◽

Acetyl Coa

The effect of vasopressin on the short-term regulation of fatty acid synthesis was studied in isolated hepatocytes from rats fed ad libitum. Vasopressin stimulates fatty acid synthesis by 30-110%. This increase is comparable with that obtained with insulin. Angiotensin also stimulates fatty acid synthesis, whereas phenylephrine does not. The dose-response curve for vasopressin-stimulated lipogenesis is similar to the dose-response curve for glycogenolysis and release of lactate plus pyruvate. Vasopression also stimulates acetyl-CoA carboxylase activity in a dose-dependent manner. Vasopressin does not relieve glucagon-inhibited lipogenesis, whereas insulin does. The action of vasopressin on hepatic lipogenesis is decreased, but not suppressed, in Ca2+-depleted hepatocytes. The results suggest that vasopressin acts on lipogenesis by increasing availability of lipogenic substrate (lactate + pyruvate) and by activating acetyl-CoA carboxylase.

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