Regulation of Mammalian Fatty-Acid Synthetase. The Roles of Carbohydrate and Insulin

The regulation of fatty-acid synthetase has been studied in liver, adipose tissue, and brain of diabetic and normal rats in relation to insulin administration and glucose or fructose feeding. The data indicate that: (1) insulin is not necessary for regulation of synthetase activity in liver but may...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1974-03, Vol.71 (3), p.889-893
Main Authors: Volpe, Joseph J., Vagelos, P. Roy
Format: Article
Language:English
Subjects:
Adipose Tissue - enzymology
Adipose tissues
Animals
Biological Sciences: Biochemistry
Brain - enzymology
Diabetes
Diabetes complications
Diabetes Mellitus - chemically induced
Diabetes Mellitus - enzymology
Diabetic diets
Dose-Response Relationship, Drug
Enzyme Activation
Enzymes
Fatty Acid Synthases - analysis
Fatty Acid Synthases - metabolism
Fructose - pharmacology
Glucose - pharmacology
Hexoses - pharmacology
Immunoassay
In Vitro Techniques
Insulin
Insulin - pharmacology
Liver
Liver - enzymology
Physiological regulation
Precipitin Tests
Rats
Stimulation, Chemical
Streptozocin
Type 1 diabetes mellitus
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Summary:The regulation of fatty-acid synthetase has been studied in liver, adipose tissue, and brain of diabetic and normal rats in relation to insulin administration and glucose or fructose feeding. The data indicate that: (1) insulin is not necessary for regulation of synthetase activity in liver but may be necessary in adipose tissue; (2) synthetase of liver can be regulated by carbohydrate, which can enter the glycolytic scheme in the absence of insulin (e.g., fructose), suggesting the possibility that regulation of synthetase may depend on the concentration of certain intermediates of the glycolytic pathway or beyond; (3) fructose feeding affects the synthetase by causing an increase in the rate of synthesis of fatty-acid synthetase; and (4) unlike fatty-acid synthetase of liver and adipose tissue, the enzyme of brain is unaffected by the diabetic state or by glucose or fructose feeding.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.71.3.889