ketogenesis


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Related to ketogenesis: ketogenic diet

ketogenesis

[¦kēd·ō′jen·ə·səs]
(biochemistry)
Production of ketone bodies.
References in periodicals archive ?
After establishing that activating the mTORC1 pathway decreases ketogenesis, Sengupta tried to find exactly where mTORC1 was acting.
When patients begin the rapid-loss diet, which is low in carbohydrates and fat, ketogenesis starts on day 2 and is in full effect by day 3 or 4.
The absence of insulin allows increased ketogenesis.
The net effect of AMPK activation is stimulation of hepatic fatty acid oxidation and ketogenesis, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipolysis and lipogenesis, stimulation of skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulation of insulin secretion by pancreatic beta-cells.
In T2DM, there is normally sufficient insulin to inhibit ketogenesis.
This effect can be attributed, at least in part, to the hypoglycemic action of sulphonylureas, since the primary actions of glucagon are to enhance the metabolism of stored glycogen, and to facilitate and/or increase gluconeogenesis and ketogenesis.
Table 1 Metabolic disorders that have presentations similar to Reye's syndrome Disorders of ureagencsis Partial ornithine transcarbamoylasc deficiency Partial carbamoylphosphatc deficicncy Partial arginosuccinic acid synthase deficiency Disorders of mitochondrial fatty acid oxidation and ketogenesis Medium-chain acyl-coenzyme A dehydrogenase deficiency Light-chain acyl-coenzyme A dehydrogenase deficiency Carnitine transport defect Organic acidurias Glutaricaciduria, type 1 Carbohydrate metabolism Respiratory-chain disorders
Because dietary short-chain fatty acids, mainly butyrate, are primary contributors to alimentary ketogenesis (Bergman, 1971), perhaps the ruminal fermentation of glycerol to butyrate increased plasma BHBA and decreased concentrations of glucose in plasma.
Fibroblast growth factor 21 regulates lipolysis in white adipose tissue but is not required for ketogenesis and triglyceride clearance in liver.
The NEFA are potential substrates for ketogenesis in the liver (Heitmann and Fernandez, 1986).
Responses of leptin to short-term fasting and refeeding in humans: a link with ketogenesis but not ketones themselves.