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Mechanisms of catecholamine effects on ketogenesis
The American Journal of Physiology
|August 1, 1984
Summary
In humans, epinephrine and norepinephrine increase ketone body production by first boosting nonesterified fatty acid (NEFA) release. These findings highlight the liver
Area of Science:
- Metabolic regulation
- Endocrinology
Background:
- Ketogenesis is a metabolic process producing ketone bodies.
- Regulation occurs at multiple sites, including lipolysis and hepatic processing of fatty acids.
Purpose of the Study:
- To investigate the control sites of ketogenesis.
- To determine the role of catecholamines in regulating ketogenesis in humans and rats.
Main Methods:
- Infusion studies in humans with epinephrine, norepinephrine, somatostatin, and dopamine.
- Studies using perfused liver or hepatocytes.
- Infusion studies in rats.
Main Results:
- In humans, epinephrine and norepinephrine increase plasma nonesterified fatty acids (NEFA), glycerol, and ketone bodies.
- Catecholamine effects on ketogenesis are minimal in perfused liver/hepatocytes.
- Rat studies showed decreased ketogenesis with catecholamine infusion.
- Somatostatin potentiates catecholamine-induced lipolysis and ketogenesis.
Conclusions:
- Catecholamine-induced ketogenesis in humans is primarily driven by increased NEFA substrate supply from adipose tissue.
- Species differences exist in the regulation of ketogenesis.
- The liver's direct response to catecholamines for ketogenesis is limited.