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Epinephrine-induced changes in hepatic glucose production after ethanol
C H Lang1, P E Molina, N Skrepnick
1Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
The American Journal of Physiology
|June 1, 1994
Summary
Acute alcohol (ethanol) intoxication impairs the body's glucose response to endotoxin by reducing the liver's glucose production, not by affecting catecholamine levels or epinephrine response.
Area of Science:
- Endocrinology
- Metabolic research
- Toxicology
Background:
- Catecholamines are crucial for glucose metabolism during endotoxin exposure.
- Acute alcohol intoxication disrupts normal metabolic responses to endotoxins.
Purpose of the Study:
- To investigate if alcohol (ethanol) attenuates endotoxin's effects by altering plasma catecholamines or epinephrine responsiveness.
- To understand alcohol's impact on glucose metabolism and the body's response to epinephrine.
Main Methods:
- Studies were conducted on fasted rats with chronic intravenous catheters, infused with either ethanol or saline.
- Plasma catecholamine levels (epinephrine, norepinephrine) were measured after endotoxin administration.
- Whole-body glucose metabolism was assessed using [3-3H]glucose infusion during epinephrine stimulation.
Main Results:
- Endotoxin administration equally increased plasma epinephrine and norepinephrine in both saline- and ethanol-infused rats.
- Epinephrine infusion caused hyperglycemia in control rats by increasing hepatic glucose production and decreasing glucose clearance.
- Ethanol infusion blunted the epinephrine-stimulated increase in hepatic glucose production without altering insulin or glucagon levels.
Conclusions:
- Ethanol intoxication impairs the metabolic response to endotoxin primarily by reducing hepatic glucose production, not by altering catecholamine levels or epinephrine's overall hyperglycemic effect.
- The impairment of glucose production by ethanol is independent of alcohol dehydrogenase activity.