The Influence of Ethanol on
Carbohydrate- and Fat-Metabolism of the Liver
H. P. T. AMMON
Abstract
In white mice the administration of alcohol enhances the glycogenolysis of the
liver and the lipolysis of adipose tissue by means of increased liberation of catecholamines from the adrenal medulla. Liver glycolysis is accelerated via glycerol1-P. The increased content of glycerol-1-P in the liver and of free fatty acids in
the serum leads to an increased formation and deposition of triglycerides in the
liver.
The liver is not only the organ frequently damaged by alcohol but also
the organ where the major part of the first step of alcohol oxidation takes
place. During this process considerable quantities of NADH2 are formed.
Furthermore alcohol leads to an increased liberation of catecholamines
from the adrenal medulla [1, 9, 13, 18]. Since both the enhanced formation
of NADH2 in the liver and the increased liberation of catecholamines
influence the carbohydrate and fat-metabolism of the liver, we investigated
the influence of alcohol on the glycolytic carbohydrate breakdown and the
metabolism of fat in this organ.
Carbohydrate Metabolism
In female white mice 10 and 30 min after the i.v. injection of 4.1 or
1.5 mg!g alcohol the contents of glycogen and pyruvate in the liver decrease whereas fructose-l,6-P 2 (FDP), dioxyacetone-P (DAP) and glycerol1-P increase. The lactate content is elevated only after 10 min. In the following hours the lactate content is below normal levels [2].
The diminution of the glycogen content and the increase of FDP, DAP
and glycerol-l-P point to an acceleration of the glycolytic carbohydrate
breakdown in the upper part of the glycolytic pathway via glycerol-l-P.
The increase of glycerol-l-P in the liver is caused by the excessive formation
of NADH2 which carries the hydrogen from alcohol to DAP forming
glycerol-l-P. The reduction of pyruvate and of lactate which is increased
for not more than 10 min show that in mice the formation of the final
products of the glycolytic pathway is reduced.
Carbohydrate- and Fat-Metabolism of the Liver
H. P. T. AMMON
Abstract
In white mice the administration of alcohol enhances the glycogenolysis of the
liver and the lipolysis of adipose tissue by means of increased liberation of catecholamines from the adrenal medulla. Liver glycolysis is accelerated via glycerol1-P. The increased content of glycerol-1-P in the liver and of free fatty acids in
the serum leads to an increased formation and deposition of triglycerides in the
liver.
The liver is not only the organ frequently damaged by alcohol but also
the organ where the major part of the first step of alcohol oxidation takes
place. During this process considerable quantities of NADH2 are formed.
Furthermore alcohol leads to an increased liberation of catecholamines
from the adrenal medulla [1, 9, 13, 18]. Since both the enhanced formation
of NADH2 in the liver and the increased liberation of catecholamines
influence the carbohydrate and fat-metabolism of the liver, we investigated
the influence of alcohol on the glycolytic carbohydrate breakdown and the
metabolism of fat in this organ.
Carbohydrate Metabolism
In female white mice 10 and 30 min after the i.v. injection of 4.1 or
1.5 mg!g alcohol the contents of glycogen and pyruvate in the liver decrease whereas fructose-l,6-P 2 (FDP), dioxyacetone-P (DAP) and glycerol1-P increase. The lactate content is elevated only after 10 min. In the following hours the lactate content is below normal levels [2].
The diminution of the glycogen content and the increase of FDP, DAP
and glycerol-l-P point to an acceleration of the glycolytic carbohydrate
breakdown in the upper part of the glycolytic pathway via glycerol-l-P.
The increase of glycerol-l-P in the liver is caused by the excessive formation
of NADH2 which carries the hydrogen from alcohol to DAP forming
glycerol-l-P. The reduction of pyruvate and of lactate which is increased
for not more than 10 min show that in mice the formation of the final
products of the glycolytic pathway is reduced.