Influence of Ethanol on Carbohydrate- and Fat-Metabolism
155
Since alcohol leads to an elevated liberation of catecholamines this
raises the question whether the glycogenolytic effect of alcohol is caused by
the catecholamines liberated by alcohol; the catecholamines activate the
phosphorylase in the liver by means of increased formation of cyclic 3,5
AMP. Results from this laboratory show that glycogenolysis following
administration of alcohol is due to the catecholamines because this effect
could be prevented in mice pretreated with the tJ-sympathicolytic K6 592
(1-(isopropylamino )-3-(m-toloxy)-J-propanol. HCl).
Fat Metabolism
Besides glycogenolysis in the liver, lipolysis in the adipose tissue is
accelerated by alcohol as is shown in a decrease of the content of fat in the
epididymal adipose tissue and an increase of free fatty acids (FF A) in the
serum of rats 2 hrs after the i. v. injection of 2 mg/g alcohol [5].
Nearly 30-50 % of the FFA offered to the liver is taken up and esterified
by glycerol-1-P to triglycerides [15, 17]. The formation of triglycerides in
the liver depends on the concentration of FFA in the blood [16]. The delivery of triglycerides from the liver seems to be limited. Therefore one finds
an increase of the fat content in the liver when the uptake of FF A and the
synthesis of triglycerides exceed the ability of the liver to deliver triglycerides. For this reason there is an increase of triglycerides in the liver which
depends on the concentration of FF A in the serum [6, 7, 11]. The composition of the triglycerides in the liver after administration of alcohol
corresponds to that found in adipose tissue [8, 14].
The increased mobilization of FF A from adipose tissue following the
administration of alcohol, bringing about an elevation of FF A in the
serum and of the content of fat in the liver, seems to be an effect in which
the catecholamines, liberated by alcohol, play an important role. The reason
for this assumption is that these effects of alcohol can be prevented by
adrenalectomy [10], ex-sympathicolytics [3] and tJ-sympathicolytics [5].
Besides the increased mobilization of FF A, the elevated content of
glycerol-l-P in the liver seems to favour the formation of triglycerides
therein [12]. It is possible that the elevated offer of glycerol-l-P in the liver
leads to an increased extraction of FF A from the serum. The latter opinion
is supported by findings of BROWN et al. [4] who could observe an increased
uptake of i.v. administered He-palmitate by the liver in the presence of
alcohol.
References
1. ABELIN, 1., CH. HERREN and W. BERLI: Helv. med. acta 25, 591 (1958).
2. AMMON, H. P. T., c.-J. ESTLER and F. HElM: Arch. into Pharmacodyn. 159,
258 (1966).
155
Since alcohol leads to an elevated liberation of catecholamines this
raises the question whether the glycogenolytic effect of alcohol is caused by
the catecholamines liberated by alcohol; the catecholamines activate the
phosphorylase in the liver by means of increased formation of cyclic 3,5
AMP. Results from this laboratory show that glycogenolysis following
administration of alcohol is due to the catecholamines because this effect
could be prevented in mice pretreated with the tJ-sympathicolytic K6 592
(1-(isopropylamino )-3-(m-toloxy)-J-propanol. HCl).
Fat Metabolism
Besides glycogenolysis in the liver, lipolysis in the adipose tissue is
accelerated by alcohol as is shown in a decrease of the content of fat in the
epididymal adipose tissue and an increase of free fatty acids (FF A) in the
serum of rats 2 hrs after the i. v. injection of 2 mg/g alcohol [5].
Nearly 30-50 % of the FFA offered to the liver is taken up and esterified
by glycerol-1-P to triglycerides [15, 17]. The formation of triglycerides in
the liver depends on the concentration of FFA in the blood [16]. The delivery of triglycerides from the liver seems to be limited. Therefore one finds
an increase of the fat content in the liver when the uptake of FF A and the
synthesis of triglycerides exceed the ability of the liver to deliver triglycerides. For this reason there is an increase of triglycerides in the liver which
depends on the concentration of FF A in the serum [6, 7, 11]. The composition of the triglycerides in the liver after administration of alcohol
corresponds to that found in adipose tissue [8, 14].
The increased mobilization of FF A from adipose tissue following the
administration of alcohol, bringing about an elevation of FF A in the
serum and of the content of fat in the liver, seems to be an effect in which
the catecholamines, liberated by alcohol, play an important role. The reason
for this assumption is that these effects of alcohol can be prevented by
adrenalectomy [10], ex-sympathicolytics [3] and tJ-sympathicolytics [5].
Besides the increased mobilization of FF A, the elevated content of
glycerol-l-P in the liver seems to favour the formation of triglycerides
therein [12]. It is possible that the elevated offer of glycerol-l-P in the liver
leads to an increased extraction of FF A from the serum. The latter opinion
is supported by findings of BROWN et al. [4] who could observe an increased
uptake of i.v. administered He-palmitate by the liver in the presence of
alcohol.
References
1. ABELIN, 1., CH. HERREN and W. BERLI: Helv. med. acta 25, 591 (1958).
2. AMMON, H. P. T., c.-J. ESTLER and F. HElM: Arch. into Pharmacodyn. 159,
258 (1966).