Ethanol consumption affects stress response and insulin binding in tissues of rats.
OBJECTIVE
The mechanisms of harmful effect of excessive chronic ethanol intake on cardiovascular and neuronal systems, metabolic processes and protective effects of low ethanol intake on cerebrovascular and cardiovascular disturbances are not yet known. The aim of present study was to investigate the effect of short-term and long-term ethanol consumption on food intake, plasma levels of corticosterone (CS), glucose (G) and insulin (INS) in intact rats and in animals exposed to immobilization stress (IMO) or restrain stress (RESTR). The insulin binding to specific membrane receptors in adipocytes, muscle and liver was also determined.


METHODS
Adult male rats were fed liquid diet without and with ethanol (5% per weight) for 9-12 days (short-term intake) and at the end the animals were exposed to acute IMO stress. The second group of rats was fed solid diet and without or with ethanol in drinking water (6% per volume) for 52 days (long-term ethanol intake). A part of these animals was exposed to repeated restrain stress during 42 days. The groups of pair fed rats with the same food intake as in ethanol diet fed animals were in both experiments. The food intake, plasma glucose, insulin and corticoster-one levelswere determined. Plasma cell membranes were isolated from adipose, liver and skeletal muscle tissues and insulin binding to specific receptors was determined.


RESULTS
Decreased food consumption was observed after ethanol intake. Increased plasma G and CS were noted in rats fed ethanol diet for a short time. Plasma insulin levels were not affected by ethanol intake. Exposure to IMO stress resulted in increase of plasma G levels in controls and pair fed groups. A higher increase of CS plasma levels after IMO stress was noted in rats with ethanol intake for a short-time, however, no changes of plasma CS were noted after repeated exposure to restrain stress. Plasma levels of insulin were decreased after IMO and restrain stresses, while in rats fed ethanol diet for a short-time insulin decrease was deeper as compared to controls. The binding capacity of insulin receptors in adipose tissue was elevated in rats fed ethanol diet and deep decrease of insulin binding was noted in rats exposed to stress. In liver insulin binding was elevated after short-term ethanol intake and stress exposure resulted in decrease of insulin binding in ethanol fed rats. The binding capacity of insulin receptors in skeletal muscle was not changed in rats fed ethanol diet.


CONCLUSIONS
The results showed 1. differences in short term and long term ethanol intake on basal glucose, insulin and corticosterone levels, 2. effects of ethanol intake on changes of insulin plasma levels and insulin binding in adipose and liver tissues after exposure to stress, 3. effects of short term ethanol intake on the response of plasma hormones to immobilization stress.
Macho
Ladislav
L
Institute of Experimental Endocrinology, Slovak Academy of Sciences, 833 06 Bratislava, Slovakia. ueenlaco@savba.sk
Zorad
Stefan
S
Radikova
Zofia
Z
Patterson-Buckedahl
Patricia
P
Kvetnansky
Richard
R
D017667:Adipocytes / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002462:Cell Membrane / Q000378:metabolism; D003345:Corticosterone / Q000097:blood; D004032:Diet; D004435:Eating; D000431:Ethanol / Q000008:administration & dosage*; D007328:Insulin / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011972:Receptor, Insulin / Q000378:metabolism; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000378:metabolism*
D001786:Blood Glucose; D007328:Insulin; D000431:Ethanol; D011972:Receptor, Insulin; D003345:Corticosterone