Tags

Type your tag names separated by a space and hit enter

Delayed pro-opiomelanocortin activation after ethanol intake in man.
Alcohol Clin Exp Res 1994; 18(5):1226-9AC

Abstract

To elucidate the effect of ethanol on the secretion of ACTH and beta-endorphin (BE) as the representatives of the pro-opiomelanocortin (POMC) system, as well as cortisol as the hypophyseally regulated peripheral hormone, we measured concentrations of serum ethanol and plasma ACTH, BE, and cortisol at 1- to 4-hr intervals for 12 hr after administration of 0.5 and 1.0 g ethanol/kg of body weight and placebo drinks between 1900-1945 hr to nine healthy volunteers according to a double-blind, cross-over design. Plasma ACTH, BE, and cortisol showed an expected diurnal rhythm with the highest levels at 0700 hr. Intake of ethanol had no statistically significant effects on plasma ACTH up to 0700 hr in the morning. The higher dose caused increased levels of BE at 0100 hr and both doses at 0200 hr. Plasma cortisol at 0400 hr was higher in subjects receiving 1.0 g ethanol/kg than in those receiving placebo (p < 0.05). Our present observation that plasma ACTH was unchanged after ethanol intake, but plasma BE was increased at 0100-0200 hr may be due to the fact that our BE antiserum cross-reacts with beta-lipotropin, which has a considerably longer half-life than ACTH or BE, and also to the long sampling interval. Thus, the POMC system may have been stimulated after ethanol intake. The nocturnal rise of plasma cortisol levels at 0400 hr, 2-3 hr after the peak in plasma BE, may be caused by the increased secretion of POMC. Because the ethanol dose of 1.0 g/kg body weight stimulated the POMC system but the 0.5 g/kg body weight did not, we conclude that higher ethanol doses induce increases in stress hormone secretion.

Authors+Show Affiliations

Department of Physiology, University of Oulu Medical School, Finland.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

7847611

Citation

Ekman, A C., et al. "Delayed Pro-opiomelanocortin Activation After Ethanol Intake in Man." Alcoholism, Clinical and Experimental Research, vol. 18, no. 5, 1994, pp. 1226-9.
Ekman AC, Vakkuri O, Vuolteenaho O, et al. Delayed pro-opiomelanocortin activation after ethanol intake in man. Alcohol Clin Exp Res. 1994;18(5):1226-9.
Ekman, A. C., Vakkuri, O., Vuolteenaho, O., & Leppäluoto, J. (1994). Delayed pro-opiomelanocortin activation after ethanol intake in man. Alcoholism, Clinical and Experimental Research, 18(5), pp. 1226-9.
Ekman AC, et al. Delayed Pro-opiomelanocortin Activation After Ethanol Intake in Man. Alcohol Clin Exp Res. 1994;18(5):1226-9. PubMed PMID: 7847611.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Delayed pro-opiomelanocortin activation after ethanol intake in man. AU - Ekman,A C, AU - Vakkuri,O, AU - Vuolteenaho,O, AU - Leppäluoto,J, PY - 1994/10/1/pubmed PY - 1994/10/1/medline PY - 1994/10/1/entrez SP - 1226 EP - 9 JF - Alcoholism, clinical and experimental research JO - Alcohol. Clin. Exp. Res. VL - 18 IS - 5 N2 - To elucidate the effect of ethanol on the secretion of ACTH and beta-endorphin (BE) as the representatives of the pro-opiomelanocortin (POMC) system, as well as cortisol as the hypophyseally regulated peripheral hormone, we measured concentrations of serum ethanol and plasma ACTH, BE, and cortisol at 1- to 4-hr intervals for 12 hr after administration of 0.5 and 1.0 g ethanol/kg of body weight and placebo drinks between 1900-1945 hr to nine healthy volunteers according to a double-blind, cross-over design. Plasma ACTH, BE, and cortisol showed an expected diurnal rhythm with the highest levels at 0700 hr. Intake of ethanol had no statistically significant effects on plasma ACTH up to 0700 hr in the morning. The higher dose caused increased levels of BE at 0100 hr and both doses at 0200 hr. Plasma cortisol at 0400 hr was higher in subjects receiving 1.0 g ethanol/kg than in those receiving placebo (p < 0.05). Our present observation that plasma ACTH was unchanged after ethanol intake, but plasma BE was increased at 0100-0200 hr may be due to the fact that our BE antiserum cross-reacts with beta-lipotropin, which has a considerably longer half-life than ACTH or BE, and also to the long sampling interval. Thus, the POMC system may have been stimulated after ethanol intake. The nocturnal rise of plasma cortisol levels at 0400 hr, 2-3 hr after the peak in plasma BE, may be caused by the increased secretion of POMC. Because the ethanol dose of 1.0 g/kg body weight stimulated the POMC system but the 0.5 g/kg body weight did not, we conclude that higher ethanol doses induce increases in stress hormone secretion. SN - 0145-6008 UR - https://www.unboundmedicine.com/medline/citation/7847611/Delayed_pro_opiomelanocortin_activation_after_ethanol_intake_in_man_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0145-6008&amp;date=1994&amp;volume=18&amp;issue=5&amp;spage=1226 DB - PRIME DP - Unbound Medicine ER -