Sexual dimorphic expression of ADH in rat liver: importance of the hypothalamic-pituitary-liver axis

Hepatic alcohol dehydrogenase (ADH) activity is higher in female than in male rats. Although sex steroids, thyroid, and growth hormone (GH) have been shown to regulate hepatic ADH, the mechanism(s) for sexual dimorphic expression is unclear. We tested the possibility that the GH secretory pattern de...

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Published in:American journal of physiology: Gastrointestinal and liver physiology 2002-09, Vol.283 (3), p.G646-G655
Main Authors: Simon, Francis R, Fortune, John, Iwahashi, Mieko, Sutherland, Eileen
Format: Article
Language:English
Subjects:
Alcohol Dehydrogenase - genetics
Alcohol Dehydrogenase - metabolism
Aldehyde Dehydrogenase - metabolism
Animals
Castration
Female
Gonadal Steroid Hormones - pharmacology
Growth Hormone - secretion
Hormones - pharmacology
Hypothalamo-Hypophyseal System - physiology
Liver - enzymology
Liver - physiology
Male
Pituitary Hormones - physiology
Protein Biosynthesis
Rats
Rats, Sprague-Dawley
RNA, Messenger - metabolism
Sex Characteristics
Weight Gain - drug effects
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Summary:Hepatic alcohol dehydrogenase (ADH) activity is higher in female than in male rats. Although sex steroids, thyroid, and growth hormone (GH) have been shown to regulate hepatic ADH, the mechanism(s) for sexual dimorphic expression is unclear. We tested the possibility that the GH secretory pattern determined differential expression of ADH. Gonadectomized and hypophysectomized male and female rats were examined. Hepatic ADH activity was 2.1-fold greater in females. Because protein and mRNA content were also 1.7- and 2.4-fold greater, results indicated that activity differences were due to pretranslational mechanisms. Estradiol increased ADH selectively in males, and testosterone selectively decreased activity and mRNA levels in females. Effect of sex steroids on ADH was lost after hypophysectomy; infusion of GH in males increased ADH to basal female levels, supporting a role of the pituitary-liver axis. However, GH and L-thyroxine (T4) replacements alone in hypophysectomized rats did not restore dimorphic differences for either ADH activity or mRNA levels. On the other hand, T4 in combination with intermittent administration of GH reduced ADH activity and mRNA to basal male values, whereas T4 plus GH infusion replicated female levels. These results indicate that the intermittent male pattern of GH secretion combined with T4 is the principal determinant of low ADH activity in male liver.
ISSN:0193-1857
1522-1547
DOI:10.1152/ajpgi.00438.2001