Role of the pituitary and neonatal androgenic imprinting in the hormonal regulation of liver alcohol dehydrogenase activity |
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| Authors: | D W Crabb W F Bosron T K Li |
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| Affiliation: | 2. Departments of Biochemistry and Molecular Biology and Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana , USA;3. Department of Pharmaceutical Sciences, South Dakota State University, Brookings, South Dakota, USA;4. Department of Psychological and Brain Sciences, University of California Santa Barbara, Santa Barbara, California, USA;1. Department of Medical Affairs, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China;2. Department of Medical Records, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China;3. Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China;4. China Center for Health Development Studies, Peking University, Beijing 100191, China;1. Soft Nano Laboratory, Physical Sciences Division, Institute of Advanced Study in Science and Technology, Vigyan Path, Paschim Boragaon, Garchuk, Guwahati, Assam 781035, India;2. Solid State Physics Division, Bhabha Atomic Research Centre, Mumbai 400085, India;3. Laboratory for Neutron Scattering, Paul Scherrer Institute, CH-5232 PSI Villigen, Switzerland;1. Department of Biomedical Sciences, Marquette University, P.O. Box 1881, SC 446, Milwaukee, WI 53201-1881, USA;2. Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;3. Department of Psychiatry, Louisiana State University Health Sciences Center, Shreveport, LA, USA |
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| Abstract: | Liver alcohol dehydrogenase activity is increased by thyroidectomy, orchidectomy, or hypophysectomy. We investigated the mechanisms of these hormonal effects by examining the effects of testosterone, dexamethasone and thyroid hormone on liver alcohol dehydrogenase activity in hypophysectomized rats and in cultured hepatocytes, and the effect of administration of androgens to neonatal female rats. Testosterone did not lower alcohol dehydrogenase activity in hypophysectomized rats, whereas dexamethasone and thyroxine produced moderate decreases in activity. Triiodothyronine reduced alcohol dehydrogenase activity of cultured hepatocytes from male and hypothyroid female rats in a dose-dependent fashion, confirming that thyroid hormone had pituitary-independent effects on the enzyme activity. Dexamethasone was required for the expression of alcohol dehydrogenase activity in cultured cells, and it increased the enzyme activity when present at supraphysiologic concentrations. Treatment of neonatal female rats with testosterone reduced the activity of the enzyme in adulthood. The difference in alcohol dehydrogenase activity in adult male and female rats appears to be determined in part by neonatal imprinting by androgens and in part by an effect of testosterone that is either mediated by or dependent upon the pituitary. Thyroid hormone reduces alcohol dehydrogenase activity by a direct effect on the liver. |
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