Premium
Hypothalamic‐Pituitary‐Thyroid Axis in Chronic Alcoholism. II. Deiodinase Activities and Thyroid Hormone Concentrations in Brain and Peripheral Tissues of Rats Chronically Exposed to Ethanol
Author(s) -
Baumgartner Andreas,
Heyne Andrea,
CamposBarros Angel,
Köhler Ralf,
Müller Frank,
Meinhold Harald,
Rommelspacher Hans,
Wolffgramm Jochen
Publication year - 1994
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1994.tb00017.x
Subject(s) - deiodinase , medicine , endocrinology , thyroid , ethanol , alcohol , iodothyronine deiodinase , triiodothyronine , chemistry , abstinence , hormone , hippocampus , cerebellum , central nervous system , striatum , psychology , dopamine , biochemistry , psychiatry
Thyroxine (T 4 ), triiodothyronine (T 3 ) concentrations, and the activities of the three deiodinase isoenzymes were measured in different brain regions and peripheral tissues of rats. According to an animal model of alcohol addiction, “behaviorally” dependent rats having lost control over their intake of ethanol were compared with alcohol‐naive controls and ethanol‐experienced, but “controlled” consumers. The two kinds of alcohol‐experienced rats were investigated either 24 hr or 3 months after ethanol withdrawal. The results of these four groups were compared with those of an ethanol‐naive control group. During withdrawal, the activities of type II 5′‐deiodinase (which catalyzes deiodination of T 4 , and T 3 in the CNS) in both the “behaviorally dependent” rats and the “controlled drinkers” were significantly lower than in the alcohol‐naive controls in the frontal cortex, parieto‐occipital cortex, hippocampus, and striatum, but not in the cerebellum or pituitary. Probably as a result, the tissue concentrations of T 4 were higher in areas of the CNS in the groups exposed to alcohol. However, the T 3 concentrations were normal. No relevant differences were seen between the activities of type III 5‐deiodinase (which catalyzes the further deiodination of T 3 ) observed in these groups. Atter 3 months of abstinence, the type II 5′‐deiodinase activities had almost returned to nomal in both “controlled drinkers” and “behaviorally dependent” animals, whereas type III 5‐deiodinase activity was inhibited, possibly to maintain physiological concentrations of T 3 during abstinence. Indeed, the tissue levels of T 3 were normal in the areas of the CNS, and the T 4 levels were still elevated. However, the liver concentrations of T 3 and T 4 were significantly lower in the “behaviorally dependent” animals than in the “controlled” drinkers after 3 months of abstinence, whereas no differences were found between the T 4 and T 3 concentrations in the areas of the CNS investigated in the two groups exposed to ethanol. These results suggest that chronic administration of ethanol affects intracellular thyroid hormone metabolism in both rat CNS and liver in a highly complex manner. No direct evidence of ethanolinduced enhancement of tissue uptake or concentrations was obtained. However, taking into account the numerous similarities between the clinical picture of hyperthyroidism and the symptomatology of alcoholism, it may be hypothesized that ethanol may directly influence any step in the as yet unknown biochemical cascade of thyroid hormone function.