Ethanol feeding and thyroid hormone monodeiodination.

Adult male rats were placed on a 3 week regimen of ethanol (as 20% of total calories) in a nutritionally adequate diet, and controls were matched equicalorically without ethanol. Serum measurements of T4, T3, FT4, rT3, and TSH were performed in both the fed and the fasted state (18 hours). In the fed state, serum hormone measurements did not differ between control and ethanol-treated rats. Overnight fasting had a significant effect in decreasing serum T3 level in both experimental and control rats and in decreasing serum T4 level in ethanol-treated animals; FT4 and rT3 levels were not affected. Fasting also decreased in vitro hepatic T4 to T3 production to an equivalent degree in control and ethanol-treated rats, but did not alter hepatic T4 to rT3 production rates in control animals. In the fed state, hepatic rT3 neogenesis in animals given ethanol declined relative to the levels observed in control fed rats; fasting restored the depressed rT3 neogenesis to the levels noted in the fed state. Because decreased rT3 production in ethanol-treated rats in the fed state could not be explained on the basis of a change in 5'-deiodinase activity, it is suggested that ethanol administered with a nutritionally adequate diet may inhibit hepatic rT3 generation by inhibiting T4(5)-deiodinase.

Ethanol inhibition of pituitary-thyroid axis: an effect secondary to nutritional deficiency.

Ethanol as either 20% or 36% of total calories in a Lieber diet was administered to male rats. At these concentrations, ethanol consumption relative to body weight did not differ. Pair-fed controls were restricted to the amount of calories consumed by rats given ethanol. Under these conditions, a direct effect of ethanol on the hypothalamic-hypophyseal-thyroid axis could not be demonstrated. There were no differences between pair-fed control and ethanol treated rats in serum or pituitary TSH, TSH response to TRH, or T4 and T3 levels. On the other hand, in rats given ethanol as 36% of total calories ("36%" ethanol-treated), and in their pair-fed controls, a marked decrease in serum T4 levels occurred (25% and 30%), relative to the corresponding "20%" groups. The decreased T4 in the "36%" groups was associated with a pronounced fall in caloric intake, decreased serum TSH, and declines in adenohypophyseal and body weights -- all of which were of similar magnitude in experimental and control rats. Thus, inanition was probably the primary cause of reduced thyroid function in the "36%" groups. An interesting aspect of this change was the finding of no difference in serum T3 levels between pair-fed control and ethanol treated rats in the 36% and 20% groups despite the reduced T4 and caloric intake in 36% animals; the lack of decrease in T3 concentration in 36% animals may reflect augmented peripheral conversion of T4 to T3 or reduced T3 clearance.