Background: Thyroid hormone has been known to affect hepatic alcohol dehydrogenase (ADH) activity. Although the liver is the principal site of ethanol metabolism, stomach is also responsible in part for ethanol oxidation. The effects of thyroid hormon...
Background: Thyroid hormone has been known to affect hepatic alcohol dehydrogenase (ADH) activity. Although the liver is the principal site of ethanol metabolism, stomach is also responsible in part for ethanol oxidation. The effects of thyroid hormone on ADH activity in gastric mucosa and other tissues of rats had not been previously examined.
Method: The effects of thyroid hormone on liver, stomach, lung, and kidney ADH activities (nM of NADH/min/mg of cytosolic protein) have been investigated in male Sprague Dawley rats treated with propylthiouracil (50 mg/kg) for 14 days.
Results: Whereas hepatic ADH activities were not changed by treatment with PTU(42.9(8.6 vs 45.2 (10.1), gastric ADH activities in PTU-treated rats increased by 258.8% of control rat (6.3 ( 0.6 vs 2.2 ( 1.2, p〈0.001). In the activities of other tissues, PTU treatment decreased lung ADH activity by 59.7% of control, and increased kidney ADH activities by 247.1% of control rats.
Conclusion: These data suggest that hypothyroidism causes an increase of gastric alcohol metabolism, and that the increase of gastric ADH activity can partly restore the first pass metabolism of ethanol in hypothyroid rats.