On the Pathogenesis of Ethanol-Induced Lipid Accumulation in the Liver - II) Effect of Stimulation of the α-Glycerophosphate Cycle on Metabolic Changes in the Liver Caused by Ethanol.[*]

Abstract

1. The effect of hyperthyroidism induced by L-triiodothyronine upon the oxidation of ethanol and ethanoldependant metabolic alterations was investigated in male rats.
2. Hyperthyroidism reduces the accumulation of α-glycerophosphate as well as the increase of the reduction of the cytoplasmic NAD-system caused by ethanol. This effect is due to the marked elevation of the activity of α-glycerophosphate oxidase, the rate limiting enzyme of the α-glycerophosphate cycle.
3. The accumulation of triglycerides in the liver by a single dose of ethanol is distinctly less in hyperthyroid rats than in euthyroid controls. In contrast, the production of β-hydroxybutyrate and acetoacetate is stimulated. These results suggest that the preferential esterification of long-chain fatty acids in the liver to triglycerides following ethanol application is partially caused by the increased α-glycerophosphate content.
4. The activity of alcohol dehydrogenase (ADH), calculated per gram of liver tissue, decreases in L-triiodothyronine treated animals. The total activity of ADH per animal did not change significantly because the liver weight increased. The elimination of alcohol from the blood is slightly elevated in hyperthyroidism.

Key words

Alcohol Dehydrogenase - Ethanol - α-Glycerophosphate Cycle - Ketone Bodies - Thyroid Hormones - Triglycerides

1 This work was supported by a grant from the Deutsche Forschungsgemeinschaft.

1 This work was supported by a grant from the Deutsche Forschungsgemeinschaft.