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Aims: Although it is commonly recognized that ethanol suppresses gluconeogenesis, the influence of alcohol intake on blood glucose levels remains controversial. Ethanol may act on both glucose production and glucose consumption in the liver. Thus, we studied each effect of ethanol on glucose oxidation, gluconeogenesis, glycogenesis and glycogenolysis in the liver. Methods: The rat liver was isolated and cyclically perfused with a medium containing 50 mmol/l ethanol. Results: Ethanol enhanced ¹⁴C-glucose oxidation in the liver from 1.09 ± 0.11 to 1.41 ± 0.14 µmol for 20 min (p < 0.05). Gluconeogenesis from ¹⁴C-lactate was markedly reduced by ethanol from 8.0 ± 1.3 to 1.5 ± 0.6 µmol for 12 min (p < 0.01). Ethanol increased glycogenolysis (net hepatic glucose output, 0.47 ± 0.10 vs. 0.22 ± 0.04 mmol/30 min, p < 0.01), and then decreased hepatic glycogen content (179 ± 38 vs. 273 ± 39 mg in the presence of 1 mU/ml insulin after 30 min of perfusion, p < 0.05). Ethanol decreased the direct glycogenesis from ¹⁴C-glucose from 0.55 ± 0.08 to 0.33 ± 0.05 µmol per 100 mg glycogen for 30 min (p < 0.01). Ethanol inhibited the indirect glycogenesis from ¹⁴C-lactate from 0.21 ± 0.04 to 0.09 ± 0.01 µmol per 100 mg glycogen for 30 min (p < 0.01). Discussion: The influence of ethanol on the blood glucose regulation by the liver seems to be different between fasted and fed states. Namely, ethanol has both the hypoglycemic effects through decreased gluconeogenesis and increased glucose oxidation and the hyperglycemic effects through decreased glycogenesis and increased glycogenolysis.

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The effect of thyroid hormone on plasma somatomedin-C (SmC) level and on SmC release from perfused rat liver was investigated. Plasma SmC levels and liver tissue SmC were significantly increased in thyroxine-treated rats. Physiological doses of triiodothyronine increased SmC release and SmC concentration in the perfused rat liver. These results indicate that thyroid hormone directly enhances the synthesis and release of SmC in the rat.

Urinary N-acetyl-beta-D-glucosaminidase (NAG) was measured in patients with hyperthyroidism. The value of urinary NAG in these patients was higher than that in normal subjects and diabetic patients without diabetic nephropathy. This high level of urinary NAG in patients with hyperthyroidism decreased to the level of normal subjects after treatment of hyperthyroidism. Why urinary NAG increases in the patients with hyperthyroidism remains unknown. On the occasion of estimating the significance of the high level of urinary NAG, however, the possibility of the existence of hyperthyroidism has to be considered in addition to renal damage or hyperglycemia which have already been found to increase urinary NAG.