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Alcohol is a potential risk factor of type 2 diabetes, but its underlying mechanism is unclear. To explore this issue, Wistar rats and mouse hepatoma cells (Hepa 1–6) were exposed to ethanol, 8 g · kg −1   · d −1  for 3 months and 100 mM for 48 h, respectively. Glucose and insulin tolerance tests  in vivo  were performed, and protein levels of 11 β -hydroxysteroid dehydrogenase type 1 (11 β -HSD1) and glucocorticoid receptor (GR) in liver and Hepa 1–6 cells were measured. Alterations of key enzymes of gluconeogenesis phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6 phosphatase (G6Pase), as well as glycogen synthase kinase 3a (GSK3  α  ), were also examined. The results revealed that glucose levels were increased, and insulin sensitivity was impaired accompanied with liver injury in rats exposed to ethanol compared with controls. The 11 β -HSD1, GR, PEPCK, G6Pase, and GSK3  α   proteins were increased in the liver of rats treated with ethanol compared with controls. Ethanol-exposed Hepa 1–6 cells also showed higher expression of 11 β -HSD1, GR, PEPCK, G6Pase, and GSK3  α   proteins than control cells. After treatment of Hepa 1–6 cells exposed to ethanol with the GR inhibitor RU486, the expression of 11 β -HSD1 and GR was significantly decreased. At the same time the increases in PEPCK, G6Pase, and GSK3  α   levels induced by ethanol in Hepa 1–6 cells were also attenuated by RU486. The results indicate that ethanol causes glucose intolerance by increasing hepatic expression of 11 β -HSD1 and GR, which leads to increased expression of gluconeogenic and glycogenolytic enzymes.

journal of diabetes research

Alteration of 11<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi mathvariant="bold-italic">β</mml:mi></mml:mrow></mml:math>-Hydroxysteroid Dehydrogenase Type 1 and Glucocorticoid Receptor by Ethanol in Rat Liver and Mouse Hepatoma Cells

Alteration of 11β-Hydroxysteroid Dehydrogenase Type 1 and Glucocorticoid Receptor by Ethanol in Rat Liver and Mouse Hepatoma Cells