| First Author | al Qatari M | Year | 1996 |
| Journal | Alcohol Alcohol | Volume | 31 |
| Issue | 1 | Pages | 89-99 |
| PubMed ID | 8672180 | Mgi Jnum | J:33350 |
| Mgi Id | MGI:80831 | Doi | 10.1093/oxfordjournals.alcalc.a008122 |
| Citation | al Qatari M, et al. (1996) Chronic ethanol consumption ameliorates the maturity-onset diabetes-obesity syndrome in CBA mice. Alcohol Alcohol 31(1):89-99 |
| abstractText | The effects of a chronic ethanol drinking schedule (20% solution for 6 weeks) on energy balance and carbohydrate and lipid metabolism have been investigated in lean (32-36 g) and obese-diabetic (40-44 g) CBA/Ca mice. The untreated obese-diabetic mice exhibited hyperglycaemia, hypertriglyceridaemia, hyper-insulinaemia and insulin resistance. The chronic ethanol treatment, which yielded plasma ethanol levels of between 1 and 11 mM, lowered the blood glucose, plasma insulin and triacylglycerol levels towards normal in the obese mice, but did not affect these parameters in the lean mice. The body weight of the obese mice tended to return to normal during the 6-week drinking period, although their total energy intake (9.2-10.0 kJ/g/week, food plus ethanol-derived calories) was almost double that of the lean mice (4.8-5.4 kJ/g/week). The blood glucose response to acute insulin injection, which was significantly reduced in the obese mice, became indistinguishable from the response of normal mice after chronic ethanol treatment. Soleus muscle glycogen synthesis in both lean and obese mice was not significantly altered by ethanol drinking, but brown adipose tissue lipogenesis was significantly increased (by 50%) in the obese mice. It is proposed that ethanol is acting chronically to restore insulin sensitivity in the obese diabetic mice at doses which have little or no effect in normal lean animals. This action is exerted, at least in part, at the level of brown adipose tissue lipogenesis. |
