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长期摄入乙醇可改善CBA小鼠的成年起病型糖尿病-肥胖综合征。

Chronic ethanol consumption ameliorates the maturity-onset diabetes-obesity syndrome in CBA mice.

作者信息

al Qatari M, Shih M F, Taberner P V

机构信息

Department of Pharmacology, School of Medical Sciences, University of Bristol, UK.

出版信息

Alcohol Alcohol. 1996 Jan;31(1):89-99. doi: 10.1093/oxfordjournals.alcalc.a008122.

Abstract

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.

摘要

在瘦型(32 - 36克)和肥胖糖尿病型(40 - 44克)CBA/Ca小鼠中,研究了长期乙醇饮用方案(20%溶液,持续6周)对能量平衡以及碳水化合物和脂质代谢的影响。未经处理的肥胖糖尿病小鼠表现出高血糖、高甘油三酯血症、高胰岛素血症和胰岛素抵抗。长期乙醇处理使血浆乙醇水平维持在1至11毫摩尔之间,肥胖小鼠的血糖、血浆胰岛素和甘油三酯水平降至正常,但对瘦型小鼠的这些参数没有影响。肥胖小鼠的体重在6周饮用期内趋于恢复正常,尽管它们的总能量摄入(9.2 - 10.0千焦/克/周,食物加乙醇衍生热量)几乎是瘦型小鼠(4.8 - 5.4千焦/克/周)的两倍。肥胖小鼠对急性胰岛素注射的血糖反应显著降低,而在长期乙醇处理后,其与正常小鼠的反应无明显差异。乙醇饮用对瘦型和肥胖小鼠的比目鱼肌糖原合成均无显著影响,但肥胖小鼠的棕色脂肪组织脂肪生成显著增加(50%)。有人提出,乙醇长期作用可恢复肥胖糖尿病小鼠的胰岛素敏感性,而在正常瘦型动物中,相同剂量的乙醇几乎没有作用或根本没有作用。这种作用至少部分是在棕色脂肪组织脂肪生成水平上发挥的。

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