Jyothirmayi G N, Jayasundaramma B, Reddi A S
Department of Medicine, UMDNJ-New Jersey Medical School, Neward 07103.
Res Commun Chem Pathol Pharmacol. 1992 Oct;78(1):113-6.
The incorporation of [14C] U-glucose into glycogen by liver, kidney and skeletal muscle and that into total lipid by adipose tissue was studied in noninsulin-dependent genetically diabetic KK mice treated either with metformin (50 mg/kg) or water for 10 weeks. Results show that glycogen synthesis was increased in the skeletal muscle from metformin-treated mice. Liver and kidney glycogen synthesis was not affected by metformin. Glucose incorporation was significantly increased into lipid in metformin-treated mice. Insulin administration stimulated lipid synthesis in adipose tissue, but had no effect on muscle glycogen synthesis in metformin-treated mice. These data suggest that chronic metformin treatment potentiates the endogenous insulin action on glucose in skeletal muscle and adipose tissue, and thus confirm our previous results of increased glycogen synthesis by skeletal muscle in metformin-treated KK mice.
在非胰岛素依赖型遗传性糖尿病KK小鼠中，研究了用二甲双胍（50毫克/千克）或水治疗10周后，肝脏、肾脏和骨骼肌将[14C] U -葡萄糖掺入糖原以及脂肪组织将其掺入总脂质的情况。结果显示，用二甲双胍治疗的小鼠骨骼肌中糖原合成增加。肝脏和肾脏的糖原合成不受二甲双胍影响。在二甲双胍治疗的小鼠中，葡萄糖掺入脂质显著增加。注射胰岛素刺激脂肪组织中的脂质合成，但对二甲双胍治疗的小鼠肌肉糖原合成没有影响。这些数据表明，长期使用二甲双胍可增强内源性胰岛素对骨骼肌和脂肪组织中葡萄糖的作用，从而证实了我们之前关于二甲双胍治疗的KK小鼠骨骼肌糖原合成增加的结果。
