Metformin HCl is one of the most effective and widely used therapeutics for treatment of type 2 diabetes. It selectively lowers the hepatic gluconeogenesis without rising insulin production, causing weight gain or hypoglycemia. [1]
AMPK (5'AMP-activated protein kinase) acts as a metabolic master switch regulating several intracellular systems including the cellular uptake of glucose, the β-oxidation of fatty acids and the biogenesis of GLUT4 (glucose transporter 4) and mitochondria.
In hepatocytes, AMPK was activated by metformin, followed by decreased ACC (acetyl-CoA carboxylase) activity, induction of fatty acid oxidization and suppression of lipogenic enzyme expression.[2] Metformin also inhibited mGPD (mitochondrial lycerophosphate dehydrogenase),a redox shuttle enzyme, leading to an altered hepatocellular redox state, decreased conversion of lactate and reduced hepatic gluconeogenesis. [1]
In rats treated with metformin, hepatic expression of SEREP-1 mRNAs/protein and activity of ACC were reduced. [2] In metformin treated mice, LKB1 in liver was essential for the ability of metformin to reduce blood glucose [3]. In ASO (Antisense oligonucleotide) knockdown of hepatic mGOD in rats, the phenotype was similar to chronic metformin treatment. It abolished mefromin-induced cytosolic redox state, reduction in plasma glucose concentration and EGP inhibition. [1]
盐酸二甲双胍是治疗2型糖尿病最有效、应用最广泛的药物之一。它选择性地降低肝脏糖异生,而不会增加胰岛素产量,导致体重增加或低血糖。[1]
AMPK(5’AMP活化的蛋白激酶)作为代谢主开关,调节几个细胞内系统,包括葡萄糖的细胞摄取、脂肪酸的β-氧化以及GLUT4(葡萄糖转运蛋白4)和线粒体的生物发生。
在肝细胞中,AMPK被二甲双胍激活,随后ACC(乙酰辅酶A羧化酶)活性降低,诱导脂肪酸氧化并抑制脂肪生成酶的表达。[2] 二甲双胍还抑制mGPD(线粒体甘油磷酸脱氢酶),这是一种氧化还原穿梭酶,导致肝细胞氧化还原状态改变,乳酸转化率降低,肝糖异生减少。[1]
在用二甲双胍治疗的大鼠中,肝脏SEREP-1 mRNA/蛋白的表达和ACC的活性降低。[2] 在二甲双胍治疗的小鼠中,肝脏中的LKB1对二甲双胍降低血糖的能力至关重要[3]。在大鼠肝mGOD的ASO(反义寡核苷酸)敲除中,表型与慢性二甲双胍治疗相似。它消除了mefromin诱导的胞质氧化还原状态、血浆葡萄糖浓度降低和EGP抑制。[1]
References:
1. Madiraju AK, Erion DM, Rahimi Y et al. Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase. Nature. 2014 Jun 26;510(7506):542-6.
2. Zhou G, Myers R, Li Y et al. Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest. 2001 Oct;108(8):1167-74.
3. Shaw RJ, Lamia KA, Vasquez D et al. The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. Science. 2005 Dec 9;310(5754):1642-6.
















