Antidiabetic agent; Autophagy modulator. Indirect modulator of mTORC1 complex; mTORC1 pathway members interact with SARS-CoV-2 N and Orf8 proteins. Gordon et al. bioRxiv, Mar 23 2020; https://doi.org/10.1101/2020.03.22.002386.
Biochemicals & reagents
1) Zhou et al. (2001), Role of AMP-activated protein kinase in mechanism of metformin action; J. Clin. Invest., 108 1167 2) Shaw et al. (2005), The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin; Science, 310 1642 3) Shi et al. (2012), Therapeutic metformin/AMPK activation blocked lymphoma cell growth via inhibition of mTOR pathway and induction of autophagy; Cell Death Dis., 3 e275 4) Rego et al. (2017) Anti-tumor effects of metgormin on head and neck carcinoma cell lines: A systemic review; Oncol. Lett., 13 554 5) Lee et al. (2017) PGC1α Activators Mitigate Diabetic Tubulopathy by Improving Mitochondrial Dynamics and Quality Control; J. Diabetes Res., 2017 6483572 6) Zheng et al. (2012) Sirtuin 1-mediated cellular metabolic memory of high glucose via the LKB1/AMPK/ROS pathway and therapeutic effects of metformin; Diabetes, 61 217 7) Katila et al. (2017) Metformin lowers α-synuclein phosphorylation and upregulates neurotrophic factor in the MPTP mouse model of Parkinson’s disease; Neuropharmacology, 125 396
Room Temperature (des.)
Metformin is a clinically useful antidiabetic agent which lowers plasma glucose levels and improves insulin sensitivity as well as inhibiting the hepatic gluconeogenesis by activation of the AMP-activated protein kinase (AMPK) pathway (1,2). This agent displays antiproliferative and pro-apoptotic actions in a variety of cancer cell lines (3,4) and induces autophagy via inhibition of the mTOR pathway. It also activates PGC1α and improves mitochondrial dynamics in renal tubular cells (5) and upregulates SIRT1 activity in endothelial cells (6). It is a neuroprotective and lowers α-synuclein phosphorylation in the Parkinson’s disease MPTP mouse model (7).