Metformin and Pancreatic Cancer Metabolism
Abstract
Numerous epidemiological studies have reported that metformin, a well-known and widely used anti-diabetic drug, may provide protective benefits in decreasing pancreatic cancer risk among the diabetic population. Following a brief introduction regarding metformin’s history and pharmacological properties, this book chapter presents epidemiological findings showing how metformin is associated with protection against pancreatic cancer. We also introduce the anti-cancer effects of metformin through AMPK-independent and AMPK-dependent manners [1-6]. These mechanisms include its inhibitory effects on the insulin growth factor-1 (IGF-1), G protein-coupled receptor (GPCR) and mTORC1 signaling pathways [3-10]. We then discuss the metabolic effects of metformin in cancer. For example, metformin has been shown to inhibit glycolysis in various cancer cell lines [11-13]. Metformin is a known inhibitor of complex I of the electron transport chain [14-18], potentially limiting the intact oxidative respiration capabilities of the cancer cell. We also discuss in depth the anti-cancer mechanisms of action of metformin in the context of lipid metabolism as reported in numerous models. These include metformin’s ability to increase fatty acid β-oxidation in adipocytes [19] and its ability to inhibit hepatic lipogenesis [2]. As shown by numerous studies [20-23], metformin also possesses antilipogenic properties, potentially limiting this critical metabolic pathway that confers cancer pancreatic…
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