Metformin—mode of action and clinical implications for diabetes and cancer
By I. Pernicova, M. Korbonits. Nature Reviews Endocrinology, 2014
1,235 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/b0aaaa464852e83365c249b05b55a686078d766f
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Citations in the corpus
- Metformin Is Associated With Higher Relative Abundance of Mucin-Degrading Akkermansia muciniphila and Several Short-Chain Fatty Acid–Producing Microbiota in the Gut (2016, background): “Metformin (1,1-dimethylbiguanide hydrochloride) is the most frequent medication used to treat type 2 diabetes (7), and findings from recent studies suggest it may also prevent cancer (7) and cardiovascular events (8).”
- Metformin-associated lactic acidosis: Current perspectives on causes and risk. (2016, background): “metformin, have a reduced threshold for the development of lactic acidosis in response to a secondary event [19,25,26,41].”
- Shared Risk Factors in Cardiovascular Disease and Cancer (2016, background): “Metformin has been thought to reduce the risk of cancer and has a plausible biological mechanism, although population studies have demonstrated mixed results.(85,86) Metformin activates adenosine monophosphate– activated protein kinase in hepatocytes, a major cellular regulator of lipid and glucose ”
- Adiponectin, Leptin, and Fatty Acids in the Maintenance of Metabolic Homeostasis Through Adipose Tissue Crosstalk (2016, background): “Treatments that enhance systemic insulin sensitivity have been shown to enhance glucose uptake by peripheral tissues while decreasing hepatic glucose output (Pernicova and Korbonits, 2014).”
- Metformin in patients with type 2 diabetes and kidney disease: a systematic review. (2014, neutral): “Thus, the final number of manuscripts was 65 (pharmacokinetic/ metabolic investigations [10]; case series [20]; cross-sectional, observational, and pharmacosurveillance studies [31]; metaanalyses [3]; and a clinical trial [1]).”
- Metformin promotes antitumor immunity via endoplasmic reticulum-associated degradation of PD-L1 (2018, neutral): “Metformin has been shown to directly induce antitumor effects by inhibiting the PI3K (phosphatidylinositol 3-kinase)-AktmTOR and Ras-MAPK (mitogen-activated protein kinase) signaling pathways critical for cancer progression or indirectly by systemically reducing glucose and insulin metabolism to att”