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- Lactate uptake by the liver is diminished with metformin use because lactate is a substrate for hepatic gluconeogenesis, a process that metformin inhibits.
- Metformin has been suggested as increasing production of lactate in the large intestine.
- Epidemiological studies first recognized a relationship with metformin use in T2DM patients and reduced colorectal cancer (CRC) risk. (2)
- metformin treatment significantly increase Escherichia coli and lowers Intestinibacter abundance.
- This effect is thought to be mediated by metformin’s effect on short-chain fatty acid (butyrate)-producing bacteria and the abundance of Akkermansia muciniphila, as well as through common biological pathways and genes encoded in different metformin-affected bacteria. (3)
-bcat-1 knockdown increases mitochondrial respiration and induces oxidative damage in neurons through mammalian target of rapamycin-independent mechanisms. Increased mitochondrial respiration, or "mitochondrial hyperactivity," is required for bcat-1(RNAi) neurotoxicity.
-Post-disease-onset administration of the type 2 diabetes medication metformin reduces mitochondrial respiration to control levels and significantly improves both motor function and neuronal viability.(4)