Microbiome & Chronic Diseases

Evidence Based Medicine

Metformin {60000057}

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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)

Shared Notes

  • [1.1
    - metformin treatment, shifts a depletion of butyrate-producing taxa in T2D patient. These in turn cause functional microbiome shifts, in part alleviated by metformin-induced changes.
  • [1.2
    - The commonly used diabetes treatment Metformin increase Akkermansia spp. abundance, and to significantly improve glucose metabolism in high-fat diet fed mice while also increasing the number of mucin-producing goblet cells.
  • [1.3
    - there is a negative association between specific species such as B. adolescentis, B. bifidum, B. pseudocatenulatum, B. longum, B. dentium and disease in patients treated with metformin or after undergoing gastric bypass surgery

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