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    Metformin, a common diabetes drug, can cause toxicity by increasing cellular reducing equivalents. Protecting fatty acid biosynthesis is crucial for buffering this stress and maximizing metformin's lifespan benefits.

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    Area of Science:

    • Biochemistry
    • Cell Biology
    • Aging Research

    Background:

    • Biguanides, like metformin, are widely used oral hypoglycemics known to extend lifespan.
    • Metformin's safety is generally assumed, with toxicity only expected at very high doses.

    Purpose of the Study:

    • To investigate the unanticipated toxicity of biguanides related to the accumulation of reducing equivalents.
    • To explore the role of fatty acid biosynthesis in mitigating biguanide-induced toxicity and promoting longevity.

    Main Methods:

    • Examined biguanide treatment effects on fatty acid biosynthesis and reducing equivalent levels (NADPH, NADH, GSH).
    • Utilized genetic models (e.g., C. elegans) with impaired fatty acid synthesis to assess survival under biguanide treatment.
    • Investigated the necessity of fatty acid biosynthesis for buffering NADPH-generating insults.

    Main Results:

    • Biguanide treatment leads to the accumulation of damaging reducing equivalents, specifically NADPH, NADH, and GSH.
    • Impaired fatty acid biosynthesis exacerbates biguanide-induced reductive stress and accelerates mortality across metazoans.
    • Fatty acid biosynthesis is essential for preventing shortened survival during NADPH-generating interventions.

    Conclusions:

    • Biguanides induce reductive stress through the accumulation of reducing equivalents, a toxicity mitigated by fatty acid biosynthesis.
    • Fatty acid biosynthesis acts as a critical defense mechanism against biguanide-induced reductive stress.
    • This pathway represents a potential vulnerability in cancer cells sensitive to reductive stress and a target for optimizing metformin's pro-longevity effects.