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Mechanistically, metformin's primary action is the inhibition of mitochondrial complex I, which reduces ATP production and alters the cellular redox state. This mitochondrial stress is a potent inducer of GDF15 expression. The significant increase in serum GDF15 (P < 0.001) observed by Kolnes 2026 provides direct human evidence for this pathway being engaged by metformin therapy. GDF15 itself has complex roles, acting as a stress-response cytokine that can influence appetite and energy expenditure.

Evidence grade: exploratory

Contradiction status: none

Publication: 5f566366-fb20-4402-ba24-c1117573f97f

Provenance: Derivation Web chain

Citation Support

  • source_1 Zaveri 2026
  • source_2 Wu 2026
  • source_3 Hong 2026
  • source_4 Lee 2026
  • source_5 Seo 2026

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