Five longevity interventions in mice converge on a liver metabolic switch driven by glucagon
On 19 September the journal npj Aging published a study from the University of Michigan that compared five interventions known to extend mouse lifespan: the diabetes drugs acarbose and canagliflozin, a calorie‑restricted diet, and two genetic alterations—Snell dwarfism and growth‑hormone‑receptor knockout (GHRKO). All five regimens were found to remodel liver metabolism in the same way.
In each case the liver lowered the activity of enzymes that break down glucose while raising the activity of enzymes that catabolize the amino acids alanine, glutamine and asparagine. The shift was driven by the hormone glucagon, which altered the liver’s fuel preference without changing its release of glucose into the bloodstream.
Previously, the only common feature of these longevity methods was suppression of the MEK1‑ERK and mTOR growth pathways and activation of chaperone‑mediated autophagy. The downstream metabolic signal had escaped detection because broad‑omics screens filtered out a weak
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Nature
Regulation of alanine glutamine asparagine catabolism is common to mouse models that extend lifespan
npj Aging - Regulation of alanine glutamine asparagine catabolism is common to mouse models that extend lifespan
September 22, 2026 12
