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Related Experiment Video

Updated: Feb 3, 2026

Frailty Assessment in an Aging Mouse Model
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Elevating Circulating L-Kynurenine Promotes Frailty in Aging Mice.

Mia Y Kawaida1, Abigail L Tice1, Samuel Alvarez1

  • 1Department of Applied Physiology and Kinesiology, The University of Florida, Gainesville, Florida, USA.

Journal of Cachexia, Sarcopenia and Muscle
|February 2, 2026
PubMed
Summary

Elevated L-Kynurenine (L-Kyn) worsens aging frailty, but skeletal muscle PGC1α overexpression protects against this decline. This protection is linked to increased muscle kynurenine aminotransferase (KAT) expression and metabolism.

Keywords:
agingfrailtymitochondriamusclephysical function

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Area of Science:

  • Aging and Metabolism
  • Skeletal Muscle Physiology
  • Mitochondrial Function

Background:

  • L-Kynurenine (L-Kyn), a tryptophan metabolite, increases with age and is linked to reduced physical function and frailty.
  • Kynurenine aminotransferases (KATs) in skeletal muscle degrade L-Kyn and are regulated by PGC1α.

Purpose of the Study:

  • To investigate if elevated L-Kyn exacerbates age-related decline in physical, muscle, and mitochondrial functions.
  • To determine if skeletal muscle-specific PGC1α (MCK-PGC1α) transgenic expression protects against age-dependent L-Kyn pathology.

Main Methods:

  • Aging mice (MCK-PGC1α transgenic and wildtype littermates, n=262) were studied longitudinally.
  • Dietary intervention increased L-Kyn levels.
  • Physical function (endurance, strength, speed, activity), muscle function (soleus contraction), and mitochondrial energetics were assessed.

Main Results:

  • L-Kyn diet decreased endurance and activity in male mice and walking speed in female mice.
  • L-Kyn increased frailty in wildtype mice, but this was mitigated by MCK-PGC1α expression.
  • MCK-PGC1α mice exhibited higher KAT expression and improved mitochondrial function compared to wildtypes.

Conclusions:

  • Skeletal muscle PGC1α overexpression mitigates L-Kyn-induced exacerbation of physical frailty in aging mice.
  • This protective effect is partly due to enhanced skeletal muscle L-Kyn metabolism via increased KAT expression driven by PGC1α.