Research

Hormonal

Caloric restriction enhances skeletal muscle insulin sensitivity in mice by activating Sirt1, which deacetylates and inactivates Stat3, thereby reducing the expression of inhibitory PI3K regulatory subunits (p55α/p50α) and improving PI3K signaling efficiency.

Caloric restriction improves how your muscles respond to insulin by activating a specific protein (Sirt1) that optimizes the cell's internal signaling machinery. This happens regardless of muscle mass changes and is driven by the energy deficit itself, likely through changes in cellular energy sensors (NAD+ levels).

GoodSupportsHIGH confidence
Mechanistically, Sirt1 was found to be required for the deacetylation and inactivation of the transcription factor Stat3 during CR, which resulted in decreased gene and protein expression of the p55α/p50α subunits of PI3K, thereby promoting more efficient PI3K signaling during insulin stimulation.
Simon Schenk et al. · Journal of Clinical Investigation · 2011

Why this rating

High-quality mechanistic evidence using genetically modified mice (muscle-specific knockout) and rigorous metabolic clamps, though limited to murine models.

Source

Sirt1 enhances skeletal muscle insulin sensitivity in mice during caloric restriction

Simon Schenk et al. · Journal of Clinical Investigation · 2011

DOI 10.1172/jci58554

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DOI resolved against Crossref · corpus check 2026-06-10

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