Skeletal muscle insulin resistance is a key component in the development of type 2 diabetes. Caloric restriction (CR) has been shown to enhance skeletal muscle insulin sensitivity, but the molecular mechanisms involved have not been fully elucidated.

Recent studies suggest that Sirt1, a NAD+-dependent deacetylase, plays a crucial role in linking CR to improved insulin action in skeletal muscle. Research in mice has demonstrated that CR increases Sirt1 deacetylase activity, which correlates with enhanced insulin-stimulated phosphoinositide 3-kinase (PI3K) signaling and glucose uptake.

These findings highlight Sirt1 as a pivotal signaling node that mediates the metabolic adaptations induced by CR, ultimately promoting greater insulin sensitivity in skeletal muscle.

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