A feeding-induced myokine modulates glucose homeostasis.

Summary

This study identifies feimin, a feeding-induced myokine, as a regulator of glucose homeostasis. Feimin binds MERTK to activate AKT, increasing glucose uptake and suppressing hepatic glucose production; co-administration with insulin synergistically improves glycaemia in mice. A human MERTK variant (R466K) reduces feimin binding and associates with higher postprandial glucose and insulin.

Key Findings

• Identification of feimin, a feeding-induced myokine secreted by skeletal muscle.
• Feimin binds MERTK and activates AKT to enhance glucose uptake and suppress glucose production.
• Feimin plus insulin synergistically improves glycaemia in mice.
• Human MERTK R466K variant reduces feimin binding and associates with elevated postprandial glucose and insulin.

Clinical Implications

While preclinical, feimin–MERTK could become a therapeutic target or biomarker to augment postprandial glucose control. The MERTK R466K variant may stratify individuals with impaired feimin signaling.

Limitations

• Preclinical study; efficacy and safety in humans are untested.
• Breadth of metabolic effects and tissue specificity beyond skeletal muscle require clarification.

Future Directions

Validate feimin–MERTK signaling in humans (pharmacokinetics, target engagement) and assess therapeutic modulation in metabolic disease models and early-phase clinical trials.