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[35] In some embodiments, the present disclosure provides a method of reducing fat mass regain in a subject after discontinuing treatment with a GLP-1 receptor agonist, wherein the method comprises administering to the subject a myostatin inhibitor in an amount effective to reduce fat mass gain as compared to a subject who has discontinued a GLP-1 receptor agonist therapy but is not treated with the myostatin inhibitor

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This targeted redox signal serves as an early alarm, acutely rewiring metabolic flux, for instance, away from the TCA cycle and towards alternative pathways like glycolysis or glutaminolysis, to meet changing energetic or biosynthetic demands, particularly under stress conditions such as inflammation or ischemia–reperfusion [86]