Metabolic adaptation is often framed as differential gene expression, yet nutrient state also remodels which transcript isoforms from a gene contribute to physiology. This review presents isoform usage as an organizing principle of endocrine and metabolic regulation: a layer that connects nutrient sensing to transcript architecture, protein function, tissue specialization, and disease vulnerability. We synthesize evidence that fasting, feeding, insulin, and metabolite availability reshape isoform outputs across metabolic organs independently of total mRNA abundance. We then integrate functional examples, nutrient-responsive RNA-processing mechanisms, human genetic and disease data, and emerging RNA-targeted interventions. These findings suggest that metabolic disease reflects not only dysregulated gene expression but also failure to maintain the appropriate isoform state required for adaptive physiology.

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Diabetologia -

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