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We read with great interest the recent study by Gilliam-Vigh et al demonstrating significant transcriptomic alterations in the intestinal mucosa of individuals with type 2 diabetes (T2D), particularly increased immune activation, altered barrier function in the large intestine and metabolic dysfunction.1 These findings provide crucial mechanistic insights that complement observations on metabolic disturbances in patients with irritable bowel syndrome (IBS), supporting the rationale for glucose-targeted interventions.