Sulforaphane as a Therapeutic Target for Sarcopenia in Type 2 Diabetes: Mechanistic Insights and Translational Evidence

Sulforaphane, a bioactive isothiocyanate abundant in cruciferous vegetables, has emerged as a potential multi-target therapeutic agent capable of mitigating these pathological processes. Here, using evidence from preclinical and clinical literature, we review the mechanistic and translational evidence linking sulforaphane with the preservation of skeletal muscle tissue in the context of sarcopenia associated with T2D. The reviewed evidence suggests sulforaphane modulates oxidative stress, inflammation, and mitochondrial dysfunction through activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and related signaling pathways. Preclinical rodent studies corroborate these findings, reporting improved muscle mass, contractility, metabolic homeostasis, and attenuation of inflammation via Nrf2/heme oxygenase (HO)-1, AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) pathways. Limited clinical evidence from two small studies in healthy adults suggest that short-term sulforaphane supplementation (30 mg/day) may reduce exercise-induced muscle damage and enhance antioxidant responses. The evidence collectively highlights sulforaphane as a promising candidate for preserving skeletal muscle integrity in T2D. However, more randomized controlled trials are required to define optimal dosing, long-term safety, and direct efficacy in patients with sarcopenia and diabetes. This review strengthens the translational value of sulforaphane while integrating mechanistic insights and therapeutic potential against T2D-associated sarcopenia.