Dihydrolipoic acid improves diabetic endothelial cell function via the H ₂ S ‐producing enzyme 3‐mercaptopyruvate sulfurtransferase

High glucose‐induced endothelial dysfunction is a hallmark of diabetic microvascular complications. Reduced hydrogen sulphide (H 2 S) levels and dysregulation of the H 2 S‐producing enzyme 3‐mercaptopyruvate sulfurtransferase (3‐MST) are linked to this dysfunction. Dihydrolipoic acid (DHLA), formed from alpha‐lipoic acid in mitochondria, has been proposed to enhance H 2 S release from 3‐MST; however, this has not been empirically tested in diabetes. Using a cell culture model, this study demonstrates that DHLA supplementation enhances H 2 S production via 3‐MST and improves endothelial function under high glucose conditions. Our results provide foundational knowledge and indicate that targeting the 3‐MST/H 2 S pathway via DHLA supplementation may have therapeutic potential to reduce or slow the onset and progression of diabetic microvascular complications.