Effect of L-Tryptophan on hyperglycemia, GLP-1, and Na⁺/K⁺-ATPase activity in a STZ-induced diabetes rat model

L-Tryptophan, an essential amino acid, precursor of serotonin, melatonin and niacin, has been implicated in glucose metabolism and gut hormone regulation. However, its role in diabetes remains obscure. This pilot study evaluated the effects of L-Tryptophan (Trp) supplementation on glycemic control, intestinal glucose absorption, biochemical markers and tissue histology in streptozotocin (STZ)-induced diabetic rats. Adult Wistar rats (n = 24) were divided into four groups: normal control, diabetic control, diabetic + Trp (50 mg/kg), and Trp control. Diabetes was induced by STZ (50 mg/kg). Trp was administered orally for 10 days. Blood glucose, serum biochemical parameters, intestinal glucose absorption, and Na⁺/K⁺-ATPase activity were assessed. Qualitative histological analysis of pancreatic and hepatic tissues was performed. Trp treatment in diabetic rats significantly reduced blood glucose and intestinal glucose absorption compared to diabetic controls. Pancreatic and intestinal Na⁺/K⁺-ATPase(NKA) remained statistically insignificant (p > 0.669 and 0.369). Improvements were observed in serum protein and cholesterol levels, pancreatic and hepatic histology as well as pancreatic GLP-1. L-Tryptophan demonstrated improved glycemia, metabolic benefits and tissue integrity in diabetic rats. These findings are preliminary and are interpreted within the limitations of a short duration. Further Mechanistic studies may elucidate Tryptophan-mediated mechanisms to evaluate its relevance in hyperglycemia.