Gmelinol ameliorates type 2 diabetes and multi-organ complications in streptozotocin-nicotinamide-induced diabetic rats.

To study ameliorative effects of gmelinol against streptozotocin (STZ) and nicotinamide (NAD) induced type-2 diabetes mellitus (T2DM) and diabetic complications. Molecular docking was conducted to validate the affinity of gmelinol with α-amylase, α-glucosidase, and sodium-glucose cotransporter 2. In vitro enzymatic assays were performed to study the inhibitory potential of gmelinol against α-amylase and α-glucosidase. The insulinomimetic potential of gmelinol was evaluated using a glucose uptake assay. Furthermore, 36 male rats were divided into six groups. Excluding the normal control (NC) group, all animals received NAD (230 mg/kg, intraperitoneally [i.p.]), followed by STZ (65 mg/kg, i.p.) to induce T2DM. Treatments were administered orally from Day 60 to Day 90. The NC and disease control group (DC) received 0.1% carboxy methyl cellulose orally, while glibenclamide (3 mg/kg) was administered orally as standard treatment. Three doses of glmelinol (25, 50, or 100 mg/kg) were administered orally to three treatment groups. Changes in body weight (BW), diabetic parameters, cardiac parameters, renal parameters, and neuronal parameters were assessed. Dissected issues were subjected to histopathology. Gmelinol exhibited notable binding affinities with α-amylase and α-glucosidase. In vitro enzymatic assays indicated inhibitory effects of gmelinol against α-amylase and α-glucosidase. Gmelinol demonstrated a dose-dependent increase in glucose uptake. Gmelinol significantly improved BW and glycemic control by regulating BGLs and diabetic parameters. Significant improvements in cardiac, renal, and neuronal parameters were observed in gmelinol-treated animals. Gmelinol demonstrated a notable improvement in the morphology of tissues. Gmelinol exhibited an ameliorative effect against T2DM and diabetic complications.