Antidiabetogenic efficiency of menthol, improves glucose homeostasis and attenuates pancreatic β-cell apoptosis in streptozotocin–nicotinamide induced experimental rats through ameliorating glucose metabolic enzymes

Abstract The phytochemical, menthol, has been reported to play many beneficial roles. However, under diabetic conditions, there is no detail mechanism of its beneficial action in the glucose homeostasis. The present study, we investigated to explore the role of menthol, on the glucose metabolic enzymes and pancreatic islet cell apoptosis of streptozotocin–nicotinamide (STZ–NA) induced diabetes in rats. Diabetes was induced by single intraperitoneal (i.p.) injection of STZ (50 mg/kg/b.w.) and NA (110 mg/kg/b.w.). Diabetic rats were treated with different dose of menthol (25, 50, and 100 mg/kg/b.w.) and glibenclamide (600 μg/kg/b.w.) daily for 45 days. The result of our study shows that menthol significantly reduced the blood glucose and glycosylated hemoglobin levels and significantly increased the total hemoglobin, plasma insulin and liver glycogen levels in diabetic rats. The altered activities of hepatic glucose metabolic enzymes, serum biomarkers of liver damage were restored to near normal. The pathological abnormalities in hepatic and pancreatic islets of diabetic rats were significantly ameliorated by menthol intervention. These effects were mediated by suppressing pancreatic β-cells apoptosis and were associated with increased anti-apoptotic Bcl-2 expression and reduced pro-apoptotic Bax expression. Findings from the current study consent us to conclude that menthol alleviates STZ–NA-induced hyperglycemia via modulating glucose metabolizing enzymes, suppression of pancreatic β-cells apoptosis and altered hepatic, pancreatic morphology. This exclusivity and dearth of any noticeable adverse efficacy proposes the opportunity of using this monoterpene as an efficient adjuvant in the management diabetes mellitus.