Role of Hentriacontane on dexamethasone-induced insulin resistance in rats

Abstract

Background

The worldwide incidence of morbidity and mortality linked to diabetes mellitus is on the ascent, with insulin resistance (IR) standing out as a key characteristic. Given the restricted safety and effectiveness observed in current therapeutic approaches, there exists a demand for novel anti-diabetic pharmaceuticals. This study aims to explore the impact of Hentriacontane, a naturally occurring long-chain alkane hydrocarbon, in an experimental model of IR induced by dexamethasone. The animals were administered dexamethasone (0.08 mg/kg b.w. s.c.) for six weeks to produce IR in the experimental animals. The animals distributed into five groups (n = 6) were: Normal group, IR group, IR + Hentriacontane low dose (2 mg/kg b.w./day p.o.), IR + Hentriacontane high dose (5 mg/kg b.w./day p.o.), and IR + Metformin (250 mg/kg b.w./day p.o.). Following the experimental period, blood/serum samples were taken for the assessment of various biochemical parameters, and a histopathological investigation of the pancreas was carried out.

Results

The inhibitory concentration (IC₅₀) value of Hentriacontane in various in-vitro assays targeting anti-diabetic and anti-oxidant effects indicates its efficacy in mitigating diabetes and scavenging free radicals. Findings from in-vivo studies demonstrate that this phytoconstituent notably lowers fasting glucose, insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) levels in dexamethasone-induced diabetic rats. Administration of hentriacontane effectively counteracts dexamethasone-induced impairments in oral glucose tolerance tests. Further, Hentriacontane normalizes lipid profiles and restores beta-cell function in diabetic rats.

Conclusion

This study has provided scientific support and evidence that Hentriacontane has a positive hypoglycemic impact on insulin-resistant rats induced by dexamethasone. Additional studies are required to ascertain the most effective dosage, duration of therapy and molecular mode of action.