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Alcoholic extract and its ethyl acetate fraction of Moringa oleifera (Lam.) (MO), (Moringaceae) bark are experimentally claimed to possess insulin-sensitizing potentials. The present study aimed to isolate and characterize the phytochemical(s) responsible for insulin sensitization in dexamethasone-induced acute and chronic rat models for insulin resistance (IR). The reported ethyl acetate fraction from the alcoholic extract of the bark of MO was prepared and subjected to bioactivity-guided sub-fractionation and isolation of phytochemicals. A component responsible for improving insulin sensitivity in rat models for IR was isolated and reported for the first time from the bark of MO and its structure was characterized as a procyanidin dimer type of polyphenol by spectroscopic techniques. [ABSTRACT FROM AUTHOR]

Objective: Alcoholic extract of the bark of Moringa oleifera Lam. (MO), (Moringaceae), has been experimentally evaluated previously for its insulin sensitizing potentials. In the quest to explore the possibility of the class of phytochemical(s) responsible for this experimental claim, the alcoholic extract was fractionated and evaluated for insulin sensitizing effect in rat model for insulin resistance. Methods: Alcoholic extract of MO was fractionated into, non-polar [petroleum ether (PEF)], moderately non-polar [ethyl acetate (EAF)] and polar [aqueous (AQF)] fractions. The fractions obtained were investigated for their insulin sensitizing properties in dexamethasone induced insulin resistance in rats. The bioactive fraction was analysed by spectroscopy for further characterization of phytochemical(s) present. Results: Acute treatment for 4 h with dexamethasone (1 mg/kg i.p.) in rats led to the development of impaired oral glucose tolerance. Treatment with pioglitazone and EAF abolished dexamethasone induced oral glucose intolerance (OGT). Dexamethasone (1 mg/kg s.c., once daily for 11 d) administration led to the development of insulin resistance, characterised by fasting hyperglycemia, hyperinsulinemia, hypertriglyceridemia, impaired OGT and increased HOMA IR index. Treatments with EAF (140 mg/kg p.o.) and pioglitazone [PIO (10 mg/kg p.o.)] significantly prevented dexamethasone induced metabolic changes. Similarly, treatment with AQF (95 mg/kg p.o.) also significantly prevented metabolic changes due to dexamethasone except impaired OGT. In contrast PEF (15 mg/kg p.o.) failed to prevent these metabolic changes except hypertriglyceridemia. Conclusion: The present study reveals that triterpenoid and the polyphenols (procyanidin) class of phytochemicals detected in EAF of alcoholic extract of MO bark may be responsible for the prevention of dexamethasoneinduced insulin resistance in rats. [ABSTRACT FROM AUTHOR]