The present study aimed to evaluate the antihyperglycemic effects of Musa paradisiaca (M. paradisiaca) leaf and fruit peel hydroethanolic extracts and to suggest their probable mode of actions in nicotinamide (NA)/streptozotocin (STZ)-induced diabetic rats. The leaf and fruit peel hydroethanolic extracts were analyzed by GC-MS that indicated the presence of phytol, octadecatrienoic acid, hexadecanoic acid, and octadecadienoic acid as major components in the leaf extract and vitamin E, octadecenamide, β-sitosterol, and stigmasterol as major phytochemicals in the fruit peel extract. Diabetes mellitus was induced by a single intraperitoneal injection of STZ (60 mg/kg body weight) dissolved in citrate buffer (pH 4.5), 15 minutes after intraperitoneal injection of NA (120 mg/kg body weight). The NA/STZ-induced diabetic rats were, respectively, treated with M. paradisiaca leaf and fruit peel hydroethanolic extracts at a dose of 100 mg/kg body weight/day by oral administration for 28 days. The treatment of NA/STZ-induced diabetic rats with leaf and fruit peel extracts significantly improved the impaired oral glucose tolerance and significantly increased the lowered serum insulin and C-peptide levels. The HOMA-IR (as the index of insulin resistance) and QUICKI (as a marker for insulin sensitivity), as well as HOMA-β cell function were significantly alleviated as a result of treatment of diabetic rats with leaf and fruit peel extracts. In association, the elevated serum-free fatty acids, TNF-α, and IL-6 levels were significantly decreased. In addition, the suppressed adipose tissue PPARγ, GLUT4, adiponectin, and insulin receptor β-subunit mRNA expressions were upregulated while the elevated adipose tissue resistin expression was downregulated in diabetic rats as a result of treatment with the leaf and peel extract. Based on these results, it can be concluded that M. paradisiaca leaf and fruit peel hydroethanolic extracts have antihyperglycemic effects which may be mediated via their insulinotropic and insulin-sensitizing effects.

This study aimed to assess antihyperlipidemic, cardiac and antioxidant effects as well as mode of actions of Musa paradisiaca (M. paradisiaca) leaf and fruit peel hydroethanolic extracts in nicotinamide (NA)/streptozotocin (STZ)‐induced diabetic rats. Experimental diabetes mellitus was induced by a single intraperitoneal injection of STZ (60 mg/kg body weight), 15 min after intraperitoneal injection of NA (120 mg/kg body weight). NA/STZ‐induced diabetic rats were orally supplemented with M. paradisiaca leaf and fruit peel hydroethanolic extracts in a dose of 100 mg/kg body weight/day for 28 days. The treatment of NA/STZ‐induced diabetic rats with M. paradisiaca leaf and fruit peel extracts significantly decreased the elevated fasting and post‐prandial serum glucose, total cholesterol, triglycerides, LDL‐cholesterol and vLDL‐cholesterol levels and significantly increased the lowered serum insulin level, liver glycogen content, serum HDL‐cholesterol level, homeostasis model assessment‐insulin resistance (HOMA‐IS) and HOMA‐β cell function. The elevated cardiovascular risk indices in diabetic rats were significantly improved due to treatment with M. paradisiaca extracts. Concomitant with the increase in liver glycogen content, the glucose‐6‐phosphatase activity significantly decreased reflecting the decrease in hepatic glucose output. The heart function was potentially ameliorated as manifested by decrease in the elevated serum creatine kinase‐MB, lactate dehydrogenase and aspartate aminotransferase activities after treatments of diabetic rats with M. paradisiaca extracts. The elevated liver lipid peroxidation and the decline in liver glutathione content and superoxide dismutase, glutathione peroxidase and glutathione‐S‐transferase activities were significantly reversed by treatments. Thus, it can be concluded that M. paradisiaca leaf and fruit peel hydroethanolic extracts may have antihyperlipidemic and cardioprotective potentials in NA/STZ‐induced diabetic rats. These effects may be mediated via improvements in the glycemic state, β‐cell function, tissue insulin sensitivity, and antioxidant defense mechanism.

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