Modulation of Diabetes and Dyslipidemia in Diabetic Insulin-Resistant Rats by Mangiferin: Role of Adiponectin and TNF-α

Mangiferin, present in Mangifera indica bark, was reported to produce hypoglycemic and antidiabetic activity in an animal model of genetic type 2 diabetes and in streptozotocin diabetic rats. Its effect on diabetic insulin-resistant animals has not been investigated. The current work aimed to explor...

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Bibliographic Details
Main Authors: SAMIRA SALEH, NABILA EL-MARAGHY, ENJI REDA, WALEED BARAKAT
Format: Article
Language:English
Published: Academia Brasileira de Ciências 2014-12-01
Series:Anais da Academia Brasileira de Ciências
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Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652014000401935&lng=en&tlng=en
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Summary:Mangiferin, present in Mangifera indica bark, was reported to produce hypoglycemic and antidiabetic activity in an animal model of genetic type 2 diabetes and in streptozotocin diabetic rats. Its effect on diabetic insulin-resistant animals has not been investigated. The current work aimed to explore the effect of mangiferin on diabetic insulin-resistant rat model. Diabetes was induced by high-fat/high fructose diet for eight weeks followed by a subdiabetogenic dose of streptozotocin (HFD-Fr-STZ). Rats were treated with mangiferin (20 mg/kg i.p.) for 28 days starting one week after STZ and its effects were compared to the standard insulin sensitizer, rosiglitazone. HFD-Fr-STZ, induced obesity, hyperglycemia and insulin resistance accompanied by depletion in liver glycogen and dyslipidemia. Moreover, there was an elevation in serum TNF-α and a reduction in adiponectin. Mangiferin ameliorated the consequences of HFD-Fr-STZ and its actions were comparable to the effects of the standard insulin sensitizer, rosiglitazone. The results obtained in this study provide evidence that mangiferin is a possible beneficial natural compound for type 2 diabetes and metabolic disorders associated with the metabolic syndrome. This effect is mediated through improving insulin sensitivity, modulating lipid profile and reverting adipokine levels to normal.
ISSN:1678-2690