Background: Diabetes Mellitus (DM) is an endocrine disorder due to improper
secretion of insulin or action of insulin regardless of hyperglycemia in the body.
Reactive oxygen species (ROS) play a major role in the development of insulin
resistance and DM.
Objective: The present study, designed to assess the role of chemically induced ROS and also the effect of chromium picolinate (CrPic) and melatonin (Mel) alone or in combination (CrPic+Mel) along with ROS on insulin resistance, blood glucose, lipid, and oxidative stress variables in alloxan induced Wistar rats. Methods: Male Wistar rats have been categorized into five groups and group consists of six rats. Group I served as untreated, while group II, III, IV, and V, were treated with alloxan (AID), alloxan+CrPic (AID+CrPic), alloxan+Mel (AID+Mel), and alloxan+CrPic+Mel (AID+CrPic+Mel) respectively.
Results: Insulin resistance was greatly increased in group AID rats compared with untreated rats. A similar increase was seen in blood glucose, total cholesterol, and triacylglycerols compared between group II and untreated (P<0.05). Significant differences were observed when group group III, group IV, and group V rats were compared with group II rats in blood glucose and lipid variables (P<0.05). But prominent significant differences were observed between group group II and group IV experimental rats in serum levels of zinc, malondialdehyde, nitric oxide, superoxide dismutase, catalase, and glutathione (P<0.05) respectively. Histopathological findings suggest that the Mel and CrPic+Mel treated rats had normal renal tubular architecture compared with group II rats. Relatively normal architecture of liver and pancreas was observed in alloxan rats treated with Mel and CrPic+Mel.
Conclusion: CrPic and Mel alone or in a combination prevented pathological alterations in the serum and in tissues due to their anti-hyperglycemic, insulinsensitizing, anti-dyslipidemia, and antioxidant activity, but Mel alone was most effective.
Zephy Doddigarla, Iqbal Parwez, Subuhi Abidi and Jamal Ahmad
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