Summary
The source of alloxan and its role in the aetiology of diabetes mellitus in man is unclear. Alloxan can be found in body fluids in man during diseases and may be formed from a related industrial material. Its structure closely, resembles pyrimidine and may be derived from uric acid. Alloxan-induced diabetes is mediated via free radical damage of pancreatic β-cells. Therefore, antioxidants or free radical scavengers may alter the diabetogenic action of the chemical. The aim and the design of the study is to test the susceptibility of the animal with various vitamin A status to diabetes after a challenge of 100 mg/Kg body weight of alloxan. Physiological and histological parameters, fasting plasma glucose and islet size and number respectively, are monitored as indexes of the severity of the induced diabetes over a period of three weeks. Since retinol has been found to stimulate β-cancer cell but not normal β-cell to secrete insulin in vitro, the effect of vitamin A supplementation on the established diabetes in vivo is also studied for three more weeks. It is concluded that vitamin A deficiency increases the susceptibility of rats to alloxan. Supplementation of retinyl palmitate at twice of normal level of intake confers no additional protective effect against alloxan damage over the control. In the vitamin A depleted rat, replenishment of retinoid does not ameliorate the elevated fasting glucose level, but does restore the total islet size (size x number of islet) comparable to the supplemented group.
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© 1992 Birkhäuser Verlag, Basel/Switzerland
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Chung, Y.M.I., Chiu, P.M.M., Wong, H.L. (1992). Modification of Alloxan Diabetes in Rats by Vitamin a Status. In: Ong, A.S.H., Packer, L. (eds) Lipid-Soluble Antioxidants: Biochemistry and Clinical Applications. Molecular and Cell Biology Updates. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7432-8_22
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DOI: https://doi.org/10.1007/978-3-0348-7432-8_22
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