title: Beneficial effect of supplementation with copper sulfate on STZ-diabetic mice (IDDM).
abstract: Trace element status is known to be altered in the diabetic state. Current evidence suggests that reactive oxygen intermediates (ROI's) do participate in the destruction of pancreatic beta cells in STZ-induced Type 1 diabetes. The copper and zinc status of diabetic patients and their descendants was also found to have changed. The aim of this study was to evaluate the potential usefulness of copper sulfate in the treatment of STZ-induced type I diabetes. We used C57BL6 female mice, in whom copper sulfate treatment was started at 6 weeks of age followed by an IP injection of 40 mg/kg body weight of STZ for five consecutive days. Its effects were evaluated at 10 weeks of age. The treatment with copper sulfate significantly decreased blood glucose levels, levels of lipid peroxidation and mRNA expression of the enzyme iNOS and the cytokines IFN-gamma and IL-4. Histological analysis of the pancreas revealed that, three out of five animals in the copper sulfate treated groups showed absence of mononuclear cell infiltration and no change in the shape and size of islets as compared to pancreas of the STZ-induced diabetic group of animals. In conclusion, our observations indicate that copper sulfate treatment can exert beneficial effects in diabetes with preservation of beta-cell function in vivo. Copper sulfate could be exerting these beneficial effects either by acting directly by reducing free radicals or through reduction in glucose levels.
authors: National Centre for Cell Science, NCCS Complex, Ganeshkhind Road, Pune 411007, India. ssitasawaad@hotmail.com
authors: S
authors: S
authors: Sitasawad
authors: M
authors: M
authors: Deshpande
authors: M
authors: M
authors: Katdare
authors: S
authors: S
authors: Tirth
authors: P
authors: P
authors: Parab
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D019327:Copper Sulfate / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism*; D005215:Fasting / Q000097:blood; D005260:Female; D007074:Immunoglobulin G / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D007515:Islets of Langerhans / Q000473:pathology; D008054:Lipid Peroxides / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D013154:Spleen / Q000166:cytology / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D007074:Immunoglobulin G; D008054:Lipid Peroxides; D015847:Interleukin-4; D007371:Interferon-gamma; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D019327:Copper Sulfate