Effect of Insulin on Arsenic Toxicity in Diabetic Rats—Liver Function Studies

• Published in: Biological trace element research Vol. 132; no. 1-3; pp. 215 - 226
• Main Authors: Singh, Neetu, Rana, Suresh Vir Singh
• Format: Journal Article
• Language: English
• Published: New York New York : Humana Press Inc 01.12.2009; Humana Press Inc; Springer Nature B.V
• Subjects: Animals; Arsenic; Arsenic - toxicity; Bilirubin; Bilirubin - pharmacology; Biochemistry; Biomedical and Life Sciences; Biotechnology; Blood Glucose - drug effects; Carbohydrates; Diabetes; Diabetes mellitus; Glucose-6-Phosphatase; Hyperglycemia; Insulin; Insulin - pharmacology; Life Sciences; Liver; Liver - drug effects; Liver - metabolism; Liver Function Tests; Male; Nutrition; Oncology; Pharmacodynamics; Pharmacokinetics; Rats; Rats, Wistar; Rodents; Secretion; Toxicity; transaminase; Transaminases - metabolism; Workers; Serum transaminases; Arsenic; Insulin; Liver; Diabetes mellitus
• ISSN: 0163-4984; 1559-0720
• DOI: 10.1007/s12011-009-8396-8

Arsenic (iAs)-induced diabetic mellitus has been debated by several workers. However, role of insulin in iAs-induced diabetes is yet to be investigated. Present report suggests that iAs promotes insulin secretion in diabetic rats and inhibits hyperglycemia. Whereas, reverse effects were recorded after insulin treatment to diabetic and iAs-treated rats. These conditions affect accumulation of iAs in liver. It decreased in diabetic and iAs-treated rats but increased after insulin treatment. Reciprocal effects were observed on serum transaminases and total bilirubin. Nevertheless, activity of glucose-6-phosphatase in the liver was stimulated by insulin treatment to diabetic and arsenic-fed rats. These results suggest that manifestations of arsenic-induced diabetes mellitus are not modulated or reversed by insulin. Observations on liver function further suggest that iAs is less toxic in diabetic rats. This protective effect has been attributed to noninsulin-dependent carbohydrate regulatory mechanisms. Diabetes certainly alters the pharmacodynamics and pharmacokinetics of iAs in rat.