Review
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World J Transl Med. Aug 12, 2014; 3(2): 96-111
Published online Aug 12, 2014. doi: 10.5528/wjtm.v3.i2.96
Arsenic-induced abnormalities in glucose metabolism: Biochemical basis and potential therapeutic and nutritional interventions
Archana Kulshrestha, Urmila Jarouliya, GBKS Prasad, SJS Flora, Prakash S Bisen
Archana Kulshrestha, Urmila Jarouliya, GBKS Prasad, Prakash S Bisen, School of Studies in Biochemistry, Jiwaji University, Gwalior 474011, India
SJS Flora, Division of Regulatory Toxicology, Defence Research and Development Establishment, Gwalior 474002, India
Author contributions: Each author had participated sufficiently in preparing this review for submission and takes responsibility for its content.
Correspondence to: Prakash S Bisen, Professor, School of Studies in Biotechnology, Jiwaji University, Mahalgaon, Gwalior 474011, India. psbisen@gmail.com
Telephone: +91-751-2462500 Fax: +91-751-4043850
Received: May 6, 2014
Revised: June 21, 2014
Accepted: July 17, 2014
Published online: August 12, 2014
Processing time: 113 Days and 20.6 Hours
Abstract

Health hazards due to the consumption of heavy metals such as arsenic have become a worldwide problem. Metabolism of arsenic produces various intermediates which are more toxic and cause toxicity. Arsenic exposure results in impairment of glucose metabolism, insulin secretion in pancreatic β-cells, altered gene expressions and signal transduction, and affects insulin-stimulated glucose uptake in adipocytes or skeletal muscle cells. Arsenic toxicity causes abnormalities in glucose metabolism through an increase in oxidative stress. Arsenic interferes with the sulfhydryl groups and phosphate groups present in various enzymes involved in glucose metabolism including pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, and contributes to their impairment. Arsenic inhibits glucose transporters present in the cell membrane, alters expression of genes involved in glucose metabolism, transcription factors and inflammatory cytokines which stimulate oxidative stress. Some theories suggest that arsenic exposure under diabetic conditions inhibits hyperglycemia. However, the exact mechanism behind the behavior of arsenic as an antagonist or synergist on glucose homeostasis and insulin secretion is not yet fully understood. The present review delineates the relationship between arsenic and the biochemical basis of its relationship to glucose metabolism. This review also addresses potential therapeutic and nutritional interventions for attenuating arsenic toxicity. Several other potential nutritional supplements are highlighted in the review that could be used to combat arsenic toxicity.

Keywords: Arsenic toxicity; Glucose metabolism; Nutritional aspects

Core tip: This review illustrated the interference caused by arsenic in enzymes, genes and transcription factors involved in glucose metabolism and possible nutritional aspects for attenuating arsenic toxicity.