Exp Clin Endocrinol Diabetes 2011; 119(10): 613-617
DOI: 10.1055/s-0031-1287782
Article
© J. A. Barth Verlag in George Thieme Verlag KG Stuttgart · New York

Low-Level Subchronic Arsenic Exposure from Prenatal Developmental Stages to Adult Life Results in an Impaired Glucose Homeostasis

M. E. Dávila-Esqueda
1   Departamento de Farmacología, Facultad de Medicina, San Luis Potosí, México
,
J. M. Morales
2   Laboratorio de Clínicos, Facultad de Ciencias Químicas, San Luis Potosí, México
,
M. E. Jiménez-Capdeville
3   Departamento de Bioquímica, San Luis Potosí, México
,
E. De la Cruz
4   Departamento de Hormonas, San Luis Potosí, México
,
R. Falcón-Escobedo
5   Departamento de Patología, Hospital Central “Ignacio Morones Prieto”, San Luis Potosí, México
,
E. Chi-Ahumada
5   Departamento de Patología, Hospital Central “Ignacio Morones Prieto”, San Luis Potosí, México
,
S. Martin-Pérez
6   Bioterio, Facultad de Medicina, Universidad Autónoma de San Luis Potosí (UASLP), San Luis Potosí, México
› Author Affiliations
Further Information

Publication History

received 04 February 2011
first decision 29 August 2011

accepted 31 August 2011

Publication Date:
08 November 2011 (online)

Abstract

We evaluated how low-level (3 ppm) subchronic inorganic arsenic (iAs) exposure from prenatal developmental stages until adult life affects glucose homeostasis. Biochemical parameters of glucose and lipid metabolism, pancreatic insulin and glycosylated haemoglobin were determined in 4-month-old female offspring of adult Wistar rats. Pancreatic histology was also performed. Statistical comparisons between control and iAs-treated groups were performed by unpaired two-tailed Student’s t-test. Statistical significance was set at p<0.05. We found that iAs treatment resulted in an impaired glucose tolerance test, suggestive of impaired glucose metabolism. This group was found to have hyperglycaemia and high levels of HOMA-IR, glycosylated haemoglobin, cholesterol and pancreatic insulin compared to control rats. However, plasma insulin, triglycerides and high-density lipoprotein cholesterol were not different from control rats. Moreover, β-cell damage found in iAs-treated rats consisted of cells with a nucleus with dense chromatin and predominance of eosinophilic cytoplasm, as well as changes in the pancreatic vasculature. The current study provided evidence that subchronic iAs exposure at 3 ppm from prenatal developmental stages to adult life resulted in damage to pancreatic β cells, affected insulin secretion and demonstrated altered glucose homeostasis, thus supporting a causal association between iAs exposure and diabetes.

 
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