title: Low-level subchronic arsenic exposure from prenatal developmental stages to adult life results in an impaired glucose homeostasis.
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.
authors: Departamento de Farmacología, Facultad de Medicina, San Luis Potosí, México. medavila@uaslp.mx
authors: M E
authors: ME
authors: Dávila-Esqueda
authors: J M V
authors: JM
authors: Morales
authors: M E
authors: ME
authors: Jiménez-Capdeville
authors: E
authors: E
authors: De la Cruz
authors: R
authors: R
authors: Falcón-Escobedo
authors: E
authors: E
authors: Chi-Ahumada
authors: S
authors: S
authors: Martin-Pérez
mesh_terms: D000818:Animals; D020261:Arsenic Poisoning / Q000503:physiopathology; D018053:Arsenites / Q000008:administration & dosage / Q000633:toxicity*; D042002:Chromatin Assembly and Disassembly / Q000187:drug effects; D003920:Diabetes Mellitus / Q000209:etiology; D005260:Female; D044882:Glucose Metabolism Disorders / Q000097:blood / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D006442:Glycated Hemoglobin / Q000032:analysis; D006937:Hypercholesterolemia / Q000209:etiology; D006943:Hyperglycemia / Q000209:etiology; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007774:Lactation; D018811:Maternal Exposure; D010179:Pancreas / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D017670:Sodium Compounds / Q000008:administration & dosage; D014886:Weaning
chemical_list: D018053:Arsenites; D006442:Glycated Hemoglobin; D007328:Insulin; D017670:Sodium Compounds; C017947:sodium arsenite