Apoptosis in pancreatic β-cells is induced by arsenic and atorvastatin in Wistar rats with diabetes mellitus type 2
Article
-
- Overview
-
- Research
-
- Identity
-
- Additional Document Info
-
- View All
-
Overview
abstract
-
Introduction Diabetes Mellitus type 2 (T2D) is a multifactorial disease. However, it is known that there is an important effect in pancreatic β-cells caused by apoptosis of pro-apoptotic proteins, possibly related to arsenic exposure and atorvastatin treatment. Objective The goal of this study was to evaluate the effects of atorvastatin treatment on apoptosis of pancreatic β-cells in Wistar rats with induced diabetes type 2 exposed to arsenic. Material %26 methods T2D in Wistar rats was induced by administration of Streptozotocin. The plasmatic glucose concentrations were measured using the glucose oxidase method, and the concentration of glycated hemoglobin (HbA1c) in whole blood was determined. Exposure to arsenic was measured from urine using atomic absorption with hydride generation, and pro-apoptotic proteins in pancreatic β-cells were observed using the Western blotting technique. Results Caspase-3 was present in rats that were treated with 10 mg/kg of oral atorvastatin and exposed to 0.01 and 0.025 mg/L of arsenic, but no others proteins were present, such as pro Caspase-8, bcl-2, and Fas. The glycemic levels were 129.2 ± 7.0 mg/dL in the control group and 161.8 ± 14.6 mg/dL and 198.3 ± 18.2 mg/dL (p <.05) in the study groups. HbA1c increased from 2.53%25 to 3.64%25 (p <.05) in the control and study groups. Conclusions Atorvastatin treatment and arsenic exposure alone are capable of generating apoptosis in pancreatic β-cells of Wistar rats with T2D. Together, all of these factors induce apoptosis in pancreatic cells. © 2017 The Authors
-
Introduction Diabetes Mellitus type 2 (T2D) is a multifactorial disease. However, it is known that there is an important effect in pancreatic β-cells caused by apoptosis of pro-apoptotic proteins, possibly related to arsenic exposure and atorvastatin treatment. Objective The goal of this study was to evaluate the effects of atorvastatin treatment on apoptosis of pancreatic β-cells in Wistar rats with induced diabetes type 2 exposed to arsenic. Material & methods T2D in Wistar rats was induced by administration of Streptozotocin. The plasmatic glucose concentrations were measured using the glucose oxidase method, and the concentration of glycated hemoglobin (HbA1c) in whole blood was determined. Exposure to arsenic was measured from urine using atomic absorption with hydride generation, and pro-apoptotic proteins in pancreatic β-cells were observed using the Western blotting technique. Results Caspase-3 was present in rats that were treated with 10 mg/kg of oral atorvastatin and exposed to 0.01 and 0.025 mg/L of arsenic, but no others proteins were present, such as pro Caspase-8, bcl-2, and Fas. The glycemic levels were 129.2 ± 7.0 mg/dL in the control group and 161.8 ± 14.6 mg/dL and 198.3 ± 18.2 mg/dL (p <.05) in the study groups. HbA1c increased from 2.53%25 to 3.64%25 (p <.05) in the control and study groups. Conclusions Atorvastatin treatment and arsenic exposure alone are capable of generating apoptosis in pancreatic β-cells of Wistar rats with T2D. Together, all of these factors induce apoptosis in pancreatic cells. © 2017 The Authors
publication date
published in
Research
keywords
-
Apoptosis; Arsenic exposure; Atorvastatin treatment; Diabetes mellitus type 2 arsenic; atorvastatin; caspase 3; caspase 8; Fas antigen; glucose; glucose oxidase; hemoglobin A1c; protein bcl 2; streptozocin; antioxidant; arsenic; atorvastatin; hydroxymethylglutaryl coenzyme A reductase inhibitor; animal cell; animal experiment; animal tissue; apoptosis; Article; atomic absorption spectrometry; controlled study; electrophoresis; female; glucose blood level; limit of quantitation; male; non insulin dependent diabetes mellitus; nonhuman; pancreas islet beta cell; polyacrylamide gel electrophoresis; priority journal; rat; Western blotting; animal; apoptosis; chemically induced; drug effect; experimental diabetes mellitus; metabolism; non insulin dependent diabetes mellitus; pancreas islet beta cell; pathology; Wistar Kyoto rat; Animals; Antioxidants; Apoptosis; Arsenic; Atorvastatin; Blood Glucose; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Female; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Insulin-Secreting Cells; Male; Rats, Inbred WKY; Streptozocin
Identity
Digital Object Identifier (DOI)
PubMed ID
Additional Document Info
start page
end page
volume