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BioMed Research International
Volume 2014, Article ID 819065, 11 pages
http://dx.doi.org/10.1155/2014/819065
Review Article

Streptozotocin-Induced Diabetes Models: Pathophysiological Mechanisms and Fetal Outcomes

1Laboratory of Experimental Research on Gynecology and Obstetrics, Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, UNESP-Universidade Estadual Paulista, Distrito de Rubião Júnior S/N, 18618-970 Botucatu, SP, Brazil
2Department of Gynecology and Obstetrics, Botucatu Medical School, UNESP-Univsidade Estadual Paulista, Distrito de Rubião Júnior S/N, 18618-970 Botucatu, SP, Brazil

Received 14 March 2014; Revised 30 April 2014; Accepted 14 May 2014; Published 27 May 2014

Academic Editor: Luis Sobrevia

Copyright © 2014 D. C. Damasceno et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Glucose homeostasis is controlled by endocrine pancreatic cells, and any pancreatic disturbance can result in diabetes. Because 8% to 12% of diabetic pregnant women present with malformed fetuses, there is great interest in understanding the etiology, pathophysiological mechanisms, and treatment of gestational diabetes. Hyperglycemia enhances the production of reactive oxygen species, leading to oxidative stress, which is involved in diabetic teratogenesis. It has also been suggested that maternal diabetes alters embryonic gene expression, which might cause malformations. Due to ethical issues involving human studies that sometimes have invasive aspects and the multiplicity of uncontrolled variables that can alter the uterine environment during clinical studies, it is necessary to use animal models to better understand diabetic pathophysiology. This review aimed to gather information about pathophysiological mechanisms and fetal outcomes in streptozotocin-induced diabetic rats. To understand the pathophysiological mechanisms and factors involved in diabetes, the use of pancreatic regeneration studies is increasing in an attempt to understand the behavior of pancreatic beta cells. In addition, these studies suggest a new preventive concept as a treatment basis for diabetes, introducing therapeutic efforts to minimize or prevent diabetes-induced oxidative stress, DNA damage, and teratogenesis.