Streptozotocin-Induced Diabetes Models: Pathophysiological Mechanisms and Fetal Outcomes

• Autor(a) principal: Damasceno, Debora Cristina [UNESP]
• Data de Publicação: 2014
• Outros Autores: Netto, A. O. [UNESP], Iessi, I. L. [UNESP], Gallego, F. Q. [UNESP], Corvino, S. B. [UNESP], Dallaqua, B. [UNESP], Sinzato, Y. K. [UNESP], Bueno, A. [UNESP], Calderon, Iracema de Mattos Paranhos [UNESP], Rudge, Marilza Vieira Cunha [UNESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.1155/2014/819065; http://hdl.handle.net/11449/112239

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.