%0 Journal Article
%T Mild Diabetes Models and Their Maternal-Fetal Repercussions
%A D. C. Damasceno
%A Y. K. Sinzato
%A A. Bueno
%A A. O. Netto
%A B. Dallaqua
%A F. Q. Gallego
%A I. L. Iessi
%A S. B. Corvino
%A R. G. Serrano
%A G. Marini
%A F. Piculo
%A I. M. P. Calderon
%A M. V. C. Rudge
%J Journal of Diabetes Research
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/473575
%X The presence of diabetes in pregnancy leads to hormonal and metabolic changes making inappropriate intrauterine environment, favoring the onset of maternal and fetal complications. Human studies that explore mechanisms responsible for changes caused by diabetes are limited not only for ethical reasons but also by the many uncontrollable variables. Thus, there is a need to develop appropriate experimental models. The diabetes induced in laboratory animals can be performed by different methods depending on dose, route of administration, and the strain and age of animal used. Many of these studies are carried out in neonatal period or during pregnancy, but the results presented are controversial. So this paper, addresses the review about the different models of mild diabetes induction using streptozotocin in pregnant rats and their repercussions on the maternal and fetal organisms to propose an adequate model for each approached issue. 1. Introduction Diabetes mellitus (DM) is considered a chronic disease characterized by hyperglycemia resulting from insulin resistance and/or insulin secondary deficiency caused by failure in beta cells (¦Â) pancreatic [1]. DM1 is an autoimmune disease in which there are deficiency of insulin and loss of control of blood glucose, caused by the destruction of pancreatic ¦Â cells mediated by T cells [2]. DM2 is characterized by ¦Â-cell dysfunction and decreased insulin action in some tissues [3]. Another classification is the gestational DM, which occurs by glucose intolerance with variable magnitude. It is first diagnosed during pregnancy and may or may not persist after delivery [4]. Human studies that explore mechanisms responsible for changes caused by diabetes are limited not only for ethical reasons but also by the many uncontrollable variables (diet, socioeconomic factors, nutrition, and genetic factors) that can alter the intrauterine environment and increase congenital malformations. So there is a need to develop a suitable experimental model [5]. The use of animal models provides an essential tool for investigating the molecular mechanisms that control cell growth. The maternal-fetal interface is no exception. Although there are some differences in the organization of rodent versus primate maternal-fetal interface, there are many similarities in the functions and in cell lines that compose it. The induction of experimental diabetes by cytotoxic drugs such as beta-streptozotocin (STZ) is well characterized [6]. Depending on the animal strain used, dose, route of drug administration, and the life period in which STZ is
%U http://www.hindawi.com/journals/jdr/2013/473575/