Animal Models in Diabetes and Pregnancy

Abstract

The worldwide increase in the incidence of diabetes, the increase in type 2 diabetes in women at reproductive ages, and the cross-generation of the intrauterine programming of type 2 diabetes are the bases for the growing interest in the use of experimental diabetic models in order to gain insight into the mechanisms of induction of developmental alterations in maternal diabetes. In this scenario, experimental models that present the most common features of diabetes in pregnancy are highly required. Several important aspects of human diabetic pregnancies such as the increased rates of spontaneous abortions, malformations, fetoplacental impairments, and offspring diseases in later life can be approached by using the appropriate animal models. The purpose of this review is to give a practical and critical guide into the most frequently used experimental models in diabetes and pregnancy, discuss their advantages and limitations, and describe the aspects of diabetes and pregnancy for which these models are thought to be adequate. This review provides a comprehensive view and an extensive analysis of the different models and phenotypes addressed in diabetic animals throughout pregnancy. The review includes an analysis of the surgical, chemical-induced, and genetic experimental models of diabetes and an evaluation of their use to analyze early pregnancy defects, induction of congenital malformations, placental and fetal alterations, and the intrauterine programming of metabolic diseases in the offspring's later life.

Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats

“…Impairment of the oxidative and nitrosative stress balance can deregulate multiple signaling pathways and cause massive cell damage, apoptotic events, and defective embryonic and fetal development (Sivan et al 1997;Reece et al 2005;Morgan et al 2008;Sugimura et al 2009). In addition, the malformation rate is clearly correlated with increased glucose concentrations (Jawerbaum and White 2010). Experimental results support the notion of hyperglycemia as a teratogen, since high glucose levels (Dienelt and Zur Nieden 2011) or maternal diabetes in vivo as well as exposure to high glucose concentration cause embryonic maldevelopment.…”

A euglycaemic/non-diabetic perinatal environment does not alleviate early beta cell maldevelopment and type 2 diabetes risk in the GK/Par rat model

“…It should be noted that this happened despite a return to normal fetal growth and pancreas weight, clearly illustrating a lack of association between fetal weight and development of BCM (and further risk of type 2 diabetes). Our findings in the oGK/pW fetus do not necessarily contradict the evidence for an adverse influence of maternal diabetes on beta cell formation, as reported in the majority of experimental studies with maternal diabetes induced (not spontaneous) in various models [24]. Beta cell development, differentiation and survival are indisputably controlled by genes.…”

Hypoglycemic and anti–hyperglycemic study of Gynura procumbens leaf extracts

“…Consequently, in the present study a preliminary dose response effect of STZ on blood glucose (standardization) was carried out to determine the optimum dose needed to produce stable hyperglycemia in Sprague Dawley rats, as data in the literature could not be relied upon due to broad variability [10,11] . The results indicated that a single intra-peritoneal injection of 40-45, 50-55 and 60-65 mg/kg body weight of STZ could induce hyperglycemia in SD rats after 6 d, but of varying intensities.…”