Abstract
BackgroundExperimental models are necessary to elucidate diabetes pathophysiological mechanisms not yet understood in humans. Objective: To evaluate the repercussions of the mild diabetes, considering two methodologies, on the pregnancy of Wistar rats and on the development of their offspring.MethodsIn the 1st induction, female offspring were distributed into two experimental groups: Group streptozotocin (STZ, n = 67): received the β-cytotoxic agent (100 mg STZ/kg body weight - sc) on the 1st day of the life; and Non-diabetic Group (ND, n = 14): received the vehicle in a similar time period. In the adult life, the animals were mated. After a positive diagnosis of pregnancy (0), female rats from group STZ presenting with lower glycemia than 120 mg/dL received more 20 mg STZ/kg (ip) at day 7 of pregnancy (2nd induction). The female rats with glycemia higher than 120 mg/dL were discarded because they reproduced results already found in the literature. In the mornings of days 0, 7, 14 and 21 of the pregnancy glycemia was determined. At day 21 of pregnancy (at term), the female rats were anesthetized and killed for maternal reproductive performance and fetal development analysis. The data were analyzed using Student-Newman-Keuls, Chi-square and Zero-inflated Poisson (ZIP) Tests (p < 0.05).ResultsSTZ rats presented increased rates of pre (STZ = 22.0%; ND = 5.1%) and post-implantation losses (STZ = 26.1%; ND = 5.7%), reduced rates of fetuses with appropriate weight for gestational age (STZ = 66%; ND = 93%) and reduced degree of development (ossification sites).ConclusionMild diabetes led a negative impact on maternal reproductive performance and caused intrauterine growth restriction and impaired fetal development.
Highlights
Experimental models are necessary to elucidate diabetes pathophysiological mechanisms not yet understood in humans
The fetuses were classified by the mean ± 1.7 SD according to the mean values of fetal weights of the non-diabetic group (ND): as small for pregnancy age (SPA) when weight was smaller than ND mean - 1.7 SD; appropriate for pregnancy age (APA) when weight was included in ND mean ± 1.7 SD; and large for pregnancy age (LPA) when weight was greater than ND mean + 1.7 SD [31]. 2.4
The STZ group showed no significant difference in the mean number of live fetuses and fetal weight compared to the ND group
Summary
Experimental models are necessary to elucidate diabetes pathophysiological mechanisms not yet understood in humans. Diabetes mellitus (DM) is characterized by disarrangement of the metabolism of carbohydrates, proteins and lipids caused by the complete or relative insufficiency of insulin secretion and/or insulin action [1]. DM is not a disease but rather a heterogeneous group of syndromes characterized by elevated glucose levels caused by the absolute or relative deficiency of insulin. Pregnancy is characterized by insulin resistance and compensatory hyperinsulinemia and is a period when maternal pancreatic functional reserve is tested. In the absence of pancreatic functional reserve, the pancreas fails to produce insulin levels with relative hypoinsulinism in the second half of pregnancy with consequent maternal hyperglycemia, characterizing DMG [3]. The pathophysiology of DMG is not fully elucidated. Its incidence is variable and occurs in 3 to 8% of pregnant women [4,5]
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