Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring

Abstract

Maternal diabetes-induced fetal programming predisposes offspring to type 2 diabetes, cardiovascular disease, and obesity in adulthood. However, lifelong health and disease trajectories depend on several factors and nutrition is one of the main ones. We intend to understand the role of maternal diabetes-induced fetal programming and its association with a high-fat diet during lifelong in the female F1 generation focusing on reproductive outcomes and the possible changes in physiological systems during pregnancy as well as the repercussions on the F2 generation at birth. For this, we composed four groups: F1 female pups from control (OC) or from diabetic dams (OD) and fed with standard (SD) or high-fat diet from weaning to full-term pregnancy. During pregnancy, glucose intolerance and insulin sensitivity were evaluated. In a full-term pregnancy, the maternal blood and liver were collected to evaluate redox status markers. The maternal blood, placental tissue, and fetal blood (pool) were collected to evaluate adiponectin and leptin levels. Maternal reproductive parameters were evaluated as well. Maternal diabetes and high-fat diet consumption, in isolation, were both responsible for increased infertility rates and fasting glucose levels in the F1 generation and fetal growth restriction in the F2 generation. The association of both conditions showed, in addition to those, increased lipoperoxidation in maternal erythrocytes, regardless of the increased endogenous antioxidant enzyme activities, glucose intolerance, decreased number of implantation sites and live fetuses, decreased litter, fetal and placental weight, increased preimplantation losses, and increased fetal leptin serum levels. Thus, our findings show that fetal programming caused by maternal diabetes or lifelong high-fat diet consumption leads to similar repercussions in pregnant rats. In addition, the association of both conditions was responsible for glucose intolerance and oxidative stress in the first generation and increased fetal leptin levels in the second generation. Thus, our findings show both the F1 and F2 generations harmed health after maternal hyperglycemic intrauterine environment and exposure to a high-fat diet from weaning until the end of pregnancy.

The Ethanolic Extract of Piper glabratum Kunth Is Teratogenic and Interferes with the Ossification Process of Swiss Mice Fetuses

“…However, in general, fetuses reduce their growth and/or stop gaining weight when there is a reduction in placental efficiency. However, the literature indicates different correlations between fetal weight, adequacy of weight for gestational age, placental weight, placental index and placental efficiency [ 17 , 18 , 19 , 21 , 22 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ].…”

“…This relationship establishes the weight of the fetus produced by the weight of the placenta that worked on this production of body mass [ 31 , 32 , 33 , 34 ]. This calculation estimates the maternal–fetal relationship established during the gestational period and is a determinant of intrauterine growth, since the placenta and its performance are responsible for the nutritional and hormonal supply that determines fetal growth and weight gain [ 29 , 30 , 31 ]. It is also known that the supply capacity of the placenta is directly influenced by its size, morphology, blood flow and transport efficiency [ 32 , 33 , 34 , 35 , 36 ].…”

Antenatal and Postnatal Sequelae of Oxidative Stress in Preterm Infants: A Narrative Review Targeting Pathophysiological Mechanisms

“…However, the impact of OS on such long-term outcomes can be modulated by specific factors, such as maternal diet and microbiome. As an example, in experimental models, low-protein and high-fat maternal intakes during pregnancy have been associated with a high susceptibility to OS and with an enhanced oxidative status in the offspring [42,43] and may be potentially associated with such generational sequelae as neurodevelopmental disorders, hypertension, increased infertility rates and diabetes [44][45][46][47][48]. Moreover, an inadequate diet during pregnancy can contribute to an unfavorable microbiome in dams and offspring [49][50][51], which has been further associated with adverse long-term outcomes related to fetal programming [52,53].…”

Effect of transgenerational diabetes via maternal lineage in female rats

“…According to intergenerational studies, the hyperglycemic intrauterine environment led to reduced glucose tolerance, high serum concentration of total cholesterol, triglycerides, VLDL-c, insulin resistance, glucose intolerance, and percentage of insulin-immunostained cells in adulthood F1 generation from diabetic rats [ 10 ]. In addition, these rats presented embryofetal losses at the end of pregnancy [ 11 ].…”