Short and long‐term repercussions of the experimental diabetes in embryofetal development

Bueno, Aline; Sinzato, Yuri Karen; Sudano, Mateus José; Alvarenga, Fernanda da Cruz Landim e; Calderon, Iracema de Mattos Paranhos; Rudge, Marilza Vieira Cunha; Damasceno, Débora Cristina

doi:10.1002/dmrr.2521

Cited by 12 publications

(5 citation statements)

References 42 publications

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“…In our laboratory, to induce mild diabetes, which is characterized by low glycemic intensity, the rats received a STZ injection (dose of 100 mg/kg body weight) subcutaneously at birth. Approximately three days after STZ administration, these animals developed hyperglycemia (>300 mg/dL) and presented low blood glucose levels (120–200 mg/dL) at adulthood [ 83 , 85 – 93 ]. This fact might be explained by the high regenerative capacity of β -cell during the neonatal period [ 94 , 95 ].…”

Section: Diabetes and Pregnancy: Experimental Modelsmentioning

confidence: 99%

Streptozotocin-Induced Diabetes Models: Pathophysiological Mechanisms and Fetal Outcomes

Damasceno

Netto

Iessi

et al. 2014

BioMed Research International

132

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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.

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Section: Diabetes and Pregnancy: Experimental Modelsmentioning

confidence: 99%

Streptozotocin-Induced Diabetes Models: Pathophysiological Mechanisms and Fetal Outcomes

Damasceno

Netto

Iessi

et al. 2014

BioMed Research International

132

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“…They adapt by altering insulin resistance and secretion, which impairs glucose tolerance in adult life and increases the risk of developing type 2 DM [6]. In addition, animal models have shown that diabetes can be transmitted to the fetus by intrauterine exposure to maternal hyperglycemia, which may contribute to a worldwide epidemic of diabetes, further emphasizing the need for adequate glycemic control during pregnancy [7,8].…”

Section: Introductionmentioning

confidence: 99%

Lentinus edodes Exposure before and after Fetus Implantation: Materno-Fetal Development in Rats with Gestational Diabetes Mellitus

et al. 2019

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Background: The presence of β-glucans and phenolic compounds in Lentinus edodes suggests this mushroom can be used as a nutritional supplement. Two gestational conditions (before and after fetus implantation) were evaluated, and Lentinus edodes exposure was performed in diabetes mellitus rat model induced by streptozotocin in pre-clinical tests. Methods: On the 20th day of pregnancy, cesarean sections were performed. Blood was collected for biochemical, hematologic parameters and oxidative stress biomarkers. Placenta and amniotic fluid were collected, and fetuses were analyzed through morphological evaluation. Results: The mushroom did not reduce the severe hyperglycemia of the mother-concept but promoted an increase in maternal insulin levels; reduced the levels of alanine aminotransferase, and aspartate aminotransferase, triglyceride and total cholesterol; protected the animals from post-implantation losses. Liver damage induced by streptozotocin was reversed in experimental groups. Conclusions: Lentinus edodes mushroom has antioxidant properties that can minimize the damage caused by gestational diabetes mellitus.

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“…Nevertheless, OD/HFD rats showed a decrease in the number of implantations and live fetuses and higher rates of embryonic losses before implantation. Studies with early embryos (from two cells to blastocyst) in culture with high mean glucose concentration ( Fraser et al, 2007 ) or in vivo study using hyperglycemic mother rats to evaluate their pre-embryos ( Bueno et al, 2014 ) showed damages caused by hyperglycemic exposure during early embryonic development. This led to reduced cell numbers and increased apoptosis rates, which caused developmental delay and affected the success of embryonic implantation.…”

Section: Discussionmentioning

confidence: 99%

Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring

Sinzato

Paula

Gallego

et al. 2022

Front. Cell Dev. Biol.

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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.

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Short and long‐term repercussions of the experimental diabetes in embryofetal development

Cited by 12 publications

References 42 publications

Streptozotocin-Induced Diabetes Models: Pathophysiological Mechanisms and Fetal Outcomes

Streptozotocin-Induced Diabetes Models: Pathophysiological Mechanisms and Fetal Outcomes

Lentinus edodes Exposure before and after Fetus Implantation: Materno-Fetal Development in Rats with Gestational Diabetes Mellitus

Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring

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