| Grant number: | 16/25207-5 |
| Support Opportunities: | Regular Research Grants |
| Start date: | July 01, 2018 |
| End date: | August 31, 2020 |
| Field of knowledge: | Health Sciences - Nutrition - Dietetics |
| Principal Investigator: | Débora Cristina Damasceno |
| Grantee: | Débora Cristina Damasceno |
| Host Institution: | Faculdade de Medicina (FMB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil |
| City of the host institution: | Botucatu |
| Associated researchers: | Gustavo Tadeu Volpato ; Yuri Karen Sinzato |
Abstract
Diabetes is a syndrome characterized by a functional change in the beta-pancreatic cell in insulin synthesis/secretion or due to an inadequate insulin action in peripheral tissues, leading to increased blood glucose concentration (hyperglycemia). The literature describes the pathophysiological mechanisms, such as oxidative stress, are involved in the repercussions of hyperglycemia in various organs and systems. Pregnancy alone causes an imbalance between free radical production and antioxidant defense system, causing oxidative stress. Due to study variables and for ethical reasons, many experimental models are used to investigate diabetes and pregnancy association. In our research laboratory, a number of models for the induction of severe diabetes (mimicking the glycemia of decompensated type 1 Diabetes mellitus) and of mild intensity (to reproduce the glycemia of DM type 2 and / or Gestational DM) were developed. These models were relevant to improve our understanding of the mechanisms in the diabetes and pregnancy in rats, especially considering the repercussions in the maternal organism (reproductive performance, hormonal analyses in the endocrine pancreas, oxidative stress and lipid profile in blood and liver), fetal growth and development and morphological evaluation, cytokine levels and oxidative stress in the placenta. In view of these results, there is evidence to confirm the fetal programming due to an unfavorable maternal intrauterine environment caused by severe diabetes and even by mild diabetes. Based on the fact that offspring born to mildly diabetic rats present altered glycemic changes in adulthood and impaired reproductive performance, and considering a parallelism between the human condiction and experimental related to children born to diabetic mothers to feed inadequately after the maternal breast-feeding during postnatal life, we objectived to evaluate the linking between these two unfavorable condictions (hyperglycemic intrauterine environment and postnatal hyperlipidic diet) in relation to reproductive parameters, oxidative stress, endocrine pancreas, lipid profile, fetal and perinatal growth. In addition, as previous results in our laboratory confirmed the beneficial effects of a calcium and vitamin D mixture in mildly diabetic rats we will also investigate how the treatment using this mixture influences offspring from diabetic rats exposed to the hyperlipid diet from weaning. This study aims at normalizing the redox state of these rats, contributing to a better condiction of the maternal organs and systems and favoring fetal programming. (AU)
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