ArticleJournal of endocrinological investigation2016
Maternal obesity and malnourishment exacerbate perinatal oxidative stress resulting in diabetogenic programming in F1 offspring.
Article in Journal of endocrinological investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- The pre-conception maternal exposure to Sofosbuvir affects the mitochondrial biogenesis in prenatal fetal tissues: Experimental study on rats.Molecular medicine (Cambridge, Mass.) · 2023Article
- Developmental Programming in Animal Models: Critical Evidence of Current Environmental Negative Changes.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Maternal atopy and offspring epigenome-wide methylation signature.Epigenetics · 2021Article
- Cardiometabolic Phenotypic Differences in Male Offspring Born to Obese Preeclamptic-Like BPH/5 Mice.Frontiers in pediatrics · 2021Article
- Endocrine Disrupting Chemicals: An Occult Mediator of Metabolic Disease.Frontiers in endocrinology · 2019Review
- Weanling Offspring of Dams Maintained on Serine-Deficient Diet Are Vulnerable to Oxidative Stress.Oxidative medicine and cellular longevity · 2018Article
- Diet in pregnancy-more than food.European journal of pediatrics · 2017Review
- Correlation between Oxidative Stress, Nutrition, and Cancer Initiation.International journal of molecular sciences · 2017Review
- Epigenetics: spotlight on type 2 diabetes and obesity.Journal of endocrinological investigation · 2016Review
- Proteome analysis of human amniotic mesenchymal stem cells (hA-MSCs) reveals impaired antioxidant ability, cytoskeleton and metabolic functionality in maternal obesity.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of in-utero environment on fetal health and survival is long-lasting, and this is known as the fetal origin hypothesis. The oxidative stress state during gestation could play a pivotal role in fetal programming and development of diseases such as diabetes. In this study, we investigated the effect of intra-uterine obesity and malnutrition on oxidative stress markers in pancreatic and peripheral tissues of F1 offspring both prenatally and postnatally. Furthermore, the effect of postnatal diet on oxidative stress profile was evaluated. The results indicated that intra-uterine obesity and malnourishment significantly increased oxidative stress in F1 offspring. Moreover, the programming effect of obesity was more pronounced and protracted than malnutrition. The obesity-induced programming of offspring tissues was independent of high-caloric environment that the offspring endured; however, high-caloric diet potentiated its effect. In addition, pancreas and liver were the most affected tissues by fetal reprogramming both prenatally and postnatally. In conclusion, maternal obesity and malnutrition-induced oxidative stress could predispose offspring to insulin resistance and diabetes.
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