title: Maternal obesity and malnourishment exacerbate perinatal oxidative stress resulting in diabetogenic programming in F1 offspring.
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.
authors.affiliation: Department of Biochemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt. m.ibrahim1988@hotmail.com.|The Ritchie Centre, Hudson Institute of Medical Research, Monash University, Melbourne, VIC, Australia. m.ibrahim1988@hotmail.com.
authors.forename: M I
authors.initials: MI
authors.lastname: Saad
authors.affiliation: Department of Human Genetics, Medical Research Institute, Alexandria University, Alexandria, Egypt.
authors.forename: T M
authors.initials: TM
authors.lastname: Abdelkhalek
authors.affiliation: Department of Biochemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt.
authors.forename: M M
authors.initials: MM
authors.lastname: Haiba
authors.affiliation: Department of Human Genetics, Medical Research Institute, Alexandria University, Alexandria, Egypt.
authors.forename: M M
authors.initials: MM
authors.lastname: Saleh
authors.affiliation: Department of Biochemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt.
authors.forename: M Y
authors.initials: MY
authors.lastname: Hanafi
authors.affiliation: Department of Molecular Medicine, University of Padova, Padua, Italy.
authors.forename: S H
authors.initials: SH
authors.lastname: Tawfik
authors.affiliation: Department of Biochemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt.
authors.forename: M A
authors.initials: MA
authors.lastname: Kamel
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000209:etiology / Q000503:physiopathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D047109:Fetal Development; D015227:Lipid Peroxidation; D044342:Malnutrition / Q000150:complications*; D009765:Obesity / Q000150:complications*; D018384:Oxidative Stress; D018743:Perinatal Care; D011247:Pregnancy; D011256:Pregnancy Outcome; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar
keywords: Apoptosis; Fetal origin of disease; Fetal programming; Malnutrition; Obesity; Oxidative stress