title: Fetal Sex Modulates Developmental Response to Maternal Malnutrition.
abstract: The incidence of obesity and metabolic diseases is dramatically high in rapidly developing countries. Causes have been related to intrinsic ethnic features with development of a thrifty genotype for adapting to food scarcity, prenatal programming by undernutrition, and postnatal exposure to obesogenic lifestyle. Observational studies in humans and experimental studies in animal models evidence that the adaptive responses of the offspring may be modulated by their sex. In the contemporary context of world globalization, the new question arising is the existence and extent of sex-related differences in developmental and metabolic traits in case of mixed-race. Hence, in the current study, using a swine model, we compared male and female fetuses that were crossbred from mothers with thrifty genotype and fathers without thrifty genotype. Female conceptuses evidence stronger protective strategies for their adequate growth and postnatal survival. In brief, both male and female fetuses developed a brain-sparing effect but female fetuses were still able to maintain the development of other viscerae than the brain (mainly liver, intestine and kidneys) at the expense of carcass development. Furthermore, these morphometric differences were reinforced by differences in nutrient availability (glucose and cholesterol) favoring female fetuses with severe developmental predicament. These findings set the basis for further studies aiming to increase the knowledge on the interaction between genetic and environmental factors in the determination of adult phenotype.
authors.affiliation: INIA, Madrid, Spain.|University of Sassari, Sassari, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: Gonzalez-Bulnes
authors.affiliation: University of Sassari, Sassari, Italy.
authors.forename: Laura
authors.initials: L
authors.lastname: Torres-Rovira
authors.affiliation: INIA, Madrid, Spain.
authors.forename: Susana
authors.initials: S
authors.lastname: Astiz
authors.affiliation: INIA, Madrid, Spain.
authors.forename: Cristina
authors.initials: C
authors.lastname: Ovilo
authors.affiliation: INIA, Madrid, Spain.
authors.forename: Raul
authors.initials: R
authors.lastname: Sanchez-Sanchez
authors.affiliation: INIA, Madrid, Spain.
authors.forename: Ernesto
authors.initials: E
authors.lastname: Gomez-Fidalgo
authors.affiliation: INIA, Madrid, Spain.
authors.forename: Mariluz
authors.initials: M
authors.lastname: Perez-Solana
authors.affiliation: INIA, Madrid, Spain.
authors.forename: Mercedes
authors.initials: M
authors.lastname: Martin-Lluch
authors.affiliation: INIA, Madrid, Spain.
authors.forename: Consuelo
authors.initials: C
authors.lastname: Garcia-Contreras
authors.affiliation: UCM, Faculty of Veterinary, Madrid, Spain.
authors.forename: Marta
authors.initials: M
authors.lastname: Vazquez-Gomez
mesh_terms: D050154:Adiposity; D000818:Animals; D001835:Body Weight; D004195:Disease Models, Animal; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D005333:Fetus / Q000378:metabolism; D008297:Male; D044342:Malnutrition / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D008431:Maternal-Fetal Exchange / Q000502:physiology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000473:pathology / Q000503:physiopathology*; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology / Q000503:physiopathology; D012727:Sex Characteristics; D034421:Sus scrofa