title: Prenatal programming of obesity in a swine model of leptin resistance: modulatory effects of controlled postnatal nutrition and exercise.
abstract: The main role of early nutritional programming in the current rise of obesity and associated diseases is well known. However, translational studies are mostly based in postnatal food excess and, thus, there is a paucity of information on the phenotype of individuals with prenatal deficiencies but adequate postnatal conditions. Thus, we assessed the effects of prenatal programming (comparing descendants from females fed with a diet fulfilling 100 or only 50% of their nutritional requirements for pregnancy) on gene expression, patterns of growth and fattening, metabolic status and puberty attainment of a swine model of obesity/leptin resistance with controlled postnatal nutrition and opportunity of exercise. Maternal restriction was related to changes in the relationships among gene expression of positive (insulin-like growth factors 1 and 2) and negative (myostatin) regulators of muscle growth, with negative correlations in gilts from restricted pregnancies and positive relationships in the control group. In spite of these differences, the patterns of growth and fattening and the metabolic features during juvenile growth were similar in control gilts and gilts from restricted pregnancies. Concomitantly, there was a lack of differences in the timing of puberty attainment. However, after reaching puberty and adulthood, females from restricted pregnancies were heavier and more corpulent than control gilts, though such increases in weight and size were not accompanied by increases in adiposity. In conclusion, in spite of changes in gene expression induced by developmental programming, the propensity for higher weight and adiposity of individuals exposed to prenatal malnutrition may be modulated by controlled food intake and opportunity of physical exercise during infant and juvenile development.
authors.affiliation: 1 Universidad Complutense de Madrid, Facultad de Veterinaria, Madrid, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Barbero
authors.affiliation: 2 Animal Reproduction Department, INIA, Madrid, Spain.
authors.forename: S
authors.initials: S
authors.lastname: Astiz
authors.affiliation: 2 Animal Reproduction Department, INIA, Madrid, Spain.
authors.forename: C
authors.initials: C
authors.lastname: Ovilo
authors.affiliation: 1 Universidad Complutense de Madrid, Facultad de Veterinaria, Madrid, Spain.
authors.forename: C J
authors.initials: CJ
authors.lastname: Lopez-Bote
authors.affiliation: 2 Animal Reproduction Department, INIA, Madrid, Spain.
authors.forename: M L
authors.initials: ML
authors.lastname: Perez-Solana
authors.affiliation: 1 Universidad Complutense de Madrid, Facultad de Veterinaria, Madrid, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Ayuso
authors.affiliation: 1 Universidad Complutense de Madrid, Facultad de Veterinaria, Madrid, Spain.
authors.forename: I
authors.initials: I
authors.lastname: Garcia-Real
authors.affiliation: 2 Animal Reproduction Department, INIA, Madrid, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Gonzalez-Bulnes
mesh_terms: D050154:Adiposity / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D020738:Leptin / Q000097:blood*; D008297:Male; D009765:Obesity / Q000097:blood* / Q000503:physiopathology / Q000628:therapy*; D010805:Physical Conditioning, Animal / Q000379:methods / Q000502:physiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000503:physiopathology; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*; D013552:Swine
chemical_list: D020738:Leptin