TY - JOUR
T1 - Obesity and Metabolic Traits after High-Fat Diet in Iberian Pigs with Low Birth Weight of Placental Origin
AU - Heras-Molina, Ana
AU - Yeste, Natalia
AU - Pesántez-Pacheco, José Luis
AU - Astiz, Susana
AU - Vázquez-Gómez, Marta
AU - Bettiga, Arianna
AU - Trevisani, Francesco
AU - García-Contreras, Consolación
AU - Luis-Lima, Sergio
AU - Bassols Teixidó, Anna Maria
AU - Porrini, Esteban
AU - Gonzalez-Bulnes, Antonio
PY - 2022
Y1 - 2022
N2 - Intrauterine growth restriction is an increasingly concerning issue for human pregnancies because of its perinatal and longer-term consequences on offspring health. We have explored, in a swine model, differences in the adult phenotype of offspring with low birth weight induced by maternal malnutrition or placental insufficiency. Intrauterine growth restriction (IUGR) and later obesity and metabolic disorders have classically been associated with maternal malnutrition, but most cases of IUGR are related to placental insufficiency. The current study, using a swine model for IUGR and obesity, aimed to determine the interaction of birth weight (categorized as low birth weight [LBW] or normal birth-weight [NBW]) and postnatal diet (categorized as maintenance diet [MD] or fattening diet [FD]) on body weight, adiposity and metabolic traits. FD induced higher body weight and adiposity (both p < 0.0001), with higher fructosamine levels (p < 0.005) and a trend toward higher HOMA-β index (p = 0.05). NBW pigs remained heavier than LBW pigs during the early juvenile period (p < 0.005), but there were no differences at later stages. There were no differences in metabolic traits during juvenile development, but there were differences in adulthood, when LBW pigs showed higher glucose and lower insulin levels than NBW pigs (both p < 0.05). These results suggest that (a) FD allows LBW offspring to achieve similar obesity in adulthood as NBW offspring, and (b) glucose metabolism is more compromised in obese LBW than obese NBW pigs. The comparison of our data with previous studies highlights significant differences between offspring with LBW induced by maternal malnutrition or placental insufficiency, which should be considered when studying the condition.
AB - Intrauterine growth restriction is an increasingly concerning issue for human pregnancies because of its perinatal and longer-term consequences on offspring health. We have explored, in a swine model, differences in the adult phenotype of offspring with low birth weight induced by maternal malnutrition or placental insufficiency. Intrauterine growth restriction (IUGR) and later obesity and metabolic disorders have classically been associated with maternal malnutrition, but most cases of IUGR are related to placental insufficiency. The current study, using a swine model for IUGR and obesity, aimed to determine the interaction of birth weight (categorized as low birth weight [LBW] or normal birth-weight [NBW]) and postnatal diet (categorized as maintenance diet [MD] or fattening diet [FD]) on body weight, adiposity and metabolic traits. FD induced higher body weight and adiposity (both p < 0.0001), with higher fructosamine levels (p < 0.005) and a trend toward higher HOMA-β index (p = 0.05). NBW pigs remained heavier than LBW pigs during the early juvenile period (p < 0.005), but there were no differences at later stages. There were no differences in metabolic traits during juvenile development, but there were differences in adulthood, when LBW pigs showed higher glucose and lower insulin levels than NBW pigs (both p < 0.05). These results suggest that (a) FD allows LBW offspring to achieve similar obesity in adulthood as NBW offspring, and (b) glucose metabolism is more compromised in obese LBW than obese NBW pigs. The comparison of our data with previous studies highlights significant differences between offspring with LBW induced by maternal malnutrition or placental insufficiency, which should be considered when studying the condition.
KW - Animal models
KW - Intrauterine growth restriction
KW - Obesity
KW - Translational medicine
U2 - 10.3390/biology11101533
DO - 10.3390/biology11101533
M3 - Article
C2 - 36290436
SN - 2079-7737
VL - 11
JO - Biology
JF - Biology
ER -