Parental Obesity Differentially Associates with Newborn Adiposity. Is Programming of the GH-IGF Axis Involved? (OR09-05-19). (13th June 2019)

• Record Type: Journal Article
• Authors: Fuentes, Eva Diaz; Cleves, Mario; Sims, Clark; Shankar, Kartik; Borsheim, Elisabet; Andres, A
• Is Part Of: Current developments in nutrition. Volume 3(2019)Supplement 1
• Publication Date: 2019-06-13
• Subjects: Nutrition -- Periodicals; Nutritional Physiological Phenomena; Nutrition; Periodicals; Periodicals; Fulltext; Internet Resources; Periodicals; 612.3
• DOI: 10.1093/cdn/nzz041.OR09-05-19
• Languages: English
• ISSNs: 2475-2991

Abstract

Abstract: Objectives: Maternal obesity is strongly associated with offspring obesity risk. However, studies show that paternal obesity also affects offspring phenotype, especially in males. Programming of the growth hormone (GH) insulin-like growth factor (IGF) axis seems to be an important mechanism in this finding, but evidence regarding this relationship in humans is scarce. The primary purpose of this study was to evaluate associations between maternal and paternal adiposity with that of their offspring. A secondary aim was to investigate associations between paternal adiposity with GH levels in male offspring. Methods: Parent-offspring trios ( n = 209) from the Glowing study were studied. Percent body fat mass (%FM) was measured using air displacement plethysmography early in pregnancy in parents, and at age 2 weeks in the offspring. Plasma GH levels were measured at birth from umbilical cord blood ( n = 31) and at age 2 years ( n = 39) in male offspring. Multiple linear regression was used to model infant's %FM (dependent variable) at 2 weeks of age using parental %FM, race, age, IQ, income, delivery method, gestational weight gain, feeding mode, and gestational age (GA) as independent variables. The best fitted models were constructed for girls and boys. Spearman correlations (ρ) between paternal %FM and offspring GH levels were adjusted for maternal %FM. Results: Girls ( n = 94): Paternal %FM did not associate with female newborn %FM. Instead, maternal %FM (β = 0.12, P = 0.010) and C-section delivery mode (β = 2.56, P = 0.011) had the strongest associations with female newborn %FM. Boys ( n = 115): Maternal %FM (β = 0.12, P = 0.006) and GA (β = 1.06, P = 0.003) were positively associated with male newborn %FM, whereas paternal %FM was negatively associated (β = −0.09, P = 0.014) with male offspring adiposity. There was no significant correlation between paternal %FM and GH measured at birth (ρ = 0.19, P = NS) in boys. However, at age 2 years, GH levels in boys decreased with increasing paternal %FM (ρ = −0.40, P = 0.015). Maternal %FM did not correlate with offspring GH level at any age. Conclusions: Parental obesity differentially associates with newborn girls' and boys' adiposity at age 2 weeks. In line with prior findings in animal models, this preliminary analysis points to programming of the GH/IGF axis in male offspring born to obese fathers. Funding Sources: USDA ARS # 6026-51000-010-05S, NIH 1UL1RR029884.