Maternal High Fat Diet Causes Changes in Pulmonary Function and Persistent Deficits in Pulmonary Vascularization

Background Maternal obesity has been associated with multiple complications for both the mother and the child including hypertensive disorders and gestational diabetes for the mother and macrosomia and congenital abnormalities for the child. Previously, we demonstrated increases in inflammation, deficits in alveolarization, and decreases in angiogenic pathways in the offspring (PN21) of mice maintained on high fat diets during pregnancy and lactation. For the current studies we tested the hypothesis that maternal obesity would impair lung function in the offspring and that angiogenic pathways would continue to be depressed into adulthood (3 mon). Methods Female mice were fed high fat diets (HFD) or control diets (CD) for 8 weeks prior to mating and through weaning. At weaning the pups were placed on either CD or HFD until 3 months of age. Pulmonary function was assessed using a Scireq Flexivent. Expressions of angiogenic pathway proteins were measured by western blot in lung tissues. Results At 3 months, pulmonary function tests indicated decreased inspiratory capacity, resistance (Rrs), elastance (Ers) and airway resistance (Rn) in the offspring that were fed HFD after weaning. These finding were exacerbated in pups having been born to and nursed by mothers fed HFD. Protein expression of PTP1B was also suppressed at 3 months. Conclusions Maternal and adult HFD results in altered pulmonary function at 3 months of age. Changes in pulmonary function may contribute to increased morbidities associated with obesity. Support or Funding Information The authors gratefully acknowledge funding from the NIH/NICHD, R01HD0880833. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .