Abstract

Introduction: Obesity in women and men of reproductive age may lead to adverse cardiovascular and metabolic developmental programing in their offspring. For example, we observed signs of cardiac diastolic dysfunction in offspring from obese rats as early as 3 weeks of age. However, the contribution from paternal and maternal obesity to increased susceptibility for developing cardiac dysfunction in their offspring early in life is unknown. Hypothesis: We hypothesized that paternal and maternal obesity both play important roles in causing impaired cardiac function and metabolic disorders such as fatty liver in their offspring early in life. Methods: Livers from male newborn Sprague-Dawley rats born from obese fathers (fHFD-offs), obese mothers (mHFD-offs), or from both parents being obese (fmHFD-offs) were weighed and analyzed for fat content by oil red-O and ECHOMRI. Additionally, within 1-3 days after weaning, male offspring were submitted to cardiac catheterization for assessment of cardiac function. Age-matched offspring from lean rats (ND-Offs) were used as controls. Results: fmHFD-Offs and mHFD-offs groups were heavier compared to fHFD-offs and ND-offs groups (61±4 and 64±2 vs 57±2 and 48±2 g, respectively) at 1-3 days after weaning. Newborn rats with at least one obese parent had more liver fat infiltration compared to ND-offs controls. Compared to ND-offs, only offspring from obese mothers (mHFD-offs) exhibited reduced dP/dt max (8998±466 vs. 10560±807, 11869±1171, and 11611±436 mmHg/s for mHFD-offs vs fHFD-offs, fmHFD-offs and ND-offs, respectively); fmHFD-offs and mHFD-offs showed additional signs of impaired diastolic function as indicated by increased Tau values (5.7±0.2 and 5.6±0.3 vs. 4.7±0.2 and 5.0±0.1 ms for fmHDF-offs and mHFD-offs vs ND-offs and fHFD-offs, respectively). Conclusions: These results indicate that while increased liver steatosis develops independent of which parent is obese, the presence of maternal obesity appears to be more critical for male offspring to develop cardiac dysfunction early in life. Additional studies in adult and aged offspring are needed to test if the impact of paternal and maternal obesity on offspring cardiometabolic function gets stronger with aging.

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