Maternal swimming mitigates liver damage caused by paternal obesity

Parents' lifestyle and nutrition can program offspring obesity in adulthood. We hypothesized that maternal swimming has beneficial effects on the adversity caused by paternal obesity on offspring.

Twelve-week-old male C57 BL/6 J mice (fed a high-fat diet, obese father [ObFa], or control diet, lean father [LFa]) were mated with female mice fed only the control diet. Mothers were trained (TMo) or untrained (UMo): swimming for 6 wk before and the first 2 wk of gestation. Pups were fed only the control diet.

Fathers showed different body mass (BM) at copulation, but not the mothers. The ObFa had 20% higher BM than the LFa. Twelve-week-old ObFa/UMo offspring showed a higher BM gain than the LFa/UMo and ObFa/TMo. There was BM sexual dimorphism in the LFa/UMo (female mice +24% than male mice). There was hyperglycemia and hyperinsulinemia in the ObFa/UMo, but low glycemia and insulin levels were seen in the ObFa/TMo. There was augmented liver steatosis in the ObFa/UMo compared with the LFa/UMo, and the ObFa/TMo compared with the LFa/TMo, but reduced steatosis in the ObFa/TMo compared with the ObFa/UMo. In addition, lipogenic markers were more expressed and beta-oxidation markers less expressed in the ObFa/UMo compared with the LFa/UMo, but the opposite was observed in the ObFa/TMo compared with the ObFa/UMo. Proinflammatory markers were higher in the liver of the ObFa/UMo compared with the LFa/UMo and lower in the ObFa/TMo compared with the ObFa/UMo.

Obese fathers produced offspring that were overweight and had altered fasting glycemia and insulin sensitivity, leading to higher liver lipogenesis and inflammation, as well as lower beta-oxidation. The swimming mother mitigated these adverse effects in mice offspring.