Paternal Zn-deficiency abolishes metabolic effects in offspring induced by diet type

Abstract

Accumulating evidence implicates that offspring are susceptible to paternal alterations in numerous fetal disorders, such as growth and metabolic defects. However, less study has been conducted to define the relationship between paternal zinc deficiency (ZnD) and energy metabolism of offspring. In the present study, we used a paternal ZnD exposure (Zn at 0.3 μg/g) model to test energy metabolism of male and female offspring with the intervention of diet type (high-fat diet and low-fat diet). Our results demonstrated that paternal ZnD decreased body weight (BW) gain per week ( P < 0.01) and ME intake per week ( P < 0.05) at 11 weeks in male offspring with high-fat diet intervention but not in female offspring. Further, anabolism and catabolism of hepatic energy products also exhibited alterations. ZnD attenuated liver glucose but increased lipids content accompanied with elevated adiponectin and reduction in leptin level in serum, which exhibited lipid metabolic disturbance and smaller ratio of liver weight to BW in male but not female offspring. The qRT-PCR and liver energy metabolites analysis revealed that paternal ZnD mainly induced reduction in glucose tolerance and lowered glucose uptaking ability in male offspring and thereby alleviated glycolysis and the tricarboxylic acid cycle (TCA) cycle, which displayed a male gender-dependency. Therefore, we propose that paternal ZnD abolishes metabolic effects in male offspring induced by diet type intervention. Our findings reveal a novel link between paternal Zn-D and offspring energy metabolism.

Paternal dietary ratio of n-6: n-3 polyunsaturated fatty acids programs offspring leptin expression and gene imprinting in mice

“…Interestingly, we found that paternal n-3 PUFAs reduced leptin levels in adult offspring in a sex-specific manner, with effects on F1 males and F2 females. In keeping with this, peri-conceptional exposure to other nutritional changes (e.g., obesity, fructose-rich diet, and Zn deficiency) is sufficient to shape offspring expression patterns of metabolism-associated genes, characterized by impacts on males instead of females in the F1 generation (82)(83)(84)(85)(86). However, inconsistent results have also been reported, with female (but not male) offspring from fathers fed a high-fat diet before mating displaying impaired pancreatic β-cell function with increased body weight (87).…”