Genetic predisposition of pigs to hypo- and hyperselenemia.

A continuing, sporadic incidence of vitamin E-selenium (Se) responsive disease among confinement-reared pigs believed to be fed complete and adequately supplemented diets prompted these studies on the potential genetic influence over vitamin E and Se metabolism in pigs. The initial study revealed a wide range of serum Se and vitamin E concentrations among age-matched, commonly housed and commonly fed growing pigs. Pigs found relatively hyposelenemic (hypo-Se) or hyperselenemic (hyper-Se) early in life retained their relative Se status while commonly reared. The persistence of vitamin E status was poor. Selected matings between identified, relatively hypo-Se gilts and boars and between relatively hyper-Se gilts and boars produced similarly affected baby pigs. In Exp. 2, representative hypo-Se (20) and hyper-Se (20) pigs were identified from a total of 107 baby pigs by 30 d of age. These pigs were allotted to an experiment to compare the responses of these two populations to .1 and .3 ppm supplemental dietary Se through 150 d of age. The difference in mean serum Se of the selected hypo- and hyper-Se pigs fed .1 ppm Se was significant at each sampling time. This difference approximated that observed between pigs (either hypo- or hyperselenemic) fed .1 and .3 ppm Se. The increase in serum Se due to .3 ppm supplemental dietary Se was greater among the selected hypo-Se pigs than among the hyper-Se pigs. Plasma Se-dependent glutathione peroxidase (GSH-Px) was a better indicator of dietary or serum Se status than was erythrocyte GSH-Px. The selected hyper-Se pigs maintained a more rapid rate of growth than did the hypo-Se pigs and were approximately 10 kg heavier at 150 d than the hypo-Se pigs.