123 Effects of a Saccharomyces Cerevisiae Fermentation Product-Supplemented Diet on Fecal Characteristics, Oxidative Stress, and Blood Gene Expression of Adult Dogs Undergoing Transport Stress

Abstract

Abstract Previously, a Saccharomyces cerevisiae fermentation product (SCFP) was shown to positively alter fecal microbiota, fecal metabolites, and circulating immune cell function of adult dogs. The objective of this study was to measure the effects of SCFP on fecal characteristics, serum oxidative stress biomarkers, and whole blood gene expression of adult dogs undergoing transport stress. Sixteen adult pointer dogs (8M, 8F; mean age = 8.35 y; mean BW = 27.13 kg) were used in a randomized crossover design study. All dogs were fed control diet for 4 wk, then randomly assigned to a control or SCFP-supplemented diet and fed to maintain BW for 11 wk. A 6-wk washout preceded the second 11-wk experimental period with dogs receiving opposite treatments. After 11 wk, fresh fecal and blood samples were collected before and after transport in a van for 45 min. Change from baseline data (i.e., before and after transport) were analyzed using the Mixed Models procedure of SAS 9.4, with P< 0.05 being significant and P< 0.10 being trends. Changes in serum malondialdehyde and 8-isoprostane:creatinine concentrations increased (P< 0.05) in dogs fed SCFP, but decreased in control dogs with transport stress. Other serum markers were unaffected by diet during transport stress. Fecal dry matter percentage tended to be affected (P< 0.10) by diet during transport stress, being reduced in control dogs, but stable in dogs fed SCFP. Other fecal characteristics were unaffected by diet during transport stress. Blood cyclooxgenase-2 and myeloperoxidase mRNA expression was affected (P< 0.05) by diet during transport stress, being increased in control dogs, but stable or decreased in dogs fed SCFP. Expression of other genes was unaffected by diet during transport stress. These data suggest that the benefits of feeding a SCFP in a novel transport stress model are mediated more so by suppressing innate immune cell activation than through decreasing lipid peroxidation.