24 Feed restriction as a model for disruption of gut homeostasis in horses: A pilot study

Abstract

Involuntary feed restriction is commonly experienced by horses during transport, in preparation for or during competition, during illness or treatment for some diseases (eg, colic), and to facilitate weight loss in overweight individuals. Short-term reduction of feed intake is known to cause intestinal barrier dysfunction and precedes disease in multiple species. Using short-term feed restriction to induce gut dysfunction could provide a means to investigate meaningful interventions, as well as inform recommendations on routine management practices. The aim of this pilot study was to evaluate blood and gut inflammatory markers in response to short-term feed restriction (STFR). Feed restriction was imposed in 2-year-old Quarter Horses for 3 d (FR, n = 4) and compared with age- and time-matched control horses (CON, n = 4). The basal diet for all horses included concentrate (0.7% BW) and ad libitum grass hay and water. During the 3-d STFR period, intake for FR was reduced to 50% of daily DE requirements (50% of DE supplied by concentrate and 50% by hay) while CON horses remained on the basal diet. All horses were routinely housed in stalls during the day and in pasture at night but remained in stalls fulltime during the STFR period. Blood and fecal samples were taken immediately before (PRE) and at the conclusion of the 3-d STFR period (0 h), and at 9, 24, 33 and 48 h post-STFR. Serum amyloid A (SAA), serumcortisol, fecal immunoglobulins and fecal zonulin were measured by ELISA and data were compared using mixed model ANOVA with repeated measures. STFR resulted in greater (P < 0.01) loss of BW in FR horses (5.74 ± 0.51% of PRE BW) than CON horses (0.80 ± 0.38%) and, despite returning to their normal ration, FR horses retained a weight loss deficit 48 h post-STFR (P = 0.003). Serum cortisol did not differ between FR and CON but did fluctuate over time (P < 0.0001), likely related to the circadian rhythm. A time*treatment interaction was observed for SAA (P = 0.03), where it tended to be higher in FR than CON following STFR. However, SAA was highly variable between horses and the response to STFR was unimpressive. Fecal dry matter changed over time (P = 0.02), where it was elevated at 9 h post-STFR but had returned to the pre-STFR moisture level by h 33. A time*treatment interaction was also observed for fecal pH (P = 0.06) and tended to be higher (P = 0.08) in FR compared with CON following STFR. Evaluation of other inflammatory markers may be informative about the response to this STFR model. Additionally, measurements obtained during STFR (not just after) would help clarify when the most pronounced effects occur.