Effect of short-term abomasal corn starch infusions on postruminal fermentation and blood measures.

It is possible that some of the systemic responses to subacute ruminal acidosis (SARA) may be caused by increased intestinal starch fermentation. The objective of this experiment was to evaluate the effect of abomasal infusion of up to 3 g of corn starch/kg body weight (approximately 1.6 kg of starch/d) on fecal measures of fermentation, plasma acute phase proteins, and white blood cell populations. Six ruminally cannulated cows in late lactation were randomly assigned to duplicate 3 × 3 Latin squares with 21-d periods. Cows were fed a 20.6% starch TMR twice daily and during the last 7 d of each period cows were abomasally infused with corn starch at 0 (CON), 1 (ST1), or 3 (ST3) g/kg body weight split into 2 bolus infusions, provided every 12 h. Fecal samples were collected at 0, 6, 12, and 18 h following feeding on d 21 and were analyzed for pH, VFA, lactic acid, and lipopolysaccharide (LPS). Composite fecal samples were used to estimate apparent total-tract nutrient digestibility using undigested neutral detergent fiber as an internal marker. Blood samples were collected at 0 and 6 h relative to feeding on d 14, 18, and 21 of each period. Concentrations of haptoglobin and serum amyloid A in plasma were measured in all samples, 0 h samples on d 14 and 21 were used to measure white blood cell populations, and 0 h samples from d 14, 18, and 21 were used for flow cytometric analysis of γδ T cells. Data were analyzed in SAS using models that included fixed effects of treatment and period and the random effects of cow and square. For blood measures, d 14 samples collected before the initiation of abomasal infusions were included as covariates. Time (d or h) was added as a repeated measure in variables that included multiple samples during the abomasal infusion period. A contrast was used to determine the linear effect of increasing abomasal corn starch. Abomasal corn starch linearly decreased fecal pH and linearly increased fecal total VFA and LPS, but effects were modest, with fecal pH, total VFA, and LPS changing from 6.96, 57.7 mM, and 4.14 log endotoxin units (EU) per gram for the CON treatment to 6.69, 64.1 mM, and 4.58 log EU/g for the ST3 treatment, respectively. This suggests that we did not induce hindgut acidosis. There were no effects of treatment on apparent total-tract starch digestibility or fecal starch content (mean of 96.9% and 2.2%, respectively). Treatment did not affect serum acute phase proteins or most circulating white blood cells, but the proportion of circulating γδ T cells tended to linearly decrease from 6.69% for CON to 4.61% for ST3. Contrary to our hypothesis, increased hindgut starch fermentation did not induce an inflammatory response in this study.