Intestinal Alkaline Phosphatase Alleviates Ruminal Acidosis in Dairy Cows Fed High‐Concentrate Diets Improves Their Overall Health

The pursuit of high milk yields via high-concentrate diets risks ruminal acidosis and microbial dysbiosis, triggering lipopolysaccharide (LPS) release, subacute ruminal acidosis (SARA) incidence, and substantial economic losses. This study evaluated the efficacy of the dietary intestinal alkaline phosphatase (IAP) against high-concentrate feeding effects, hypothesizing it prevents SARA by degrading LPS, modulating microbiota, stabilizing ruminal pH, and improving gut health. Thirty-six lactating cows were stratified into three groups (n = 12): a high-concentrate diet group (HC, 5:5 concentrate:forage), an HC group supplemented with IAP (HC + IAP), and a low-concentrate control group (LC, 3:7). Key biomarkers such as ruminal pH, ruminal and fecal LPS, inflammatory cytokines (IL-6, IL-1β), and acute-phase proteins (SAA, LBP)--were monitored at 30-day intervals from calving through lactation. SARA status was defined by ruminal pH: < 5.6 (SARA), 5.6-5.8 (at-risk), and ≥ 5.8 (healthy). Fecal microbiome analysis was conducted on HC and HC + IAP cows at 90 days in milk (DIM). The HC group exhibited a high incidence of SARA, peaking between 90 and 120 DIM. In stark contrast, dietary supplementation with IAP (0.5 kg per 1000 kg of concentrate feed) effectively stabilized ruminal fluid pH, thereby completely preventing the incidence of SARA throughout the entire lactation period. This prophylactic effect was associated with significantly reduced systemic concentrations of SAA, LBP, IL-6, and IL-1β. Moreover, IAP treatment markedly enhanced gut microbial diversity and the relative abundance of beneficial bacteria. Therefore, IAP acted primarily in the rumen to detoxify LPS, thereby stabilizing pH and preventing the occurrence of SARA, while also entering the intestine to regulate the structure of gut microbiota, thereby maintaining the health of dairy cows under high-concentrate feeding conditions.