(P03-057-23) Characterization of Lipid Oxidation Products-Elicited Metabolic Changes in Gastrointestinal Digesta After Feeding Oxidized Soybean Oil to Nursery Pigs

Objectives: Consumption of fried food by humans and feeding recycled cooking oils to animals introduce significant amount of primary lipid oxidation products (LOPs), such as peroxidized fatty acids, and secondary LOPs, mainly lipidic aldehydes, into their gastrointestinal tracts (GIT), but the metabolic fates of those LOPs and their metabolic interactions with dietary components in the GIT were barely examined. In the current study, oxidized lipids-elicited metabolic changes in the GIT were characterized by a nursery pig feeding trial and comprehensive metabolomic and biochemical analyses.

Methods: Oxidized soybean oil (OSO) was prepared by heating control soybean oil (CSO) at 187 °C for 6 hours with a constant airflow of 30 L/min and included as 10% (w/w) of nursery diet. Total 60 nursery pigs at age of 28 days) were randomly allocated to two groups (3 pigs/pen, 10 pens/group) and fed with CSO and OSO diets for 28 days. At the end of the feeding, one focal pig per pen was sacrificed to collect digesta samples at stomach, duodenum, jejunum, ileum, cecum, and colon. OSO-elicited metabolic changes were defined by metabolomic analysis, biochemical analysis, multivariate modeling, and correlation analysis.

Results: Compared to CSO, OSO compromised the growth performance of nursery pigs in both weight gain and feed intake. OSO elevated the concentrations of lipidic aldehydes in all segments of the GI tract, especially nonanal, hexanal, and pentanal in cecum and colon. This observation was correlated with the increases of carbonylated protein in digesta. Besides direct influences of aldehydes, OSO decreased free amino acids and elastase activity in the small intestine and decreased short-chain fatty acids and bile acids in the large intestine.

Conclusions: Our results indicated that extensive influences of OSO on the digesta metabolome in the GI tract were caused by both direct contribution of LOPs and the metabolic interactions of LOPs with proteins, digestive enzymes, and microbiota. These observations provide insights into the metabolic fates of lipidic aldehydes and subsequent disruptions of nutrient and microbial metabolism and chemical environment in the GIT.

Funding Sources: Research efforts are partially supported by the NIFA project MIN-18-125