Abstract: To explore the association between metabolic inflammation and systemic immune homeostasis imbalance in obese pig models induced by a high-fat feed, this study selected 24 healthy 40 day old white pigs and randomly divided them into two groups, the control group (fed a basal feed) and the high-fat group (fed a high-fat feed), with 12 pigs in each group. The experiment lasted for 12 weeks. Western blot was used to detect the expression levels of inflammation-related proteins (NF-κB p65, IκBα) in adipose tissue. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to determine the relative mRNA expression levels of pro-inflammatory factors (TNF-α, IL-6, IL-1β) and anti-inflammatory factors (IL-10, TGF-β) in peripheral blood mononuclear cells, liver, and adipose tissue. The results showed that compared with the control group, the final body weight, Lee's index, and fat coefficient of pigs in the high-fat group were significantly increased (P＜0.05); the phosphorylation level of NF-κB p65 in adipose tissue was significantly increased (P＜0.05), while the protein expression level of IκBα was significantly decreased (P＜0.05); the mRNA expression levels of TNF-α, IL-6, and IL-1β in peripheral blood mononuclear cells, liver and adipose tissue were significantly up-regulated (P＜0.05), whereas the mRNA expression levels of IL-10 and TGF-β were significantly down-regulated (P＜0.05). In conclusion, pigs with obesity induced by a high-fat feed exhibit obvious metabolic inflammatory responses, and the mechanism may be related to the activation of the NF-κB signaling pathway. Meanwhile, they were accompanied by systemic immune homeostasis imbalance, which was manifested as an imbalanced state of high expression of pro-inflammatory factors and low expression of anti-inflammatory factors. This study provided an ideal large animal model basis for the research on the pathogenesis and intervention of obesity-related metabolic diseases.

Key words: pig, high-fat feed, obesity, pig model, metabolic inflammation, immune homeostasis, NF-κB signaling pathway