Abstract: Objective A liver-specific Trappc11 gene knockout mouse model(Trappc11^flox/flox-Alb-Cre^+/-) was established using the Cre-loxP system to investigate the pathogenesis of fatty liver disease. Methods Trappc11 homozygous mice with a loxP site(Trappc11^flox/flox) were crossed with Alb-Cre transgenic mice (Alb-Cre^+/-), and the genotypes of the offspring were identified. Progeny with the Trappc11^/flox-Alb-Cre^+/- genotype were selected, and liver-specific knockout mice were obtained through further breeding with Trappc11^flox/flox mice. Three groups of mice, including Trappc11^flox/flox-Alb-Cre^+/-、Trappc11^flox/+-Alb-Cre^+/- and Trappc11^flox/flox-Alb-Cre^-/-, aged 3-4 weeks, were selected, DNA was extracted from tissue samples to assesst the knockout efficiency and specificity of Trappc11. with further validation at the mRNA and protein levels. By the forth week, parameters such as food intake and body weight were measured. Results We successfully generated liver-specific Trappc11 gene knockout mice. Although the expression of Trappc11 gene was not affected in various tissues, including the heart, spleen, lung, kidney, pancreas, muscle, fat and brain, our model achieved a knockout efficiency of over 85 % at the mRNA level, significantly decreasing the TRAPPC11 protein level. The knockout mice are currently in good health, exhibiting normal growth, diet and water intake, making them suitable for subsequent breeding and mechanistic studies. Conclusion The successfully constructed Trappc11^flox/flox-Alb-Cre^+/- mice provide a valuable in vivo model for investigating the physiological and pathological roles of Trappc11 in the liver.

Key words: Trafficking Protein Particle Complex Subunit 11, Cre-loxP recombinase system, Tissue specific knockout