Abstract: Objective To identify mRNA expression of 26S proteasome non-ATPase regulatory subunit 13(PSMD13) in Chinese hamsters with type Ⅱ diabetes mellitus (T2DM), analyze its physicochemical properties, signal peptides, subcellular localization, and functional domains, and provide a theoretical basis to study its function. Methods PSMD13 mRNA expression in the liver, skeletal muscle, fat and small intestinal tissues of Chinese hamsters with or without T2DM was determined by RT-qPCR. The amino acid sequence of PSMD13 was downloaded from the NCBI website and amino acid homology analysis was performed using DNAman software. Physicochemical properties of PSMD13 were analyzed by the Prot Param online tool. Hydrophobicity, signal peptides, and subcellular localization of PSMD13 were analyzed by Prot Scale software. The functional domain and secondary structure of PSMD13 were analyzed using the Conserved Domain database and SOPMA tool, respectively. The interacting proteins and functional networks of PSMD13 were analyzed using STRING databases. Results RT-qPCR showed that PSMD13 mRNA expression was decreased in adipose tissue of T2MD Chinese hamsters compared with that in normal Chinese hamsters. PSMD13 was located on chromosome 3, contained 13 exons, encoded a protein containing 378 amino acid residues, and its relative molecular mass was 42 942. 48. PSMD13 was an acidic protein and its theoretical isoelectric point was 6. 1. Amino acid sequence homology of PSMD13 with mice, rats, Drosophilae melanogaster, orangutans, and humans was as high as 97. 78%. PSMD13 protein had no signal peptide or transmembrane structure, and was mainly located in the cytoplasm. The carboxyl terminal of the PSMD13 protein contained a PCI domain that interacted with PSMD7, PSMD8, PSMA3, PSMC1, and USP14 to participate in ubiquitin-dependent protein catabolism. Conclusions The PSMD13 protein is highly conserved in evolution and its expression is low in adipose tissue of T2DM Chinese hamsters. PSMD13 is involved in the proteasome degradation pathway, and its downregulation in adipose tissue may be involved in the occurrence and development of T2MD.