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Aims/Introduction  The putative tumor suppressor gene,  KBTBD11 , might play a role in tumorigenesis, and is associated with cellular apoptosis and proliferation in colorectal cancer cells. However, the function of  Kbtbd11  during adipogenesis is unknown. The aim of the present study was to investigate the role of  Kbtbd11  in the differentiation of 3T3‐L1 preadipocytes.    Materials and Methods  For the fasting–refeeding protocol, mice were subjected to fasting for 24 h, followed by a chow diet for 12 h. Adenovirus infection methods were used to examine the effect of  Kbtbd11 , and 3T3‐L1 cells were analyzed with Oil Red O staining and real‐time polymerase chain reaction.    Results  The white adipose tissue expression of  Kbtbd11  messenger ribonucleic acid (mRNA) was significantly higher in the re‐fed state than in the fasted state.  Kbtbd11  mRNA levels were markedly increased in epididymal white adipose tissue of diet‐induced obesity mice compared with those in the mice fed a chow diet. In addition,  Kbtbd11  mRNA expression was increased in a differentiation‐dependent manner in 3T3‐L1 cells. Knockdown of  Kbtbd11  mRNA through the infection with adenoviral vectors remarkably inhibited triglyceride accumulation and adipocyte differentiation in 3T3‐L1 cells. In contrast, the overexpression of  Kbtbd11  promoted the differentiation of 3T3‐L1 adipocytes.    Conclusions  The present findings show that  Kbtbd11  expression might be involved in nutritional regulation and is increased in obese adipose tissue. In addition,  Kbtbd11  appears to be required for the differentiation of adipocytes in 3T3 ‐ L1 cells. Collectively, these results show a novel link between the expression of  Kbtbd11  and fat accumulation, and suggest that  Kbtbd11  is a new therapeutic target for obesity.

Kbtbd11 gene expression in adipose tissue increases in response to feeding and affects adipocyte differentiation