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

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.