Obesity is an epidemic problem in most societies around the world. The obesity-related study has become the important topics in nutrition research. One early study showed that the transcription factor HBP1 is highly expressed in the adipose tissue in rat, wherein the HBP1 mRNA is more abundant in the fully differentiated adipocytes than those of the undifferentiated ones. In the current study, we confirm the previous finding that HBP1expression is not increased until the late stage of the 3T3-L1 adipocyte differentiation. These observations lead us to hypothesize that HBP1 may have stage-specific function during adipocyte differentiation. To test the hypothesis, in the early Mitotic Clonal Expansion (MCE) stage, we treated 3T3-L1 cells with querceuin to increase HBP1 expression, resulting in the growth arrest in G1 phase and consequent incompletion of adipocytes differentiation. Oppositely, HBP1 siRNA which down-regulates HBP1 leads to accelerated cell growth with early appearance of G2/M phase in MCE. These results indicate that HBP1 is involved in cell cycle regulation in MCE phase. Interestingly, although HBP1knockdown causes early MCE completion, the full adipogenesis process is impaired. This indicates that HBP1 activation during terminal differentiation stage is necessary for full adipogenesis. We further hypothesize that HBP1 is a potential target of PPARγfunction during terminal differentiation. First, the CHIP-Mapper search discovers 2 putative PPARγbinding sites in HBP1 promoter. Moreover, GW9662 (PPARγantagonist) inhibits the activation of a -2kb HBP1promoter and decreases HBP1 mRNA expression. Taken together, the results of the current study will further characterize HBP1 as a key marker of adipocyte differentiation, which may serve as a potential biological target in the intervention of obesity treatment.
