脂肪生成
内科学
内分泌学
脂肪细胞
生物
基因敲除
锌指
白色脂肪组织
脂肪组织
细胞生物学
转录因子
基因
医学
生物化学
作者
Eun-Su Kim,Sun Ah Ham,Jae Joon Hwang,Jun Pil Won,Hyuk Gyoon Lee,Joon Hur,Han Geuk Seo
标识
DOI:10.1016/j.mce.2022.111838
摘要
Zinc finger protein (ZFP) 251 is a member of the C2H2 ZFP family containing a Krüppel-associated box domain that might mainly act as a transcriptional repressor. However, its cellular function remains largely unknown. Here, we discovered that ZFP251 deficiency caused glucose intolerance in mice. This phenotype was associated with impaired insulin signaling due to hypertrophic changes in white adipose tissue (WAT). Gene ontology analysis revealed that ZFP251 deficiency affected the expression of genes associated with adipocyte differentiation and lipid and fatty acid metabolism. Consistent with in vivo results, hypertrophic changes were observed in Zfp251 knockdown (KD) 3T3-L1 adipocytes. In addition, Zfp251 KD 3T3-L1 preadipocytes exhibited cell cycle arrest in G0/G1 phase, leading to impaired differentiation into mature adipocytes, upon which abnormal mitotic clonal expansion and reduced expression of adipogenic markers were exhibited. These results suggest that ZFP251 deficiency causes impaired adipogenesis and adipocyte hypertrophy, leading to dysfunction of WAT.
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