Transcription Coactivator BCL3 Acts as a Potential Regulator of Lipid Metabolism Through the Effects on Inflammation.
Transcription Coactivator BCL3 Acts as a Potential Regulator of Lipid Metabolism Through the Effects on Inflammation.
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转录辅激活因子 BCL3 通过影响炎症发挥脂质代谢的潜在调节作用
DOI：
10.2147/jir.s327858
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发表时间：
2021
影响因子：
4.5
通讯作者：
Wang H
中科院分区：
文献类型：
--
作者：
Zhang S;Gao J;Liu S;Yu L;Zhang W;Liang Y;Wang H
转录共激活因子B细胞淋巴瘤3（BCL 3）是NF-κB通路抑制剂IκB家族的成员，调节NF-κB通路的活性。然而，BCL 3与脂质代谢的关系尚不清楚。本研究探讨BCL 3对肥胖小鼠免疫和代谢的影响。通过CRISPR/Cas9技术构建Bcl 3-KO小鼠。通过高脂饲料喂养16周，建立Bcl 3-KO小鼠肥胖模型，并分析一些代谢相关指标。结果表明，KO小鼠在高脂肪饮食中体重增加明显减少，而食物摄入量没有变化。KO小鼠的肝脏脂肪变性和脂肪组织肥大有显著改善。KO小鼠SREBP 1及其下游脂肪酸合成酶FAS和ACC表达下调，脂肪组织和肝脏炎症进一步减轻。这些结果表明，BCL 3可能是一个新的因素，在调节脂质代谢的肥胖的发展。
Transcriptional coactivator B-cell lymphoma-3 (BCL3) is a member of the IκB family of NF-κB inhibitors and regulates the activity of the NF-κB pathway. However, the relationship between BCL3 and lipid metabolism remains unclear. The present study investigates the effects of BCL3 in immune and metabolism in obese mice. Construct Bcl3-KO mice through CRISPR/Cas9 technology. Obesity model was induced in Bcl3-KO mice by feeding a high-fat diet for 16 weeks, and some metabolic-related indicators were analysed. The results showed that the KO mice gained significantly less body weight on a high fat diet without a change in food intake. There was significant improvement in hepatic steatosis and adipose tissue hypertrophy in KO mice. The expression of SREBP1 and its downstream fatty acid synthetase FAS and ACC were down-regulated in KO mice, and the inflammation in adipose tissue and liver was further reduced. These results suggest that BCL3 may be a novel factor in regulating lipid metabolism in the development of obesity.