Acetyl-coenzyme A acetyltransferase 1 promotes brown adipogenesis by activating the AMPK-PGC1α signaling pathway

IF 3.9 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2023-10-01 DOI:10.1016/j.bbalip.2023.159369
Kaixiang Zhu , Ling Ni , Jianxiong Han , Zhongkang Yan , Yin Zhang , Feifei Wang , Lili Wang , Xingyuan Yang
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Abstract

Brown adipose tissue (BAT) is thermogenic, expressing high levels of uncoupling protein-1 to convert nutrient energy to heat energy, bypassing ATP synthesis. BAT is a promising therapeutic target for treatment of obesity and type 2 diabetes since it converts fatty acids into heat but mechanisms controlling brown adipogenesis remain unclear. Knockdown of acetyl-Coenzyme A acetyltransferase 1 (ACAT1) in C3H10T1/2 cells suppressed brown adipocyte maturation during the current study and ACAT1 overexpression promoted brown adipocyte maturation. The downstream target of AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma coactivator-1-α (PGC1α), was involved in the action of ACAT1 on brown adipocyte maturation. ACAT1 overexpression enhanced AMPK phosphorylation and promoted PGC1α expression. It is suggested that ACAT1 promotes brown adipocyte maturation by activating the AMPK-PGC1α signaling pathway.

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乙酰辅酶A乙酰转移酶1通过激活AMPK-PGC1α信号通路促进棕色脂肪生成。
棕色脂肪组织(BAT)产热,表达高水平的解偶联蛋白-1,绕过ATP合成,将营养能量转化为热能。BAT是治疗肥胖和2型糖尿病的一个有前景的治疗靶点,因为它将脂肪酸转化为热量,但控制棕色脂肪生成的机制尚不清楚。在当前的研究中,敲除C3H10T1/2细胞中的乙酰辅酶A乙酰转移酶1(ACAT1)抑制了棕色脂肪细胞的成熟,而ACAT1过表达促进了棕色脂肪电池的成熟。AMP活化蛋白激酶(AMPK)的下游靶标,过氧化物酶体增殖物活化受体γ共活化因子-1-α(PGC1α),参与ACAT1对棕色脂肪细胞成熟的作用。ACAT1过表达增强AMPK磷酸化并促进PGC1α的表达。提示ACAT1通过激活AMPK-PGC1α信号通路促进棕色脂肪细胞成熟。
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来源期刊
CiteScore
11.00
自引率
2.10%
发文量
109
审稿时长
53 days
期刊介绍: BBA Molecular and Cell Biology of Lipids publishes papers on original research dealing with novel aspects of molecular genetics related to the lipidome, the biosynthesis of lipids, the role of lipids in cells and whole organisms, the regulation of lipid metabolism and function, and lipidomics in all organisms. Manuscripts should significantly advance the understanding of the molecular mechanisms underlying biological processes in which lipids are involved. Papers detailing novel methodology must report significant biochemical, molecular, or functional insight in the area of lipids.
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