Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, Villejuif, France.
INSERM U1138, Centre de Recherche des Cordeliers, Sorbonne Université, Université de Paris, Paris, France.
Adipocyte. 2020 Dec;9(1):116-119. doi: 10.1080/21623945.2020.1736734.
We recently identified acyl coenzyme A-binding protein (ACBP)/diazepam binding inhibitor (DBI) as a novel 'hunger factor': a protein that is upregulated in human or murine obesity and that, if administered to mice, causes hyperphagy, adipogenesis and obesity. Conversely, neutralization of ACBP/DBI by systemic injection of neutralizing monoclonal antibodies or autoantibodies produced after auto-immunization against ACBP/DBI has anorexigenic and lipolytic effects. Thus, neutralization of ACBP/DBI results in reduced food intake subsequent to the activation of anorexigenic neurons and the inactivation of orexigenic neurons in the hypothalamus. Moreover, ACBP/DBI neutralization results into enhanced triglyceride lipolysis in white fat, a surge in free fatty acids in the plasma, enhanced incorporation of glycerol-derived carbon atoms into glucose, as well as an increase in β-oxidation, resulting in a net reduction of fat mass. Importantly, ACBP/DBI neutralization also stimulated an increase in autophagy in various organs, suggesting that it might mediate anti-ageing effects.
我们最近发现酰基辅酶 A 结合蛋白（ACBP）/地西泮结合抑制剂（DBI）是一种新型的“饥饿因子”：一种在人类或小鼠肥胖中上调的蛋白质，如果给予小鼠，会导致过度摄食、脂肪生成和肥胖。相反，通过全身注射中和单克隆抗体或针对 ACBP/DBI 自身免疫产生的自身抗体中和 ACBP/DBI，会产生厌食和脂肪分解作用。因此，ACBP/DBI 的中和会导致下丘脑厌食神经元的激活和摄食神经元的失活，从而减少食物摄入。此外，ACBP/DBI 的中和会导致白色脂肪中甘油三酯的脂肪分解增强，血浆中游离脂肪酸增加，甘油衍生碳原子掺入葡萄糖增加，以及β-氧化增加，从而导致脂肪量的净减少。重要的是，ACBP/DBI 的中和也刺激了各种器官中自噬的增加，表明它可能介导抗衰老作用。
