Recently, we reported that, in mice, hunger causes the autophagy-dependent release of a protein called "acyl-CoA-binding protein" or "diazepam binding inhibitor" (ACBP/DBI) from cells, resulting in an increase in plasma ACBP concentrations. Administration of extra ACBP is orexigenic and obesogenic, while its neutralization is anorexigenic in mice, suggesting that ACBP is a major stimulator of appetite and lipo-anabolism. Accordingly, obese persons have higher circulating ACBP levels than lean individuals, and anorexia nervosa is associated with subnormal ACBP plasma concentrations. Here, we investigated whether ACBP might play a phylogenetically conserved role in appetite stimulation. We found that extracellular ACBP favors sporulation in Saccharomyces cerevisiae, knowing that sporulation is a strategy for yeast to seek new food sources. Moreover, in the nematode Caenorhabditis elegans, ACBP increased the ingestion of bacteria as well as the frequency pharyngeal pumping. These observations indicate that ACBP has a phylogenetically ancient role as a 'hunger factor' that favors food intake.

中文翻译：

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酰基辅酶A结合蛋白（ACBP）：一种系统发育保守的食欲刺激剂。

最近，我们报道说，在小鼠中，饥饿会导致细胞自噬依赖性释放一种称为“酰基辅酶A结合蛋白”或“地西泮结合抑制剂”（ACBP/DBI）的蛋白质，从而导致血浆 ACBP 浓度增加. 额外的 ACBP 的给药是食欲和肥胖，而它的中和在小鼠中是厌食的，这表明 ACBP 是食欲和脂肪合成代谢的主要刺激物。因此，肥胖者的循环 ACBP 水平高于瘦人，神经性厌食症与低于正常的 ACBP 血浆浓度有关。在这里，我们调查了 ACBP 是否可能在食欲刺激中发挥系统发育保守的作用。我们发现细胞外 ACBP 有利于酿酒酵母的孢子形成，知道孢子形成是酵母寻找新食物来源的一种策略。此外，在秀丽隐杆线虫中，ACBP 增加了细菌的摄入以及咽部抽吸的频率。这些观察结果表明，ACBP 作为一种有利于食物摄入的“饥饿因素”在系统发育上具有古老的作用。