Department CIBIO, University of Trento, Trento, Italy.
Université de Paris, Paris, France.
Appl Environ Microbiol. 2021 May 26;87(12):e0047121. doi: 10.1128/AEM.00471-21.
Acyl coenzyme A (CoA) binding protein (ACBP), also called diazepam-binding inhibitor (DBI), is a phylogenetically conserved protein that is expressed by all eukaryotic species as well as by some bacteria. Since elevated ACBP/DBI levels play a major role in the inhibition of autophagy, increase in appetite, and enhanced lipid storage that accompany obesity, we wondered whether ACBP/DBI produced by the human microbiome might affect host weight. We found that the genomes of bacterial commensals rarely contain ACBP/DBI homologues, which are rather encoded by genomes of some pathogenic or environmental taxa that were not prevalent in human feces. Exhaustive bioinformatic analyses of 1,899 gut samples from healthy individuals refuted the hypothesis that bacterial ACBP/DBI might affect the body mass index (BMI) in a physiological context. Thus, the physiological regulation of BMI is unlikely to be affected by microbial ACBP/DBI-like proteins. However, at the speculative level, it remains possible that ACBP/DBI produced by potential pathogenic bacteria might enhance their virulence by inhibiting autophagy and hence subverting innate immune responses. Acyl coenzyme A (CoA) binding protein (ACBP) can be encoded by several organisms across the domains of life, including microbes, and has shown to play major roles in human metabolic processes. However, little is known about its presence in the human gut microbiome and whether its microbial counterpart could also play a role in human metabolism. In the present study, we found that microbial ACBP/DBI sequences were rarely present in the gut microbiome across multiple metagenomic data sets. Microbes that carried ACBP/DBI in the human gut microbiome included Saccharomyces cerevisiae, Lautropia mirabilis, and Comamonas kerstersii, but these microorganisms were not associated with body mass index, further indicating an unconvincing role for microbial ACBP/DBI in human metabolism.
酰基辅酶 A（CoA）结合蛋白（ACBP），也称为地西泮结合抑制剂（DBI），是一种在所有真核生物以及一些细菌中表达的进化上保守的蛋白质。由于升高的 ACBP/DBI 水平在肥胖症相关的自噬抑制、食欲增加和脂质储存增加中起着主要作用，我们想知道人类微生物组产生的 ACBP/DBI 是否可能影响宿主体重。我们发现，细菌共生体的基因组很少包含 ACBP/DBI 同源物，而是由一些在人类粪便中不常见的致病或环境分类单元的基因组编码的。对来自健康个体的 1899 个肠道样本的详尽生物信息学分析反驳了细菌 ACBP/DBI 可能在生理背景下影响体重指数（BMI）的假说。因此，微生物 ACBP/DBI 样蛋白不太可能影响 BMI 的生理调节。然而，在推测层面上，潜在的致病性细菌产生的 ACBP/DBI 可能通过抑制自噬从而颠覆先天免疫反应来增强其毒力仍然是有可能的。酰基辅酶 A（CoA）结合蛋白（ACBP）可以由生命领域中的几个生物体编码，包括微生物，并且已被证明在人类代谢过程中发挥主要作用。然而，关于其在人类肠道微生物组中的存在以及其微生物对应物是否也可以在人类代谢中发挥作用，知之甚少。在本研究中，我们发现微生物 ACBP/DBI 序列在多个宏基因组数据集的肠道微生物组中很少存在。在人类肠道微生物组中携带 ACBP/DBI 的微生物包括酿酒酵母、奇异变形菌和库莫氏菌，但这些微生物与体重指数无关，进一步表明微生物 ACBP/DBI 在人类代谢中的作用不太可信。
