Zhang Pengyi, Meng Xiangjing, Li Dongmei, Calderone Richard, Mao Dewei, Sui Bo
Sport Science Research Center, Shandong Sport University, Jinan, China.
Department of Microbiology & Immunology, Georgetown University Medical Center, Washington, DC, United States.
Front Physiol. 2018 Jan 8;8:1122. doi: 10.3389/fphys.2017.01122. eCollection 2017.
Gut microbiota and their metabolites have been linked to a series of chronic diseases such as obesity and other metabolic dysfunctions. Obesity is an increasingly serious international health issue that may lead to a risk of insulin resistance and other metabolic diseases. The relationship between gut microbiota and the host is both interdependent and relatively independent. In this review, the causality of gut microbiota and its role in the pathogenesis and intervention of obesity is comprehensively presented to include human genotype, enterotypes, interactions of gut microbiota with the host, microbial metabolites, and energy homeostasis all of which may be influenced by dietary nutrition. Diet can enhance, inhibit, or even change the composition and functions of the gut microbiota. The metabolites they produce depend upon the dietary substrates provided, some of which have indispensable functions for the host. Therefore, diet is a key factor that maintains or not a healthy commensal relationship. In addition, the specific genotype of the host may impact the phylogenetic compositions of gut microbiota through the production of host metabolites. The commensal homeostasis of gut microbiota is favored by a balance of microbial composition, metabolites, and energy. Ultimately the desired commensal relationship is one of mutual support. This article analyzes the clues that result in patterns of commensal homeostasis. A deeper understanding of these interactions is beneficial for developing effective prevention, diagnosis, and personalized therapeutic strategies to combat obesity and other metabolic diseases. The idea we discuss is meant to improve human health by shaping or modulating the beneficial gut microbiota.
肠道微生物群及其代谢产物与一系列慢性疾病有关,如肥胖和其他代谢功能障碍。肥胖是一个日益严重的国际健康问题,可能导致胰岛素抵抗和其他代谢疾病的风险。肠道微生物群与宿主之间的关系既相互依存又相对独立。在这篇综述中,全面阐述了肠道微生物群的因果关系及其在肥胖发病机制和干预中的作用,包括人类基因型、肠型、肠道微生物群与宿主的相互作用、微生物代谢产物以及能量稳态,所有这些都可能受到饮食营养的影响。饮食可以增强、抑制甚至改变肠道微生物群的组成和功能。它们产生的代谢产物取决于所提供的饮食底物,其中一些对宿主具有不可或缺的功能。因此,饮食是维持或不维持健康共生关系的关键因素。此外,宿主的特定基因型可能通过产生宿主代谢产物影响肠道微生物群的系统发育组成。肠道微生物群的共生稳态有利于微生物组成、代谢产物和能量的平衡。最终,理想的共生关系是相互支持的关系。本文分析了导致共生稳态模式的线索。对这些相互作用的更深入理解有利于制定有效的预防、诊断和个性化治疗策略,以对抗肥胖和其他代谢疾病。我们讨论的观点旨在通过塑造或调节有益的肠道微生物群来改善人类健康。