Tain You-Lin, Hsu Chien-Ning
Division of Pediatric Nephrology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.
Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.
Nutrients. 2024 Feb 28;16(5):683. doi: 10.3390/nu16050683.
Metabolic syndrome (MetS) denotes a constellation of risk factors associated with the development of cardiovascular disease, with its roots potentially traced back to early life. Given the pivotal role of oxidative stress and dysbiotic gut microbiota in MetS pathogenesis, comprehending their influence on MetS programming is crucial. Targeting these mechanisms during the early stages of life presents a promising avenue for preventing MetS later in life. This article begins by examining detrimental insults during early life that impact fetal programming, ultimately contributing to MetS in adulthood. Following that, we explore the role of oxidative stress and the dysregulation of gut microbiota in the initiation of MetS programming. The review also consolidates existing evidence on how gut-microbiota-targeted interventions can thwart oxidative-stress-associated MetS programming, encompassing approaches such as probiotics, prebiotics, postbiotics, and the modulation of bacterial metabolites. While animal studies demonstrate the favorable effects of gut-microbiota-targeted therapy in mitigating MetS programming, further clinical investigations are imperative to enhance our understanding of manipulating gut microbiota and oxidative stress for the prevention of MetS.
代谢综合征(MetS)指的是一组与心血管疾病发生相关的危险因素,其根源可能追溯到生命早期。鉴于氧化应激和肠道微生物群失调在MetS发病机制中的关键作用,了解它们对MetS编程的影响至关重要。在生命早期针对这些机制是预防日后发生MetS的一个有前景的途径。本文首先研究生命早期影响胎儿编程的有害因素,这些因素最终导致成年期的MetS。在此之后,我们探讨氧化应激和肠道微生物群失调在MetS编程启动中的作用。本综述还整合了现有证据,说明针对肠道微生物群的干预措施如何能够阻止与氧化应激相关的MetS编程,包括益生菌、益生元、后生元以及调节细菌代谢产物等方法。虽然动物研究表明针对肠道微生物群的疗法在减轻MetS编程方面具有有益效果,但仍需进一步的临床研究,以加深我们对通过操纵肠道微生物群和氧化应激来预防MetS的理解。