Park Ji-Eun, Park Ho-Young, Kim Young-Soo, Park Miri
Food Functionality Research Division, Korea Food Research Institute, Jeonju 55365, Republic of Korea.
Department of Food Science and Technology, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Metabolites. 2024 Dec 13;14(12):704. doi: 10.3390/metabo14120704.
: Dietary patterns, including high-fat and high-carbohydrate diets (HFDs and HCDs), as well as non-dietary factors such as food additives and antibiotics, are strongly linked to metabolic endotoxemia, a critical driver of low-grade chronic inflammation. This review explores the mechanisms through which these factors impair intestinal permeability, disrupt gut microbial balance, and facilitate lipopolysaccharide (LPS) translocation into the bloodstream, contributing to metabolic disorders such as obesity, type 2 diabetes mellitus, and inflammatory bowel disease. : The analysis integrates findings from recent studies on the effects of dietary components and gut microbiota interactions on intestinal barrier function and systemic inflammation. Focus is given to experimental designs assessing gut permeability using biochemical and histological methods, alongside microbiota profiling in both human and animal models. : HFDs and HCDs were shown to increase intestinal permeability and systemic LPS levels, inducing gut dysbiosis and compromising barrier integrity. The resulting endotoxemia promoted a state of chronic inflammation, disrupting metabolic regulation and contributing to the pathogenesis of various metabolic diseases. Food additives and antibiotics further exacerbated these effects by altering microbial composition and increasing gut permeability. : Diet-induced alterations in gut microbiota and barrier dysfunction emerge as key mediators of metabolic endotoxemia and related disorders. Addressing dietary patterns and their impact on gut health is crucial for developing targeted interventions. Further research is warranted to standardize methodologies and elucidate mechanisms for translating these findings into clinical applications.
饮食模式,包括高脂肪和高碳水化合物饮食(HFDs和HCDs),以及食品添加剂和抗生素等非饮食因素,与代谢性内毒素血症密切相关,代谢性内毒素血症是低度慢性炎症的关键驱动因素。本综述探讨了这些因素损害肠道通透性、破坏肠道微生物平衡以及促进脂多糖(LPS)进入血液的机制,这些机制导致了肥胖、2型糖尿病和炎症性肠病等代谢紊乱。:该分析整合了近期关于饮食成分和肠道微生物群相互作用对肠道屏障功能和全身炎症影响的研究结果。重点关注使用生化和组织学方法评估肠道通透性的实验设计,以及人类和动物模型中的微生物群分析。:研究表明,HFDs和HCDs会增加肠道通透性和全身LPS水平,导致肠道生态失调并损害屏障完整性。由此产生的内毒素血症促进了慢性炎症状态,破坏了代谢调节,导致各种代谢疾病的发病机制。食品添加剂和抗生素通过改变微生物组成和增加肠道通透性进一步加剧了这些影响。:饮食引起的肠道微生物群改变和屏障功能障碍是代谢性内毒素血症及相关疾病的关键介质。解决饮食模式及其对肠道健康的影响对于制定有针对性的干预措施至关重要。有必要进一步研究以规范方法,并阐明将这些发现转化为临床应用的机制。