Department of Oncology and Metabolism, University of Sheffield, Sheffield, UK.
Ekatani Scientific Limited, Yenagoa, Bayelsa, Nigeria.
Br J Nutr. 2020 May 28;123(10):1127-1137. doi: 10.1017/S0007114520000380. Epub 2020 Feb 3.
The global obesity epidemic has necessitated the search for better intervention strategies including the exploitation of the health benefits of some gut microbiota and their metabolic products. Therefore, we examined the gut microbial composition and mechanisms of interaction with the host in relation to homoeostatic energy metabolism and pathophysiology of dysbiosis-induced metabolic inflammation and obesity. We also discussed the eubiotic, health-promoting effects of probiotics and prebiotics as well as epigenetic modifications associated with gut microbial dysbiosis and risk of obesity. High-fat/carbohydrate diet programmes the gut microbiota to one predominated by Firmicutes (Clostridium), Prevotella and Methanobrevibacter but deficient in beneficial genera/species such as Bacteroides, Bifidobacterium, Lactobacillus and Akkermansia. Altered gut microbiota is associated with decreased expression of SCFA that maintain intestinal epithelial barrier integrity, reduce bacterial translocation and inflammation and increase expression of hunger-suppressing hormones. Reduced amounts of beneficial micro-organisms also inhibit fasting-induced adipocyte factor expression leading to dyslipidaemia. A low-grade chronic inflammation (metabolic endotoxaemia) ensues which culminates in obesity and its co-morbidities. The synergy of high-fat diet and dysbiotic gut microbiota initiates a recipe that epigenetically programmes the host for increased adiposity and poor glycaemic control. Interestingly, these obesogenic mechanistic pathways that are transmittable from one generation to another can be modulated through the administration of probiotics, prebiotics and synbiotics. Though the influence of gut microbiota on the risk of obesity and several intervention strategies have been extensively demonstrated in animal models, application in humans still requires further robust investigation.
全球肥胖症流行，促使人们寻求更好的干预策略，包括利用某些肠道微生物群及其代谢产物的健康益处。因此，我们研究了与内稳态能量代谢和肠道微生物失调引起的代谢性炎症和肥胖的病理生理学有关的肠道微生物组成和与宿主相互作用的机制。我们还讨论了益生菌和益生元的生态平衡、促进健康的作用，以及与肠道微生物失调和肥胖风险相关的表观遗传修饰。高脂肪/碳水化合物饮食使肠道微生物群向厚壁菌门（梭菌）、普雷沃氏菌属和甲烷短杆菌为主的方向发展，但缺乏有益的属/种，如拟杆菌属、双歧杆菌属、乳杆菌属和阿克曼氏菌属。肠道微生物群的改变与 SCFA 表达减少有关，SCFA 可维持肠道上皮屏障完整性，减少细菌易位和炎症，并增加抑制饥饿的激素表达。有益微生物数量的减少也会抑制禁食诱导的脂肪细胞因子表达，导致血脂异常。随后会出现低度慢性炎症（代谢性内毒素血症），最终导致肥胖及其合并症。高脂肪饮食和肠道微生物失调的协同作用，启动了一个表观遗传程序，使宿主更容易肥胖和血糖控制不佳。有趣的是，这些可传递给下一代的肥胖发病机制途径，可以通过益生菌、益生元和合生菌的给药来调节。尽管肠道微生物群对肥胖风险的影响及其几种干预策略已在动物模型中得到广泛证实，但在人类中的应用仍需要进一步的有力研究。
