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.

中文翻译：

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微生物失调引起的肥胖：肠道微生物群在能量代谢稳态中的作用

全球肥胖流行病需要寻找更好的干预策略，包括利用一些肠道微生物群及其代谢产物的健康益处。因此，我们研究了肠道微生物组成和与宿主相互作用的机制，这些机制与稳态能量代谢和生态失调引起的代谢性炎症和肥胖的病理生理学有关。我们还讨论了益生菌和益生元的有益健康、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/碳水化合物饮食将肠道微生物群设定为以厚壁菌门为主的微生物群（梭菌属),普雷沃泰拉和甲烷短杆菌但缺乏有益的属/种，例如拟杆菌属,双歧杆菌,乳酸杆菌和阿克曼西亚. 改变的肠道微生物群与维持肠上皮屏障完整性、减少细菌易位和炎症以及增加抑制饥饿激素的表达的 SCFA 表达降低有关。减少量的有益微生物也抑制导致血脂异常的禁食诱导的脂肪细胞因子表达。随之而来的是低度慢性炎症（代谢性内毒素血症），最终导致肥胖及其合并症。高脂肪饮食和失调的肠道微生物群的协同作用启动了一种配方，该配方对宿主进行表观遗传编程，以增加肥胖和血糖控制不佳。有趣的是，可以通过益生菌、益生元和合生元的施用来调节这些可从一代传递到另一代的致肥胖机制途径。