《生命科学》 2017, 29(7): 695-706
摘 要：摘 要：膳食营养是影响肠道菌群结构和功能最为重要，也较为迅速的因素，并由此影响宿主的代谢状况。高脂等不健康饮食习惯会引起肠道菌群的失调，使肠道通透性增加，形成全身的慢性、低水平炎症，进一步破坏胰岛素的信号转导通路，最终导致包括胰岛素抵抗、肥胖、糖尿病等在内的代谢综合征的发生。高纤维饮食可能通过富集短链脂肪酸(SCFAs) 产生菌，增加肠道内SCFAs 浓度，降低内毒素产生菌水平，进而减少脂多糖(LPS) 入血引起的组织器官炎症。这类饮食还能抑制某些能产生有害物质，如三甲胺(TMA)和吲哚的有害菌，从而改善宿主的代谢状况。益生元能减少宿主的脂肪积累，降低宿主的炎症水平并增加胰岛素敏感性，同时还伴随着食欲因子、胃肠肽水平和肠道中某些益生菌丰度的增加。此外，蔬菜、水果、奶制品等食物也能通过调节肠道菌群进而改善宿主的代谢状况。虽然越来越多的研究表明，肠道菌群可能在调节宿主的代谢状况中存在着因果关系，但是在食物- 肠道菌群- 代谢这条通路中到底存在着一种怎样的机制，有待进一步研究。
Abstract: Abstract: Diet played most important and relative immediate roles in the regulation of the structure and function of gut microbiota. The unhealthy diet such as high fat diet could impair the gut microbiota structure and increase the gut permeability， leading to the systemic， chronic and low-grade inflammation， impairment of the insulin signal transduction pathway and at last， the occurrence of the metabolic syndromes including the insulin resistance， fat， diabetes mellitus and so on. High fiber diet might enrich the short-chain fatty acids (SCFAs) producing bacteria so that increase the SCFAs levels in the intestinal tract， decrease the abundance of the lipopolysaccharide (LPS) producers and further suppress the tissue and organic inflammation induced by LPS. High fiber diet could also inhibit some potential opportunistic pathogens which could produce harmful materials such as trimethylamine (TMA) and indole. As a result， the metabolic homeostasis would be improved. Prebiotics could reduce the fat accumulation， down-regulate the inflammation levels and improve the insulin sensitivity accompanied by the increase of the neuropeptides and gastrointestinal peptides and the abundance of several beneficial bacteria. Furthermore， some other foods including vegetables， fruits and dairy products could improve the metabolic homeostasis through regulating the gut microbiota structure as well. Although more and more research implied that gut microbiota might play the causative roles in the regulation of the metabolic homeostasis of the host， the mechanism of the diet-gut microbiota-metabolism pathway still remains unclear.
