Akash Muhammad Sajid Hamid, Fiayyaz Fareeha, Rehman Kanwal, Sabir Shakila, Rasool Muhammad Hidayat
Department of Pharmaceutical Chemistry, Government College University Faisalabad, Pakistan.
Department of Pharmaceutical Chemistry, Government College University Faisalabad, Pakistan; Department of Microbiology, Government College University Faisalabad, Pakistan.
Crit Rev Immunol. 2019;39(4):223-237. doi: 10.1615/CritRevImmunol.2019030614.
Human gut microbiota consist of numerous microorganisms, but the most abundant species are Bacteroides and Firmicutes. Each human possesses a specific gut microbiota, which can be altered by diet, antibiotics, lifestyle, and genetic background. Gut microbiota perform vital functions, but in this article, we aimed to elaborate the effects of modified composition of microbiota on host metabolism. Ligands for G protein coupled receptors (GPCRs) are short-chain fatty acids (SCFAs) located on endocrine glands, epithelial cells, and adipocytes. SCFAs are produced in the distal gut by bacterial fermentation of nondigestible polysaccharides; they induce the various beneficial effects including decrease serum glucose level, insulin resistance, as well as inflammation; and they increase glucagon-like peptide-1 (GLP-1) secretion. Fasting-induced adipose factor (FIAF) is suppressed by gut microbiota and results in the increased storage of fatty acids in the adipose tissues and liver. An increased lipopolysaccharide level due to altered gut microflora cause the initiation of inflammation associated with type 2 diabetes mellitus (T2DM). Intestinal dysbiosis and metabolic endotoxemia are considered key mechanisms that seem to be associated with the development of T2DM and obesity. Therapeutic interventions that can be used for the treatment of diabetes include metformin, dietary modulation, probiotics, prebiotics, fecal microbiota transplantation and bariatric surgery.
人类肠道微生物群由众多微生物组成,但数量最多的种类是拟杆菌和厚壁菌。每个人都拥有特定的肠道微生物群,其会受到饮食、抗生素、生活方式和遗传背景的影响而发生改变。肠道微生物群发挥着重要功能,但在本文中,我们旨在阐述微生物群组成改变对宿主代谢的影响。G蛋白偶联受体(GPCRs)的配体是位于内分泌腺、上皮细胞和脂肪细胞上的短链脂肪酸(SCFAs)。SCFAs由肠道远端细菌对不可消化多糖的发酵产生;它们能产生多种有益作用,包括降低血糖水平、改善胰岛素抵抗以及减轻炎症;还能增加胰高血糖素样肽-1(GLP-1)的分泌。禁食诱导脂肪因子(FIAF)受到肠道微生物群的抑制,导致脂肪酸在脂肪组织和肝脏中的储存增加。肠道微生物群改变导致脂多糖水平升高,引发与2型糖尿病(T2DM)相关的炎症。肠道生态失调和代谢性内毒素血症被认为是与T2DM和肥胖症发展相关的关键机制。可用于治疗糖尿病的治疗干预措施包括二甲双胍、饮食调节、益生菌、益生元、粪便微生物群移植和减肥手术。