Biotechnology Institute, Ankara University, Gumusdere, Ankara, Turkey.
Adv Exp Med Biol. 2024;1460:357-372. doi: 10.1007/978-3-031-63657-8_12.
Gut microbiota is an indispensable commensal partner of human superorganism. The wealth of genetic repertoire provided by these microorganisms extends host's substrate processing capability. Energy and nutrient harvesting machinery primarily depends on the proper function of these organisms. However, the dynamic composition of microbiota changes with age, lifestyle, stress factors, infections, medications, and host pathophysiological conditions. Host immune system is primarily responsible for shaping up the microbial community and sustaining the symbiotic state. This involves controlling the delicate balance between agility toward pathobionts and tolerance toward symbionts. When things go wrong with this crosstalk, dysbiosis may arise.Metabolic syndrome is a multisystemic, low-grade chronic inflammatory disease that involves dyslipidemia, glucose intolerance, insulin resistance, and central obesity. Excess caloric intake with high-sugar and high-fat diet promote high energy harvesting and lipogenesis. The secretion of adipokines accompanies lipid spillover from fat cells, which contribute to insulin resistance and the expansion of adipose tissue in ectopic sites. Proinflammatory cytokines from adipose tissue macrophages increase the extent of adipose dysfunction.The inflammatory nature of obesity and metabolic syndrome recall the connection between dysbiosis and immune dysfunction. A remarkable association exits between obesity, inflammatory bowel disease, gluten-sensitive enteropathy, and dysbiosis. These conditions compromise the gut mucosa barrier and allow lipopolysaccharide to enter circulation. Unresolved chronic inflammation caused by one condition may overlap or trigger the other(s). Experimental studies and therapeutic trials of fecal microbiota transplantation promise limited improvement in some of these conditions.Typically, metabolic syndrome is considered as a consequence of overnutrition and the vicious cycle of lipogenesis, lipid accumulation, and chronic low-level inflammation. Because of the complex nature of this disorder, it remains inconclusive whether dysbiosis is a cause or consequence of obesity and metabolic syndrome.
肠道微生物群是人类超级生物体不可或缺的共生伙伴。这些微生物提供的丰富遗传资源扩展了宿主的基质处理能力。能量和营养收获机制主要依赖于这些生物的正常功能。然而，微生物群的动态组成会随着年龄、生活方式、应激因素、感染、药物和宿主病理生理状况而变化。宿主免疫系统主要负责塑造微生物群落并维持共生状态。这涉及到控制对病原体的敏感性和对共生体的耐受性之间的微妙平衡。当这种交流出现问题时，可能会出现失调。代谢综合征是一种多系统、低度慢性炎症性疾病，涉及血脂异常、葡萄糖不耐受、胰岛素抵抗和中心性肥胖。高糖高脂饮食导致热量摄入过多，促进了能量的高效获取和脂肪生成。脂肪细胞的脂质溢出伴随着脂肪细胞的脂滴溢出，导致胰岛素抵抗和异位脂肪组织的扩张。来自脂肪组织巨噬细胞的促炎细胞因子增加了脂肪组织功能障碍的程度。肥胖和代谢综合征的炎症性质让人想起了失调与免疫功能障碍之间的联系。肥胖、炎症性肠病、麸质敏感肠病和失调之间存在显著的相关性。这些情况会损害肠道黏膜屏障，使内毒素进入循环。一种疾病引起的未解决的慢性炎症可能会重叠或引发其他疾病。粪便微生物群移植的实验研究和治疗试验承诺在某些情况下会有一定程度的改善。通常，代谢综合征被认为是营养过剩和脂肪生成、脂质积累和慢性低度炎症的恶性循环的结果。由于这种疾病的复杂性，失调是否是肥胖和代谢综合征的原因或后果仍不确定。
