The immunity-diet-microbiota axis in the development of metabolic syndrome

被引:39
作者
Brandsma, Eelke [1 ]
Houben, Tom [2 ]
Fu, Jingyuan [3 ]
Shiri-Sverdlov, Ronit [2 ]
Hofker, Marten H. [1 ]
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Dept Pediat, Mol Genet, NL-9713 AV Groningen, Netherlands
[2] Maastricht Univ, Dept Mol Genet, NL-6200 MD Maastricht, Netherlands
[3] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, NL-9713 AV Groningen, Netherlands
关键词
endotoxemia; innate immunity; metabolic syndrome; microbiota; short-chain fatty acids; CHAIN FATTY-ACIDS; GUT MICROBIOTA; INTESTINAL MICROBIOTA; RECEPTOR; MICE; PROMOTES; MUCOSAL; DYSBIOSIS; HOST; PHOSPHATIDYLCHOLINE;
D O I
10.1097/MOL.0000000000000154
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Purpose of review Recent evidence demonstrates that the gut-microbiota can be considered as one of the major factors causing metabolic and cardiovascular diseases. Recent findings Pattern recognition receptors as well as antimicrobial peptides are a key factor in controlling the intestinal microbiota composition. Deficiencies in these genes lead to changes in the composition of the gut-microbiota, causing leakage of endotoxins into the circulation, and the development of low-grade chronic inflammation and insulin resistance. Dietary composition can also affect the microbiota: a diet rich in saturated fats allows the expansion of pathobionts that damage the intestinal epithelial cell layer and compromise its barrier function. In contrast, a diet high in fiber supports the microbiota to produce short-chain fatty acids, thereby promoting energy expenditure and protecting against inflammation and insulin resistance. Summary The interactions between the microbiota, innate immunity, and diet play an important role in controlling metabolic homeostasis. A properly functioning innate immune system, combined with a low-fat and high-fiber diet, is important in preventing dysbiosis and reducing the susceptibility to developing the metabolic syndrome and its associated cardiovascular diseases.
引用
收藏
页码:73 / 81
页数:9
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