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本文引用的文献

1
Do SCFA have a role in appetite regulation?短链脂肪酸(SCFA)在食欲调节中起作用吗?
Proc Nutr Soc. 2011 Feb;70(1):119-28. doi: 10.1017/S0029665110004039.
2
Composition and energy harvesting capacity of the gut microbiota: relationship to diet, obesity and time in mouse models.肠道微生物群的组成和能量收集能力:与饮食、肥胖和小鼠模型时间的关系。
Gut. 2010 Dec;59(12):1635-42. doi: 10.1136/gut.2010.215665. Epub 2010 Oct 6.
3
A role for intestinal alkaline phosphatase in the maintenance of local gut immunity.肠碱性磷酸酶在维持局部肠道免疫中的作用。
Dig Dis Sci. 2011 Apr;56(4):1020-7. doi: 10.1007/s10620-010-1396-x. Epub 2010 Sep 16.
4
Butyrate and other short-chain fatty acids as modulators of immunity: what relevance for health?丁酸盐和其他短链脂肪酸作为免疫调节剂:对健康有什么影响?
Curr Opin Clin Nutr Metab Care. 2010 Nov;13(6):715-21. doi: 10.1097/MCO.0b013e32833eebe5.
5
Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa.通过对欧洲和非洲农村儿童的比较研究揭示饮食对肠道微生物群的影响。
Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14691-6. doi: 10.1073/pnas.1005963107. Epub 2010 Aug 2.
6
Effects of four Bifidobacteria on obesity in high-fat diet induced rats.四株双歧杆菌对高脂饮食诱导大鼠肥胖的影响。
World J Gastroenterol. 2010 Jul 21;16(27):3394-401. doi: 10.3748/wjg.v16.i27.3394.
7
Lactobacillus plantarum DSM 2648 is a potential probiotic that enhances intestinal barrier function.植物乳杆菌 DSM 2648 是一种有潜力的益生菌,能增强肠道屏障功能。
FEMS Microbiol Lett. 2010 Aug 1;309(2):184-92. doi: 10.1111/j.1574-6968.2010.02038.x. Epub 2010 Jun 16.
8
Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation.大鼠高脂肪饮食诱导肥胖的倾向与肠道微生物群和肠道炎症的变化有关。
Am J Physiol Gastrointest Liver Physiol. 2010 Aug;299(2):G440-8. doi: 10.1152/ajpgi.00098.2010. Epub 2010 May 27.
9
Short-chain fructooligosaccharide regulates hepatic peroxisome proliferator-activated receptor alpha and farnesoid X receptor target gene expression in rats.短链果糖寡糖调节大鼠肝过氧化物酶体增殖物激活受体α和法尼醇 X 受体靶基因表达。
J Agric Food Chem. 2010 Jun 9;58(11):7007-12. doi: 10.1021/jf1006616.
10
Absence of intestinal microbiota does not protect mice from diet-induced obesity.肠道微生物群的缺失并不能保护小鼠免受饮食诱导的肥胖。
Br J Nutr. 2010 Sep;104(6):919-29. doi: 10.1017/S0007114510001303. Epub 2010 May 5.

肥胖与肠道微生物群:促进结肠发酵能否预防肥胖和代谢性疾病?

Obesity and the gut microbiota: does up-regulating colonic fermentation protect against obesity and metabolic disease?

机构信息

Nutrition and Nutrigenomics Group, Research and Innovation Centre, FEM-IASMA, 38010, S. Michele a.A, Trento, Italy,

出版信息

Genes Nutr. 2011 Aug;6(3):241-60. doi: 10.1007/s12263-011-0230-1. Epub 2011 May 11.

DOI:10.1007/s12263-011-0230-1
PMID:21559992
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3145060/
Abstract

Obesity is now considered a major public health concern globally as it predisposes to a number of chronic human diseases. Most developed countries have experienced a dramatic and significant rise in obesity since the 1980s, with obesity apparently accompanying, hand in hand, the adoption of "Western"-style diets and low-energy expenditure lifestyles around the world. Recent studies report an aberrant gut microbiota in obese subjects and that gut microbial metabolic activities, especially carbohydrate fermentation and bile acid metabolism, can impact on a number of mammalian physiological functions linked to obesity. The aim of this review is to present the evidence for a characteristic "obese-type" gut microbiota and to discuss studies linking microbial metabolic activities with mammalian regulation of lipid and glucose metabolism, thermogenesis, satiety, and chronic systemic inflammation. We focus in particular on short-chain fatty acids (SCFA) produced upon fiber fermentation in the colon. Although SCFA are reported to be elevated in the feces of obese individuals, they are also, in contradiction, identified as key metabolic regulators of the physiological checks and controls mammals rely upon to regulate energy metabolism. Most studies suggest that the gut microbiota differs in composition between lean and obese individuals and that diet, especially the high-fat low-fiber Western-style diet, dramatically impacts on the gut microbiota. There is currently no consensus as to whether the gut microbiota plays a causative role in obesity or is modulated in response to the obese state itself or the diet in obesity. Further studies, especially on the regulatory role of SCFA in human energy homeostasis, are needed to clarify the physiological consequences of an "obese-style" microbiota and any putative dietary modulation of associated disease risk.

摘要

肥胖现在被认为是一个全球性的主要公共卫生关注点,因为它易导致许多慢性人类疾病。自 20 世纪 80 年代以来,大多数发达国家的肥胖率急剧上升,肥胖显然伴随着全球范围内“西方”饮食和低能量消耗生活方式的采用。最近的研究报告表明,肥胖受试者的肠道微生物群落异常,肠道微生物代谢活动,特别是碳水化合物发酵和胆汁酸代谢,可以影响与肥胖相关的许多哺乳动物生理功能。本综述的目的是提出特征性“肥胖型”肠道微生物群落的证据,并讨论将微生物代谢活性与哺乳动物对脂质和葡萄糖代谢、产热、饱腹感和慢性全身炎症的调节联系起来的研究。我们特别关注纤维在结肠发酵产生的短链脂肪酸 (SCFA)。尽管据报道肥胖个体粪便中的 SCFA 升高,但它们也被认为是哺乳动物调节能量代谢所依赖的生理检查和控制的关键代谢调节剂。大多数研究表明,瘦人和肥胖个体的肠道微生物群落组成不同,饮食,特别是高脂肪低纤维的西方饮食,对肠道微生物群落有显著影响。目前尚不清楚肠道微生物群是否在肥胖中起因果作用,还是对肥胖状态本身或肥胖中的饮食进行调节。需要进一步的研究,特别是关于 SCFA 在人类能量平衡中的调节作用,以阐明“肥胖型”微生物群的生理后果以及任何可能的饮食对相关疾病风险的调节。