高脂饮食通过菌群代谢产物对肠道稳态影响的研究进展

肠道稳态失调受到遗传、环境、饮食习惯等多种因素的影响,高脂饮食作为影响因素之一,可能通过影响肠道菌群代谢产物,破坏肠黏膜屏障的完整性以及诱发肠道免疫功能紊乱,进而引发肠道稳态失衡,导致消化系统疾病发生。该文对近年来高脂饮食通过菌群代谢产物对肠道稳态影响的研究进展进行综述。     

肠道生态与环境化学物质之间的相互作用是否促发肥胖和糖尿病?

[背景]肠道菌群是肥胖和糖尿病发病的重要因素,但对于肠道菌群在环境化学物质的毒理动力学中所起的作用却知之甚少,包括那些最近发现具有致肥作用和致糖尿病作用的物质. [目的]我们把肠道生态和环境化学物质与肥胖及糖尿病之间具有独立关联的证据整合起来,为对这些环境因子如何与这些疾病相互作用提供一个框架,并确定未来的研究需求. [方法]通过调查在无菌或抗生素处理过的实验动物和人类中评估饮食改变和微生物变化如何影响肥胖和糖尿病的研究,对那些评估环境化学物质暴露会如何影响肥胖和糖尿病研究的优缺点进行总结,并辨认出肠道生态会如何影响环境化学物质处置的研究空白. [结果]越来越多的证据表明,肠道菌群的组成成分与环境化学物质暴露一样均可影响肥胖和糖尿病.毒理学和药理学文献也表明,肠道菌群的个体差异可能会通过如下途径来影响化学物质代谢:直接激活化学物质、生物转化所需代谢产物的耗竭、宿主生物转化酶的活性变化、改变肝肠循环、改变环境化学物质和/或食物中抗氧化剂的生物利用度、肠道蠕动和屏障功能的改变. [结论]肠道菌群的变化可能会影响人体毒理动力学,并增加个体对致肥物质和致糖尿病物质的暴露.与肥胖和糖尿病的全球流行作斗争需要多管齐下,其中应该包括:更加重视理解和控制肠道微生物个体差异对人体内环境化学物质处置的影响.     

青春期肠道菌群特征及性别二态性研究进展

肠道菌群在人类生命的不同阶段会经历一个动态的定殖和发育过程。在青春期时受性激素水平影响，此阶段开始性别特异性肠道菌群的发育。性激素水平与肠道菌群具有潜在联系，表明肠道菌群与性激素之间很可能具有双向交互作用。此外，微生物群在人类健康中的双向作用证据不断出现。文章通过分析肠道菌群性别二态性、青春期肠道菌群特征及其最新研究进展，探索肠道菌群与性早熟、生殖系统疾病之间的密切联系，并进一步阐释考虑性别因素在肠道微生物群与青春期性早熟及生殖系统相关疾病中的影响机制及治疗措施。     

肠道菌群与妊娠期糖代谢相关性及益生菌应用相关研究进展

肠道菌群是居住在人体肠道黏膜表面的微生物群, 在正常妊娠期间随妊娠进展肠道菌群构成可发生动态改变;妊娠糖尿病是一种常见妊娠并发症, 可影响母婴肠道菌群, 通过增加胰岛素抵抗、引发炎症反应等机制影响母婴远期糖代谢。通过饮食结构调整及益生菌应用可能调节肠道微生物群, 改善妊娠糖尿病母婴糖代谢状况。文章综述了肠道菌群与妊娠期糖代谢的相关性, 并讨论了饮食及益生菌对肠道菌群的影响。     

健康新知

<正>正常饮食可维持菌群平衡人们已知体内微生物的平衡对全身健康非常重要。最近,日本研究人员证明,正常饮食可以在人的口腔和肠道中建立和维持菌群平衡。人体是人类细胞与微生物的共生体,这些微生物对人体的众多生理功能都有调节作用。研究已经证明,菌群失衡与人的消化、睡眠、情绪、身体对药物的反应,以及糖尿病、自闭症、肥胖症和癌症的易感性均有关。     

2型糖尿病与肠道菌群相关性的研究进展

2型糖尿病（type 2 diabetes mellitus,T2DM）是以胰岛素抵抗和慢性低水平炎症为特征的代谢性疾病,病因复杂,涉及遗传和环境因素。人体肠道菌群参与多种营养物质代谢,与T2DM的联系密切,影响人体健康。肠道菌群失调可能是T2DM的危险因素,肠道菌群特征随T2DM进展而变化,肠道菌群产物短链脂肪酸、吲哚、脂多糖和次级胆汁酸等均对T2DM有影响。本文从不同门类的肠道菌群、T2DM不同疾病进程的肠道特征以及肠道菌群代谢产物三方面阐述T2DM与肠道菌群的相关性,为T2DM防治提供新的线索。     

生命不同阶段肠道菌群变化及其影响因素

人体肠道是一个温度恒定、可以为菌群提供充足营养的微生态系统,维持肠道内稳态至关重要,共生菌群的结构功能和代谢功能可以抑制肠道病原体的定植。然而,肠道是一个动态的栖息地,其生理参数持续、快速地变化着,生命不同阶段有不同的特征,多种环境因素影响了肠道菌群的形成、组成和衰老,例如出生方式、喂养方式、饮食习惯、生活方式、卫生条件以及抗生素的使用等。本文综述了生命不同阶段肠道菌群的变化及其影响因素,肠道菌群与不同年龄阶段常见疾病之间的相关关系。     

肠道菌群及微生态调节剂在儿科临床中的作用

人类的微生物系统由寄生的微生物群以及人体构成,微生物在人体成长与发展的过程中发挥着不可替代的生理作用,如果人体与微生物之间出现失衡的情况,那么人体就会受到疾病的侵袭。肠道菌群对人体有着极为重要的影响,其在人体微生物中可以占到78%以上的比重,因此加强对肠道菌群的关注是十分重要且必要的。儿童年龄小,身体机能较差,因此很容易出现肠道菌群紊乱等问题,如果不对患儿予以有效的治疗,患儿的生命健康将受到严重的威胁。文中将对肠道菌群进行必要的分析,并提出利用微生态调节剂治疗儿科相关疾病的作用。     

早期饮食如何影响婴儿肠道微生态

<正>婴儿肠道微生物对新生儿免疫激活、未来身体发育起到至关重要的作用。以婴儿生长发育的实际情况来看,婴儿的早期饮食为母乳,哺乳过程形成母乳源型微生物是抑制病原菌、促进有益肠道菌群形成的媒介。本文即基于婴儿早期饮食——母乳,分析其如何影响婴儿肠道微生态,母乳中包含的各类物质是否能够影响婴儿肠道中的各类微生物,对婴儿起到何种影响。     

抗生素药物与人类肠道菌群关系的研究现状

人类肠道内菌群为人体内最大的内毒素池人体本身因素、外界环境因素及菌群自身因素对肠道菌群的动态平衡均有着不同的影响,当肠道菌群的动态平衡失衡时人类健康将造成危害。抗生素的应用恢复肠道菌群的失衡在一定程度上起着不可或缺的作用,但抗生素药物影响致病菌的同时,也会影响肠道内的正常菌群。对肠道内细菌菌群的影响以及影响的程度,取决于相关抗生素药物的抗菌谱系、给药的途径(口服、静脉、体外等)、给药的方式、肠道内抗生素药物的浓度等。肠道内菌群之间的相互作用也影响着抗生素药物对机体所起的作用道本身也是人体内最大的免疫器官,如抗生素药物与肠道菌群之间可以达到最佳的相互作用,将对人类健康的影响起着至关重要的作用。     

The obese gut microbiome across the epidemiologic transition

The obesity epidemic has emerged over the past few decades and is thought to be a result of both genetic and environmental factors. A newly identified factor, the gut microbiota, which is a bacterial ecosystem residing within the gastrointestinal tract of humans, has now been implicated in the obesity epidemic. Importantly, this bacterial community is impacted by external environmental factors through a variety of undefined mechanisms. We focus this review on how the external environment may impact the gut microbiota by considering, the host’s geographic location ‘human geography’, and behavioral factors (diet and physical activity). Moreover, we explore the relationship between the gut microbiota and obesity with these external factors. And finally, we highlight here how an epidemiologic model can be utilized to elucidate causal relationships between the gut microbiota and external environment independently and collectively, and how this will help further define this important new factor in the obesity epidemic.     

Diarrhea Predominant-Irritable Bowel Syndrome (IBS-D): Effects of Different Nutritional Patterns on Intestinal Dysbiosis and Symptoms

Irritable Bowel Syndrome (IBS) is a chronic functional gastrointestinal disorder characterized by abdominal pain associated with defecation or a change in bowel habits. Gut microbiota, which acts as a real organ with well-defined functions, is in a mutualistic relationship with the host, harvesting additional energy and nutrients from the diet and protecting the host from pathogens; specific alterations in its composition seem to play a crucial role in IBS pathophysiology. It is well known that diet can significantly modulate the intestinal microbiota profile but it is less known how different nutritional approach effective in IBS patients, such as the low-FODMAP diet, could be responsible of intestinal microbiota changes, thus influencing the presence of gastrointestinal (GI) symptoms. The aim of this review was to explore the effects of different nutritional protocols (e.g., traditional nutritional advice, low-FODMAP diet, gluten-free diet, etc.) on IBS-D symptoms and on intestinal microbiota variations in both IBS-D patients and healthy subjects. To date, an ideal nutritional protocol does not exist for IBS-D patients but it seems crucial to consider the effect of the different nutritional approaches on the intestinal microbiota composition to better define an efficient strategy to manage this functional disorder.     

Combined Physical Exercise and Diet: Regulation of Gut Microbiota to Prevent and Treat of Metabolic Disease: A Review

Background: Unhealthy diet and sedentary lifestyle have contributed to the rising incidence of metabolic diseases, which is also accompanied by the shifts of gut microbiota architecture. The gut microbiota is a complicated and volatile ecosystem and can be regulated by diet and physical exercise. Extensive research suggests that diet alongside physical exercise interventions exert beneficial effects on metabolic diseases by regulating gut microbiota, involving in the changes of the energy metabolism, immune regulation, and the microbial-derived metabolites. Objective: In this review, we present the latest evidence in the modulating role of diet and physical exercise in the gut microbiota and its relevance to metabolic diseases. We also summarize the research from animal and human studies on improving metabolic diseases through diet-plus-exercise interventions, and new targeted therapies that might provide a better understanding of the potential mechanisms. Methods: A systematic and comprehensive literature search was performed in PubMed/Medline and Web of Science in October 2022. The key terms used in the searches included “combined physical exercise and diet”, “physical exercise, diet and gut microbiota”, “physical exercise, diet and metabolic diseases” and “physical exercise, diet, gut microbiota and metabolic diseases”. Conclusions: Combined physical exercise and diet offer a more efficient approach for preventing metabolic diseases via the modification of gut microbiota, abating the burden related to longevity.     

Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Disease

The gastrointestinal (GI) microbiota is the collection of microbes which reside in the GI tract and represents the largest source of non-self antigens in the human body. The GI tract functions as a major immunological organ as it must maintain tolerance to commensal and dietary antigens while remaining responsive to pathogenic stimuli. If this balance is disrupted, inappropriate inflammatory processes can result, leading to host cell damage and/or autoimmunity. Evidence suggests that the composition of the intestinal microbiota can influence susceptibility to chronic disease of the intestinal tract including ulcerative colitis, Crohn’s disease, celiac disease and irritable bowel syndrome, as well as more systemic diseases such as obesity, type 1 diabetes and type 2 diabetes. Interestingly, a considerable shift in diet has coincided with increased incidence of many of these inflammatory diseases. It was originally believed that the composition of the intestinal microbiota was relatively stable from early childhood; however, recent evidence suggests that diet can cause dysbiosis, an alteration in the composition of the microbiota, which could lead to aberrant immune responses. The role of the microbiota and the potential for diet-induced dysbiosis in inflammatory conditions of the GI tract and systemic diseases will be discussed.     

A Crosstalk between Diet,Microbiome and microRNA in Epigenetic Regulation of Colorectal Cancer

A still growing interest between human nutrition in relation to health and disease states can be observed. Dietary components shape the composition of microbiota colonizing our gastrointestinal tract which play a vital role in maintaining human health. There is a strong evidence that diet, gut microbiota and their metabolites significantly influence our epigenome, particularly through the modulation of microRNAs. These group of small non-coding RNAs maintain cellular homeostasis, however any changes leading to impaired expression of miRNAs contribute to the development of different pathologies, including neoplastic diseases. Imbalance of intestinal microbiota due to diet is primary associated with the development of colorectal cancer as well as other types of cancers. In the present work we summarize current knowledge with particular emphasis on diet-microbiota-miRNAs axis and its relation to the development of colorectal cancer.     

The human gut microbiota and its interactive connections to diet

The microbiota of the gastrointestinal tract plays an important role in human health. In addition to their metabolic interactions with dietary constituents, gut bacteria may also be involved in more complex host interactions, such as modulation of the immune system. Furthermore, the composition of the gut microbiota may be important in reducing the risk of contracting particular gut infections. Changes in the microbiota during an individual's lifespan are accompanied by modifications in multiple health parameters, and such observations have prompted intense scientific efforts aiming to understand the complex interactions between the microbiota and its human host, as well as how this may be influenced by diet.     

Intestinal Microbiota and Celiac Disease: Cause,Consequence or Co-Evolution?

It is widely recognized that the intestinal microbiota plays a role in the initiation and perpetuation of intestinal inflammation in numerous chronic conditions. Most studies report intestinal dysbiosis in celiac disease (CD) patients, untreated and treated with a gluten-free diet (GFD), compared to healthy controls. CD patients with gastrointestinal symptoms are also known to have a different microbiota compared to patients with dermatitis herpetiformis and controls, suggesting that the microbiota is involved in disease manifestation. Furthermore, a dysbiotic microbiota seems to be associated with persistent gastrointestinal symptoms in treated CD patients, suggesting its pathogenic implication in these particular cases. GFD per se influences gut microbiota composition, and thus constitutes an inevitable confounding factor in studies conducted in CD patients. To improve our understanding of whether intestinal dysbiosis is the cause or consequence of disease, prospective studies in healthy infants at family risk of CD are underway. These studies have revealed that the CD host genotype selects for the early colonizers of the infant’s gut, which together with environmental factors (e.g., breast-feeding, antibiotics, etc.) could influence the development of oral tolerance to gluten. Indeed, some CD genes and/or their altered expression play a role in bacterial colonization and sensing. In turn, intestinal dysbiosis could promote an abnormal response to gluten or other environmental CD-promoting factors (e.g., infections) in predisposed individuals. Here, we review the current knowledge of host-microbe interactions and how host genetics/epigenetics and environmental factors shape gut microbiota and may influence disease risk. We also summarize the current knowledge about the potential mechanisms of action of the intestinal microbiota and specific components that affect CD pathogenesis.     

Diet–Microbiota Interactions in Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD is largely unknown, it is widely thought that diet contributes to the development of IBD. Diet shapes the composition of the gut microbiota, which plays critical roles in intestinal homeostasis. In contrast, intestinal inflammation induces gut dysbiosis and may affect the use of dietary nutrients by host cells and the gut microbiota. The interaction of diet and the gut microbiota is perturbed in patients with IBD. Herein, we review the current knowledge of diet and gut microbiota interaction in intestinal homeostasis. We also discuss alterations of diet and gut microbiota interaction that influence the outcome and the nutritional treatment of IBD. Understanding the complex relationships between diet and the gut microbiota provides crucial insight into the pathogenesis of IBD and advances the development of new therapeutic approaches.     

Nutrition and Microbiome Interactions in Human Cancer

Individual physiologic responses to changes in dietary patterns can vary widely to affect cancer risk, which is driven by multiple host-specific factors (eg, genetics, epigenetics, inflammatory and metabolic states, and the colonizing microbiome). Emerging evidence indicates that diet-induced microbiota alterations are key modulators of several host functions important to tumor etiology, progression, and response to cancer therapy. Thus, diet may potentially be used to target alterations of the microbiota as an effective means to improve outcomes across the cancer continuum (from cancer prevention to tumor development and progression, to effects on treatment and survivorship). This review will focus on recent examples of functional interactions between dietary components (nutrients and non-nutrients) and the gastrointestinal microbiome, which are 2 critical and malleable environmental variables in cancer risk that affect host immune, metabolic, and cell signaling functions and may provide insights for novel cancer therapeutic and preventive strategies.     

Gut-Brain-Microbiota Axis: Antibiotics and Functional Gastrointestinal Disorders

Gut microbiota composition and function are major areas of research for functional gastrointestinal disorders. There is a connection between gastrointestinal tract and central nervous system and this is mediated by neurotransmitters, inflammatory cytokines, the vagus nerve and the hypothalamic-pituitary-adrenal axis. Functional gastrointestinal disorders are prevalent diseases affecting more than one third of the population. The etiology of these disorders is not clarified. Visceral hyperalgesia is the main hypothesis for explaining clinical symptoms, however gut-brain axis disorder is a new terminology for functional disorders. In this review, microbiota-gut-brain axis connection pathways and related disorders are discussed. Antibiotics are widely used in developed countries and recent evidence indicates antibiotic-induced dysbiosis as an important factor for functional disorders. Antibiotics exert negative effects on gut microbiota composition and functions. Antibiotic-induced dysbiosis is a major factor for occurrence of post-infectious irritable bowel syndrome. Cognitive and mood disorders are also frequent in functional gastrointestinal disorders. Animal and human trials show strong evidence for the causal relationship between gut microbiota and brain functions. Therapeutic implications of these newly defined pathogenic pathways are also discussed.