肠道菌群与多囊卵巢综合征代谢异常的研究进展

多囊卵巢综合征(polycystic ovary syndrome,PCOS)患者的高雄激素血症、胰岛素抵抗和肥胖之间相互影响,其代谢异常成为PCOS患者急需解决的问题之一.人体肠道中存在着丰富的微生物,肠道菌群与宿主终生相伴,互利共生,成为肿瘤、免疫性疾病和代谢性疾病的研究热点,近年对PCOS患者肠道菌群及其与代谢异...     

婴儿肠道菌群的建立及其与健康的关系

在漫长的进化过程中,与人体共生的微生物形成了复杂的微生态系统,参与机体的生理功能.肠道菌群是人体重要的微生态系统之一,直接参与人体的消化、营养吸收、能量供应、脂肪代谢、免疫调节等多方面功能,相当于人体的一个重要"器官"[1].研究发现,多种疾病可能与肠道菌群有关,包括胃癌、结肠癌、非炎症性肠病、坏死性小肠结肠炎、免疫性疾病,以及慢性代谢性疾病,例如肥胖、糖尿病等[2-3].     

肠道菌群在代谢疾病中作用的研究进展

正随着社会的发展和人们生活方式、饮食结构的变化,代谢性疾病如肥胖、糖尿病等的发病率显著上升。有研究发现,肠道菌群与代谢疾病的发生发展密切相关。肠道菌群是一个庞大的微生态系统,其可参与人体的多种生理反应,尤其是机体代谢相关酶的合成,如淀粉酶、纤维分解酶和果胶酶等的合成都需要肠道菌群及其代谢产物的参与~([1-3])。因此,探究肠道菌群在代谢疾病中的作用机制可为代谢疾病的预防和治疗找到一条新思路。本文主要对肠道菌群与代谢疾病之间的关系进行总结,分析肠道菌群失衡诱发人体代谢疾病的原因。     

肠道微生态,保护人健康

在每一个人的肠道内都有一大群微生物栖息,构成肠道内的正常菌群,总量可达1000克左右,占人体各部位正常菌群总量的78%以上。肠道内正常栖息的微生物,绝大多数对人体健康并无害处,反而是维持人体健康之必须。因为它们的存在可与人体细胞之间互换能量、互通代谢、互惠共生、传递信息。这些微生物所产生的酶类     

高脂膳食诱导肠道菌群失调与认知功能损害关系研究进展

长期高脂膳食不仅可导致肥胖、2型糖尿病、心血管疾病等多种代谢性疾病,还可引发认知功能下降。人体肠道中寄居着种类繁多的微生物,这些微生物统称为肠道菌群。肠道菌群组成与膳食因素密切有关,高脂膳食可使肠道菌群的组成发生改变,导致菌群构成比例失衡,即肠道菌群失调。新近提出的"肠道菌群–肠–脑轴"观点认为,肠道菌群失调是介导高脂膳食引起认知功能损害的重要机制之一。本文对高脂膳食、肠道菌群与认知功能的关系进行研究,并对高脂膳食、肠道菌群影响认知功能的可能机制作一综述。     

肠道菌群与肥胖以及相关代谢性疾病关系的研究

肥胖通常会引起高血压、高血脂、糖尿病及心血管类疾病,对人们生活质量及健康水平造成严重影响,治疗肥胖及相关代谢性疾病已成为当前比较重要的公共健康问题。大量研究结果表明人体的营养、免疫及代谢功能通常会受到肠道菌群代谢活动的影响,同时,肠道菌群也是影响代谢性疾病以及肥胖的一个重要因素。所以,本文就肠道菌群与肥胖及相关代谢性疾病关系研究进行综述。     

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。     

揭秘微生物与健康的关系

正美国科学家近日发现,肠道菌群会产生一种名为N-酰基酰胺的小型有机复合物,它们与受体相互作用,参与包括免疫等方面的多种人体生理活动,而这可能就是人类微生物组影响人体健康的机制之一。科学家们早已意识到人类基因组并不能完全解释人类疾病与健康的关键问题,因为我们对自身体内存在的大规模与人体共生的微生物菌群还缺乏了解。美国国立卫生研究院于2007年宣布启动"人类微生物组计划",以解析微生物菌群结构变化对人类健康的影响。     

肠道菌群与2型糖尿病研究进展

2型糖尿病是一种代谢疾病,其发病率日益增加,造成了巨大的社会经济负担。肠道菌群指定居于人体肠道的微生物群体,作为与人类紧密联系的环境因素,参与人体生长发育、生理过程,甚至疾病状态。近年来关于肠道菌群与2型糖尿病的关系的研究已经成为内分泌代谢领域的热点问题。本文拟就2型糖尿病与肠道菌群的关系做一综述,梳理该方面研究的最新进展,提示这一领域的进一步研究方向。     

呼吸道微生态和健康与疾病的相关性研究进展

呼吸道微生物组学在健康和疾病中的作用一直是人们研究的热点,研究表明,吸烟、肠道菌群与呼吸道微生态之间有关联。呼吸道菌群是决定呼吸道健康与否的关键因素,健康和疾病人体呼吸道微生态环境及菌群的构成有差异。本文综述了国内外关于呼吸道微生物组学的发展历程和研究现状,健康和疾病状态下呼吸道微生物组学的差异及呼吸道、肠道微生态与呼吸系统疾病之间的联系。     

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.     

Synthetic Microbiomes on the Rise—Application in Deciphering the Role of Microbes in Host Health and Disease

The intestinal microbiota conveys significant benefits to host physiology. Although multiple chronic disorders have been associated with alterations in the intestinal microbiota composition and function, it is still unclear whether these changes are a cause or a consequence. Hence, to translate microbiome research into clinical application, it is necessary to provide a proof of causality of host–microbiota interactions. This is hampered by the complexity of the gut microbiome and many confounding factors. The application of gnotobiotic animal models associated with synthetic communities allows us to address the cause–effect relationship between the host and intestinal microbiota by reducing the microbiome complexity on a manageable level. In recent years, diverse bacterial communities were assembled to analyze the role of microorganisms in infectious, inflammatory, and metabolic diseases. In this review, we outline their application and features. Furthermore, we discuss the differences between human-derived and model-specific communities. Lastly, we highlight the necessity of generating novel synthetic communities to unravel the microbial role associated with specific health outcomes and disease phenotypes. This understanding is essential for the development of novel non-invasive targeted therapeutic strategies to control and modulate intestinal microbiota in health and disease.     

Chewing the Fat with Microbes: Lipid Crosstalk in the Gut

It is becoming increasingly important for any project aimed at understanding the effects of diet on human health, to also consider the combined effect of the trillions of microbes within the gut which modify and are modified by dietary nutrients. A healthy microbiome is diverse and contributes to host health, partly via the production and subsequent host absorption of secondary metabolites. Many of the beneficial bacteria in the gut rely on specific nutrients, such as dietary fiber, to survive and thrive. In the absence of those nutrients, the relative proportion of good commensal bacteria dwindles while communities of opportunistic, and potentially pathogenic, bacteria expand. Therefore, it is unsurprising that both diet and the gut microbiome have been associated with numerous human diseases. Inflammatory bowel diseases and colorectal cancer are associated with the presence of certain pathogenic bacteria and risk increases with consumption of a Western diet, which is typically high in fat, protein, and refined carbohydrates, but low in plant-based fibers. Indeed, despite increased screening and better care, colorectal cancer is still the 2nd leading cause of cancer death in the US and is the 3rd most diagnosed cancer among US men and women. Rates are rising worldwide as diets are becoming more westernized, alongside rising rates of metabolic diseases like obesity and diabetes. Understanding how a modern diet influences the microbiota and how subsequent microbial alterations effect human health will become essential in guiding personalized nutrition and healthcare in the future. Herein, we will summarize some of the latest advances in understanding of the three-way interaction between the human host, the gut microbiome, and the specific class of dietary nutrients, lipids.     

Prebiotics and the Human Gut Microbiota: From Breakdown Mechanisms to the Impact on Metabolic Health

The colon harbours a dynamic and complex community of microorganisms, collectively known as the gut microbiota, which constitutes the densest microbial ecosystem in the human body. These commensal gut microbes play a key role in human health and diseases, revealing the strong potential of fine-tuning the gut microbiota to confer health benefits. In this context, dietary strategies targeting gut microbes to modulate the composition and metabolic function of microbial communities are of increasing interest. One such dietary strategy is the use of prebiotics, which are defined as substrates that are selectively utilised by host microorganisms to confer a health benefit. A better understanding of the metabolic pathways involved in the breakdown of prebiotics is essential to improve these nutritional strategies. In this review, we will present the concept of prebiotics, and focus on the main sources and nature of these components, which are mainly non-digestible polysaccharides. We will review the breakdown mechanisms of complex carbohydrates by the intestinal microbiota and present short-chain fatty acids (SCFAs) as key molecules mediating the dialogue between the intestinal microbiota and the host. Finally, we will review human studies exploring the potential of prebiotics in metabolic diseases, revealing the personalised responses to prebiotic ingestion. In conclusion, we hope that this review will be of interest to identify mechanistic factors for the optimization of prebiotic-based strategies.     

The Interplay between the Gut Microbiome and the Immune System in the Context of Infectious Diseases throughout Life and the Role of Nutrition in Optimizing Treatment Strategies

Infectious diseases and infections remain a leading cause of death in low-income countries and a major risk to vulnerable groups, such as infants and the elderly. The immune system plays a crucial role in the susceptibility, persistence, and clearance of these infections. With 70–80% of immune cells being present in the gut, there is an intricate interplay between the intestinal microbiota, the intestinal epithelial layer, and the local mucosal immune system. In addition to the local mucosal immune responses in the gut, it is increasingly recognized that the gut microbiome also affects systemic immunity. Clinicians are more and more using the increased knowledge about these complex interactions between the immune system, the gut microbiome, and human pathogens. The now well-recognized impact of nutrition on the composition of the gut microbiota and the immune system elucidates the role nutrition can play in improving health. This review describes the mechanisms involved in maintaining the intricate balance between the microbiota, gut health, the local immune response, and systemic immunity, linking this to infectious diseases throughout life, and highlights the impact of nutrition in infectious disease prevention and treatment.     

Utilization of gut environment-mediated control system of host immunity in the development of vaccine adjuvants

Vaccination is one of the most powerful strategies for the preventive and therapeutic control of infectious diseases and other diseases such as cancer. To maximize the effectiveness of vaccines, it is necessary to modify the immune responses by means of adjuvants. The gut environment, including commensal bacteria and dietary components, has been proven to be able to mediate host immunity. An understanding of gut microbiota–related regulation of immune responses has revealed the potential adjuvanticity of particular microbiota-derived compounds, driving exploration into their development as vaccine adjuvants. In this review, we discuss how commensal bacteria and compounds derived from them regulate host immune responses, and we propose the potential application of these compounds as vaccine adjuvants.     

Probiotics in inflammatory bowel diseases and associated conditions

A complex set of interactions between the human genes encoding innate protective functions and immune defenses and the environment of the intestinal mucosa with its microbiota is currently considered key to the pathogenesis of the chronic inflammatory bowel diseases (IBD). Probiotics offer a method to potentially alter the intestinal microbiome exogenously or may provide an option to deliver microbial metabolic products to alter the chronicity of intestinal mucosal inflammation characterizing IBD. At present, there is little evidence for the benefit of currently used probiotic microbes in Crohn's disease or associated conditions affecting extra-intestinal organs. However, clinical practice guidelines are now including a probiotic as an option for recurrent and relapsing antibiotic sensitive pouchitis and the use of probiotics in mild ulcerative colitis is provocative and suggests potential for benefit in select patients but concerns remain about proof from trials.     

HDHL-INTIMIC: A European Knowledge Platform on Food,Diet, Intestinal Microbiomics,and Human Health

Studies indicate that the intestinal microbiota influences general metabolic processes in humans, thereby modulating the risk of chronic diseases such as type 2 diabetes, allergy, cardiovascular disease, and colorectal cancer (CRC). Dietary factors are also directly related to chronic disease risk, and they affect the composition and function of the gut microbiota. Still, detailed knowledge on the relation between diet, the microbiota, and chronic disease risk is limited. The overarching aim of the HDHL-INTIMIC (INtesTInal MICrobiomics) knowledge platform is to foster studies on the microbiota, nutrition, and health by assembling available knowledge of the microbiota and of the other aspects (e.g., food science and metabolomics) that are relevant in the context of microbiome research. The goal is to make this information findable, accessible, interoperable, and reusable (FAIR) to the scientific community, and to share information with the various stakeholders. Through these efforts a network of transnational and multidisciplinary collaboration has emerged, which has contributed to further develop and increase the impact of microbiome research in human health. The roles of microbiota in early infancy, during ageing, and in subclinical and clinically manifested disease are identified as urgent areas of research in this knowledge platform.     

Microbiota’s Role in Diet-Driven Alterations in Food Intake: Satiety,Energy Balance,and Reward

The gut microbiota plays a key role in modulating host physiology and behavior, particularly feeding behavior and energy homeostasis. There is accumulating evidence demonstrating a role for gut microbiota in the etiology of obesity. In human and rodent studies, obesity and high-energy feeding are most consistently found to be associated with decreased bacterial diversity, changes in main phyla relative abundances and increased presence of pro-inflammatory products. Diet-associated alterations in microbiome composition are linked with weight gain, adiposity, and changes in ingestive behavior. There are multiple pathways through which the microbiome influences food intake. This review discusses these pathways, including peripheral mechanisms such as the regulation of gut satiety peptide release and alterations in leptin and cholecystokinin signaling along the vagus nerve, as well as central mechanisms, such as the modulation of hypothalamic neuroinflammation and alterations in reward signaling. Most research currently focuses on determining the role of the microbiome in the development of obesity and using microbiome manipulation to prevent diet-induced increase in food intake. More studies are necessary to determine whether microbiome manipulation after prolonged energy-dense diet exposure and obesity can reduce intake and promote meaningful weight loss.