不同摄入量小米对小鼠肠道菌群和短链脂肪酸的影响

摄入一定量杂粮可降低一些慢性代谢疾病的发病率,但目前杂粮摄入量没有统一的标准,尚不清楚杂粮摄入过多是否会对健康产生不良影响。以小米添加量为20%、40%、60%、80%的饲料喂养3周龄C57BL/6J小鼠,持续12周,采用自动血生化分析仪、16S rRNA高通量基因测序、气相色谱-质谱联用仪分析了不同摄入量小米对小鼠血脂水平、肠道菌群和粪便短链脂肪酸的影响。结果发现,80%摄入量的小米显著增加了小鼠血清的总胆固醇、高密度脂蛋白胆固醇和低密度脂蛋白胆固醇的水平,同时增加了肠道丙酸、丁酸、异丁酸和戊酸的含量。肠道菌群分析结果表明,所有小米干预组的拟杆菌门(Bacteroidota)、Muribaculaceae的丰度上升,厚壁菌门(Firmicutes)、放线菌门(Actinobacteriota)、乳杆菌科(Lactobacillaceae)、双歧杆菌属 (Bifidobacterium)的丰度下降。摄入不同添加量小米的小鼠肠道菌群组成具有较大差异,其中20%小米摄入量组的小鼠菌群中显著富集了另枝菌属(Alistipes)、副拟杆菌属(Parabacteroides)、肠杆菌属(Enterorhabdus),而80%摄入量小米显著降低了小鼠菌群中的粪杆菌属(Faecalibaculum)、布劳特氏菌属(Blautia)和罗氏菌属(Roseburia)的丰度。研究结果表明,20%摄入量的小米就能有效调节小鼠肠道菌群,而过高摄入量(80%)的小米使小鼠血脂水平升高,降低了肠道菌群的多样性和均匀度以及有益菌的丰度,所以要理性看待杂粮的营养价值,避免过量摄入。     

Intake of Pro- and/or Prebiotics as a Promising Approach for Prevention and Treatment of Colorectal Cancer

Colorectal cancer (CRC) is the third most common type of cancer, posing a serious threat to human life. It is widely believed that dietary factors may be crucial modifiers of CRC risk, with pro-and/or prebiotics being especially promising. In this review, a synthesis of CRC prevention and treatment of strategies relying on usage of pro- and/or prebiotics supplements is given, as well as discuss mechanisms underlying the contribution of pro-and/or prebiotics to the suppression of colonic carcinogenesis. Furthermore, a framework for personalizing such supplements according to the composition of an individual's gut microbiome is suggested. Various factors including diversity of one's intestinal microflora, integrity of their intestinal barrier, and the presence of mutagenic/carcinogenic/genotoxic and beneficial compounds are known to have a prominent influence on the development of CRC; thus, clarifying the role of pro- and/or prebiotics will yield valuable insight toward optimizing interventions for enhanced patient outcomes in the future.     

Effects of deep frying vegetable oils rich in PUFAs on gut microbiota in rats

Vegetable oils rich in PUFAs are widely used in daily cooking and food industry, and PUFAs could be utilised by gut microbiota and present prebiotic effects. However, PUFAs are unstable in high-temperature cooking like frying. In the current study, we aimed to explore the influence of thermally oxidised oils rich in PUFA on gut microbiota. Two vegetable oils: omega-3 alpha-linolenic acid (ALA)-rich perilla oil or omega-6 linoleic acid-rich sunflower oil were heated at 180 °C for 10 h, and then fed to male SD rats for 14 weeks. Administration of heated perilla oil dramatically increased the relative abundance of Akkermansia muciniphila, a recent identified probiotics which may weaken intestinal mucus barrier, and inhibited the expression of several tight junction-related genes including occludin and claudin-1 in colon. Consumption of thermally oxidised sunflower oil stimulated the proliferation of Bifidobacterium. Our findings suggested that thermally processing has complicated effects on the prebiotic effects of vegetable oils rich in PUFAs, and perilla oil fried foods may be potential sources to stimulate Akkermansia proliferation in gut.     

魔芋甘露寡糖对ApoE-/-小鼠动脉粥样硬化的调节作用及机制

魔芋甘露寡糖(konjac mannan oligosaccharides,KMOS)具有多种有益人体健康的功能活性,但目前尚缺乏其对动脉粥样硬化(atherosclerosis,AS)的调节作用及机制方面的研究。采用高脂饮食(high fat diet,HFD)饲喂ApoE-/-小鼠14周,建立AS模型,探究KMOS干预后小鼠主动脉脂质堆积和血清脂质、炎症因子等的变化,并运用高通量测序技术,分析KMOS对于AS小鼠肠道菌群的调节作用。研究结果表明:KMOS干预显著抑制了HFD诱导引起的ApoE-/-小鼠体质量和肝脏质量的增加,主动脉窦的斑块病变面积比和总面积较HFD组分别降低57.4%和57.9%;血清中总胆固醇及低密度脂蛋白胆固醇含量分别降低21.1%和31.1%,高密度脂蛋白胆固醇含量增加了63.0%,AS小鼠肝脏脂质堆积情况明显改善;与AS模型组相比,KMOS组小鼠血清炎症因子(肿瘤坏死因子α、白介素-6、白介素-1β和单核细胞趋化蛋白-1)含量显著降低,肝脏胆固醇逆向转运相关基因的表达显著提高;此外,KMOS抑制了HFD诱导引起的ApoE-/-小鼠肠道菌群失调,增加了g_norank_f_Lachnospiraceae、g_Alistipes、g_norank_f_Ruminococcaceae的相对丰度;同时,KMOS可以增加小鼠盲肠短链脂肪酸含量,促进肠道紧密连接蛋白表达以抑制小鼠肠道屏障功能损伤。因此,KMOS可能通过调节胆固醇代谢和肠道菌群,抑制HFD诱导的ApoE-/-小鼠AS的发展,研究结果旨在为KMOS相关功能性食品的开发提供理论依据。     

The behavior of dietary fiber in the gastrointestinal tract determines its physiological effect

A diet rich in dietary fiber (DF) is considered healthy and recommended dietary intake of DF is established all over the world. The physiological effect of DF is mostly related to its behavior during digestion. In this review, the behavior of DF in the human digestive tract is discussed and linked to its physiological effect with special attention to four aspects of such behavior: (i) the modulation of bioavailability by the plant cell walls, (ii) the effect of DF on the rheological and colloidal state of digesta, (iii) the binding of DF with phenolic compounds, bile salts, mineral ions, and digestive enzymes, and (iv) DF fermentation in the large intestine and the corresponding effect on microbiota composition. It is stressed that the detailed chemical characterization of DF is crucial to explain its effect on health and that DF behavior in the digestive tract can be modulated by interactions with other food and meal components so that information of the bare content in DF of food is not sufficient to predict its physiological effect.     

Food processing increases casein resistance to simulated infant digestion

The objective of this study was to determine whether processing could modify the resistance of casein (CN) to digestion in infants. A range of different dairy matrices was manufactured from raw milk in a pilot plant and subjected to in vitro digestion using an infant gut model. Digestion products were identified using MS and immunochemical techniques. Results obtained showed that CNs were able to resist digestion, particularly κ‐ and αs₂‐CN. Resistant areas were identified and corresponded to fragments hydrophobic at pH 3.0 (gastric conditions) and/or carrying post‐translational modifications (phosphorylation and glycosylation). Milk processing led to differences in peptide patterns and heat treatment of milk tended to increase the number of peptides found in digested samples. This highlights the likely impact of milk processing on the allergenic potential of CNs.     

How Microbes Affect Depression: Underlying Mechanisms via the Gut–Brain Axis and the Modulating Role of Probiotics

Accumulating evidence suggests that the gut microbiome influences the brain functions and psychological state of its host via the gut–brain axis, and gut dysbiosis has been linked to several mental illnesses, including major depressive disorder (MDD). Animal experiments have shown that a depletion of the gut microbiota leads to behavioral changes, and is associated with pathological changes, including abnormal stress response and impaired adult neurogenesis. Short-chain fatty acids such as butyrate are known to contribute to the up-regulation of brain-derived neurotrophic factor (BDNF), and gut dysbiosis causes decreased levels of BDNF, which could affect neuronal development and synaptic plasticity. Increased gut permeability causes an influx of gut microbial components such as lipopolysaccharides, and the resultant systemic inflammation may lead to neuroinflammation in the central nervous system. In light of the fact that gut microbial factors contribute to the initiation and exacerbation of depressive symptoms, this review summarizes the current understanding of the molecular mechanisms involved in MDD onset, and discusses the therapeutic potential of probiotics, including butyrate-producing bacteria, which can mediate the microbiota–gut–brain axis.     

The Association between Gut Microbiota and Osteoarthritis: Does the Disease Begin in the Gut?

Some say that all diseases begin in the gut. Interestingly, this concept is actually quite old, since it is attributed to the Ancient Greek physician Hippocrates, who proposed the hypothesis nearly 2500 years ago. The continuous breakthroughs in modern medicine have transformed our classic understanding of the gastrointestinal tract (GIT) and human health. Although the gut microbiota (GMB) has proven to be a core component of human health under standard metabolic conditions, there is now also a strong link connecting the composition and function of the GMB to the development of numerous diseases, especially the ones of musculoskeletal nature. The symbiotic microbes that reside in the gastrointestinal tract are very sensitive to biochemical stimuli and may respond in many different ways depending on the nature of these biological signals. Certain variables such as nutrition and physical modulation can either enhance or disrupt the equilibrium between the various species of gut microbes. In fact, fat-rich diets can cause dysbiosis, which decreases the number of protective bacteria and compromises the integrity of the epithelial barrier in the GIT. Overgrowth of pathogenic microbes then release higher quantities of toxic metabolites into the circulatory system, especially the pro-inflammatory cytokines detected in osteoarthritis (OA), thereby promoting inflammation and the initiation of many disease processes throughout the body. Although many studies link OA with GMB perturbations, further research is still needed.     

Profiling of the Bacterial Microbiota along the Murine Alimentary Tract

Here, the spatial distribution of the bacterial flora along the murine alimentary tract was evaluated using high throughput sequencing in wild-type and Tff3-deficient (Tff3^KO) animals. Loss of Tff3 was linked to increased dextran sodium sulfate-induced colitis. This systematic study shows the results of 13 different regions from the esophagus to the rectum. The number of bacterial species (richness) increased from the esophagus to the rectum, from 50 to 200, respectively. Additionally, the bacterial community structure changed continuously; the highest changes were between the upper/middle and lower gastrointestinal compartments when comparing adjacent regions. Lactobacillus was the major colonizer in the upper/middle gastrointestinal tract, especially in the esophagus and stomach. From the caecum, a drastic diminution of Lactobacillus occurred, while members of Lachnospiraceae significantly increased. A significant change occurred in the bacterial community between the ascending and the transverse colon with Bacteroidetes being the major colonizers with relative constant abundance until the rectum. Interestingly, wild-type and Tff3^KO animals did not show significant differences in their bacterial communities, suggesting that Tff3 is not involved in alterations of intraluminal or adhesive microbiota but is obviously important for mucosal protection, e.g., of the sensitive stem cells in the colonic crypts probably by a mucus plume.