Human Core Temperature Responses during Exercise and Subsequent Recovery: An Important Interaction between Diurnal Variation and Measurement Site

Chronobiological investigations into core temperature during and after exercise can involve ambulatory measurements of intestinal temperature during actual competitions, esophageal temperature measurements in laboratory simulations, or rectal temperature, which can be measured in both the field and laboratory. These sites have yet to be compared during both morning and afternoon exercise and subsequent recovery. At 08∶00 and 17∶00 h, seven recreationally active males exercised at 70% peak oxygen uptake for 30 min and then recovered passively for 30 min. During the experiment, esophageal, rectal, intestinal, and skin temperatures, plus sweat loss, heart rate, and ratings of perceived exertion (RPE), were monitored. We found that the diurnal variation in intestinal temperature responses (0.45±0.32°C; mean±SD) was significantly larger compared with rectal (0.33±0.24°C) and, particularly, esophageal temperature responses (0.21±0.20°C; p= 0.019). This reflected a greater difference of 0.25–0.40°C between the esophagus and the other two sites in the afternoon, compared to inter‐site differences of only 0.13–0.16°C in the morning. Diurnal variation was small for skin temperature, heart rate, sweat loss, and RPE responses during exercise (p>0.05). Our data suggest that the relative differences between intestinal, rectal, and esophageal temperature during exercise and subsequent recovery depend on time of day to the extent that inferences from studies on experimental and applied chronobiology will be affected.     

Role of Glycoside Phosphorylases in Mannose Foraging by Human Gut Bacteria

To metabolize both dietary fiber constituent carbohydrates and host glycans lining the intestinal epithelium, gut bacteria produce a wide range of carbohydrate-active enzymes, of which glycoside hydrolases are the main components. In this study, we describe the ability of phosphorylases to participate in the breakdown of human N-glycans, from an analysis of the substrate specificity of UhgbMP, a mannoside phosphorylase of the GH130 protein family discovered by functional metagenomics. UhgbMP is found to phosphorolyze β-d-Manp-1,4-β-d-GlcpNAc-1,4-d-GlcpNAc and is also a highly efficient enzyme to catalyze the synthesis of this precious N-glycan core oligosaccharide by reverse phosphorolysis. Analysis of sequence conservation within family GH130, mapped on a three-dimensional model of UhgbMP and supported by site-directed mutagenesis results, revealed two GH130 subfamilies and allowed the identification of key residues responsible for catalysis and substrate specificity. The analysis of the genomic context of 65 known GH130 sequences belonging to human gut bacteria indicates that the enzymes of the GH130_1 subfamily would be involved in mannan catabolism, whereas the enzymes belonging to the GH130_2 subfamily would rather work in synergy with glycoside hydrolases of the GH92 and GH18 families in the breakdown of N-glycans. The use of GH130 inhibitors as therapeutic agents or functional foods could thus be considered as an innovative strategy to inhibit N-glycan degradation, with the ultimate goal of protecting, or restoring, the epithelial barrier.     

The protective effect of trefoil factor 3 on the intestinal tight junction barrier is mediated by toll-like receptor 2 via a PI3K/Akt dependent mechanism

Trefoil factor peptides are highly conserved secreted molecules characterized by heat and enzymatic digestion resistance. Intestinal trefoil factor 3 (TFF3) protects and repairs the gastrointestinal mucosa and restores normal intestinal permeability, which is dependent on the integrity of the tight junction (TJ) barrier and the TJ associated proteins claudin-1, zona occludens-1 (ZO-1) and occludin. Despite the important role of intestinal barrier dysfunction in the pathogenesis of inflammatory bowel diseases, the underlying mechanisms and associated molecules remain unclear. In the present study, we show that TFF3 and toll-like receptor 2 (TLR2) are functionally linked and modulate intestinal epithelial permeability via a mechanism that involves the PI3K/Akt pathway. We used the Caco-2 cell model to show that TLR2 and TFF3 inhibit the IL-1β induced increase in permeability and release of proinflammatory cytokines, and that this effect is mediated by activation of PI3K/Akt signaling. TLR2 silencing downregulated the expression of TFF3 and overexpression of TLR2 and TFF3 increased the levels of phospho-Akt. TFF3 overexpression significantly upregulated the expression of ZO-1, occludin and claudin-1 and this effect was abrogated by inhibition of the PI3K/Akt pathway. Taken together, our results indicate that TLR2 signaling selectively enhances intestinal TJ barrier integrity through a mechanism involving TFF3 and the activation of the PI3K/Akt pathway.     

中药甘草对大鼠肠平滑肌运动的影响

目的观察甘草对大鼠肠道平滑肌运动的影响,了解甘草与胃肠运动之间的关系。方法实验分成正常组、甘草制成煎剂4．8、16、32、64g／kg剂量组,每日1次灌胃给药。末次给药1h后观察大鼠胃半排时间;采用灌胃给予炭末,测定胃推进率。结果甘草煎剂剂量大小对大鼠小肠蠕动有直接的影响,较小剂量对大鼠小肠的推进功能有抑制作用,较大剂量对大鼠的肠推进有促进作用。     

砂仁对抗生素所致肠道菌群失调小鼠调节作用的探讨

【摘要】 目的 通过建立抗生素诱导小鼠肠道菌群失调模型,应用PCR-变性梯度凝胶电泳(PCR-DGGE)技术分析小鼠肠道菌群失调前后经服用中药砂仁调理后肠道菌群指纹图谱的变化。方法 选用10只昆明种小鼠,正常培养7 d,适应环境后每天取粪便1次,连续3 d;菌群稳定后按100 mg/kg的头孢拉啶灌胃,每天灌胃2次,连续5 d,每天取粪便1次;上述小鼠随机分为两个组,自然恢复组(饲喂基础饲料)和砂仁处理组,每组5只。3 d后每天取粪便1次,连续3 d,提取细菌总DNA,以16S rRNA基因V3区通用引物扩增,对扩增的PCR产物进行DGGE电泳及指纹图谱分析并切胶测序比对。结果 抗生素处理后小鼠肠道菌群与正常小鼠差异有统计学意义,致病菌增加,砂仁处理组小鼠与正常小鼠的肠道菌群指纹图谱有很大的相似性,但与自然恢复组差异有统计学意义。结论 抗生素可导致小鼠肠道菌群失调,而中药砂仁对肠道菌群失调有明显的恢复作用。     

抗性淀粉对HFA小鼠肠道菌群的影响

目的 以人源菌群(HFA)小鼠为研究模型,观察抗性淀粉(RS)对高脂饮食诱导的肥胖小鼠肠道菌群的多样性的影响.方法 将30只无菌小鼠接种健康人志愿者的粪便悬液构建HFA小鼠模型后,随机分成3组,一组喂养含20％的抗性淀粉的高脂饲料(RS组),一组喂养纯高脂饲料(CK组),一组喂养普通饲料(CONV组),取第0周和第8周的小鼠新鲜粪便,用PCR-DGGE分析3组小鼠的肠道菌群的相似性和多样性.结果 3组小鼠在第0周时肠道菌群多样性的相似度达到79％～87％,与人的肠道菌群相似性达到39％,说明构建HFA小鼠模型成功,第8周时,3组之间的均匀度(E)和Shannon指数差异无统计学意义(P＞0.05),而丰富度(S)在高脂组(CK)与普通饲料组(CONV)和抗性淀粉组(RS)之间差异都有统计学意义(P＜0.05),说明高脂饮食引起肠道菌群多样性增加,而抗性淀粉则能降低这种多样性.结论 抗性淀粉可以显著影响HFA小鼠的肠道菌群多样性.     

肠道微生物群落与炎症性肠病关系研究进展

目的炎症性肠病（IBD）包括克罗恩病（CD）和溃疡性结肠炎（UC）,以持续性肠道非特异性炎症为特征,通常反复发作、迁延不愈,临床上仍无特效性的治疗手段。IBD确切的发病机制尚不清楚,涉及免疫、环境及遗传等因素,这些因素共同诱导肠道炎症、黏膜损伤和修复。肠道微生物群落及其代谢产物、宿主基因易感性及肠道黏膜免疫三方面共同参与了IBD的发病机制。本文从消化道微生态角度出发,对目前IBD相关的肠道微生物群落研究现状、宿主-微生物间免疫应答及益生菌治疗等内容进行探讨。     

肠道菌群与疾病发生及中草药调节和治疗作用的研究概述

肠道正常菌群及微生态稳定对人体极具重要性,中草药对肠道菌群具有调节作用.本文综述了人体的肠道正常菌群与疾病产生和发展的关系,结合中草药对肠道菌群调节作用的研究,探讨中药调节肠道菌群与其发挥疾病防治效果之间的相关性,以期为中草药的临床应用及药理学研究提供一定的参考依据.     

植物性发酵乳杆菌对免疫系统的生理活性、抗高血糖和促进肠蠕动的影响

研究植物源性发酵乳杆菌对免疫系统生理活性、抗高血糖和促进肠蠕动的影响.β-内啡肽对免疫系统有重要作用,阿片-促黑素细胞皮质素原(POMC)是β-内啡肽的前体物质,为了探讨发酵乳杆菌对免疫功能的影响,检测小鼠下丘脑和脑垂体中POMC的基因表达水平.通过喂食发酵乳杆菌时间和浓度的不同及测量β一内啡肽表达水平的方式,来分析血液中B-内啡肽的变化情况.此外,测定了三种小鼠模型的血糖变化,即常规的WT小鼠模型、D-葡萄糖诱导的急性高血糖模型和链唑霉素(STZ)诱导的糖尿病模型,以证实发酵乳杆菌的降血糖效果,并对降血糖效果进行了验证.通过检测血糖随喂食发酵乳杆菌浓度和时间而变化的情况,已证实给药浓度和时间对血糖浓度有很好的影响.另外,为证实发酵乳杆菌对肠蠕动的影响测定了胃肠通过时间,证明发酵乳杆菌对肠蠕动有极好的促进作用.通过此项研究,证实发酵乳杆菌对提高人体免疫系统的生理活性、抗高血糖和促进小肠蠕动有极佳的效果.     

双歧杆菌四联活菌片对肝硬化白发性细菌性腹膜炎患者肠黏膜屏障和炎症因子的影响

目的探讨双歧杆菌四联活菌片对肝硬化自发性细菌性腹膜炎（SBP）患者肠黏膜屏障和炎症因子的影响。方法选择乙肝后肝硬化SBP患者68例,分为治疗组和对照组。两组患者均予以低盐饮食、护肝利尿、补充白蛋白和抗感染等基础治疗。治疗组在此基础上予以双歧杆菌四联活菌片口服,1．5g／次,3次／d,连用6周。结果治疗6周后,两组血浆内毒素、PCT和尿L／M比值比较均有明显下降（对照组比较P〈0．05,或治疗组比较P〈0．01）,且治疗组下降幅度明显优于对照组（P〈0．05）;两组血浆TNF-α、IL-6和IL-10水平均有明显下降（对照组比较P〈0．05,或治疗组比较P〈0．01）,且治疗组下降幅度明显优于对照组（P〈0．05）。治疗组临床总有效率明显高于对照组（χ2=8．17,P〈0．01）,治疗期间未发生严重的药物不良反应。结论双歧杆菌四联活菌片治疗肝硬化SBP患者具有较好的临床疗效及安全性,对患者肠黏膜屏障功能具有良好保护和改善作用,并能下降血浆TNF—α、IL-6和IL-10水平,具有辅助治疗肝硬化作用。