益生菌干预对高脂高糖饮食诱导肥胖小鼠肠道菌群及脂代谢影响的研究

目的探讨益生菌干预对高脂高糖饮食诱导肥胖小鼠肠道菌群及脂代谢的影响。方法 C57BL/6J雌性小鼠30只随机分为正常对照组、肥胖组和益生菌干预组,每组10只,分别给予标准饲料、高脂高糖饲料以及高脂高糖饲料同时给予益生菌干预,连续喂养6周,测量并分析三组小鼠的体重。留取小鼠粪便样本,应用PCR-DGGE法分析菌群,应用酶反应比色法分析三组小鼠血脂情况。结果与正常对照组小鼠相比,肥胖小鼠体重明显增加,益生菌干预组小鼠体重略有增加;肥胖组小鼠肠道菌群紊乱,与正常对照组分别聚为两大类,益生菌干预组小鼠肠道菌群与正常对照组聚为一大类。肥胖小鼠血清总胆固醇、低密度脂蛋白含量升高,益生菌干预组小鼠较肥胖组血清总胆固醇、低密度脂蛋白含量降低,但与正常对照组仍有差异。结论高脂高糖饮食诱导肥胖小鼠存在肠道菌群结构失调及脂代谢异常,益生菌干预可以改善肥胖小鼠菌群失调以及脂代谢紊乱。     

母代高脂饮食诱导子代在小鼠生命早期出现糖脂代谢紊乱且具有雄性易感性

目的：探讨孕期和哺乳期的高脂饮食能否导致子代在生命早期出现糖脂代谢紊乱。方法成年雌性C57BL/6J小鼠与正常饮食雄性小鼠进行交配,孕鼠随机分为高脂饮食组和正常饮食组,在孕期和哺乳期喂养高脂饲料或正常饲料,至交配后第一代鼠断乳时（3周龄）观察其糖脂代谢相关性指标以及肝脏病理表现。结果较正常饮食组子鼠相比,高脂饮食子鼠出生体重更低（ P＜0.05）。在断乳时,高脂饮食组雄性子鼠体重较重（ P ＝0.038）,腹腔糖耐量实验30 min和60 min血糖明显升高（P值分别为＜0.001和＜0.01）,糖耐量曲线下面积较大（P＝0.0016）,HOMA-IR值较大（P＜0.05）,雌性子鼠腹腔糖耐量实验在30 min血糖高于正常组（P＜0.01）,而糖耐量曲线下面积和HOMA-IR值在两组之间无明显统计学意义。雄性和雌性子代小鼠空腹胆固醇水平高脂饮食组均高于正常饮食组（ P值分别为＜0.0001和0.0004）,而两组雄性和雌性子代小鼠空腹胰岛素和甘油三酯水平差异均无显著性（ P均＞0.05）。另外,在断乳时高脂饮食子鼠出现肝脏脂肪变性,雌性和雄性子鼠无明显差异。结论母鼠孕期和哺乳期高脂饮食能够诱导子代在生命早期就能出现糖脂代谢紊乱并且雄性子鼠更易出现肥胖、糖耐量异常、胰岛素抵抗。     

益生菌干预对肥胖小鼠肝脏miR-33 和miR-122表达的影响

目的探讨益生菌干预对高脂饮食诱导肥胖小鼠肝脏miR-33和miR-122表达的影响。方法 18只雌性C57BL/6J小鼠随机分为对照组、肥胖组和益生菌干预组,每组6只,分别给予标准饲料、高脂饲料以及高脂饲料+益生菌合剂灌胃,自由采食及饮水,连续喂养6周。每周测量3组小鼠的体质量,6周后,留取小鼠血液样本采用全自动生化仪检测小鼠血脂,安乐法处死小鼠,留取小鼠肝脏样本Hair-pin RT-PCR法检测miR-33和miR-122的含量。结果与对照组小鼠相比,肥胖组小鼠体质量明显增加(t_(2周)=3.985,t_(3周)=4.751,t_(4周)=4.380,t_(5周)=4.728,t_(6周)=4.112,均P0.01);益生菌干预组小鼠体质量较肥胖组明显降低(t_(3周)=3.694,t_(4周)=4.415,t_(5周)=3.752,t_(6周)=3.392,均P0.01);肥胖组小鼠血清总胆固醇、低密度脂蛋白含量较对照组明显升高(t=10.850,t=7.024,均P0.01),益生菌干预组小鼠较肥胖组小鼠血清总胆固醇、低密度脂蛋白含量降低(t=3.034,t=2.881,均P0.05),但与对照组仍有差异。与对照组小鼠相比,肥胖组小鼠肝脏miR-122的表达升高(t=9.170,P0.01),miR-33的表达降低(t=3.420,P0.05),益生菌干预组小鼠较肥胖组小鼠miR-122的表达降低(t=3.204,P0.05),miR-33的表达升高(t=2.070,P0.05)。结论益生菌干预能够影响高脂饮食小鼠肝脏miR-33和miR-122的表达,这可能是益生菌干预改善高脂饮食小鼠肝脏脂代谢的机制之一。     

泽泻对高脂高糖饮食大鼠肠道菌群多样性的影响

目的研究泽泻对高脂高糖饮食大鼠的降血脂作用与肠道菌群多样性的相关性,并测定高脂高糖饮食大鼠肠道菌群丰度与多样性的变化。方法将32只健康雄性SD大鼠随机分成正常组(control group,CON)、高脂高糖模型组(high-fat and high-sucrose diet group,HFS)、高脂高糖饲料加二甲双胍干预组(metformin treatment group,MET)和高脂高糖饲料加泽泻醇提取物干预组(Alisma orientale extract group,AOE)。每组8只,造模4周后分别灌胃给予相应药物,连续4周。CON组和HFS组灌胃给予生理盐水。检测血清TC、TG、LDL-C及HDL-C水平及其他指标,提取肠道菌群总DNA,分析肠道微生物的变化。结果 HFS组的TC、LDL-C水平明显高于CON组(Ps0.05),给药4周后,AOE组TC、LDL-C水平均显著性降低(Ps0.05)。高通量测序结果显示,AOE组中与脂质代谢、多聚糖生物合成与代谢相关的肠道菌群多样性及丰度增加显著,肠道菌群的生态环境得以改善,形成了新的肠道菌群稳态。结论泽泻醇提取物可以有效降低高脂高糖饮食大鼠的血脂水平,对其肝脏具有保护作用。泽泻醇提取物也能通过改变肠道菌群的丰度、多样性和功能类群等靶标进行脂质代谢调节。     

不同配方益生菌在高脂饮食诱导小鼠肥胖发生中的差异化作用

【目的】基于肠道微生物与宿主代谢的相互关系,研究不同配方的益生菌对小鼠肥胖的影响。【方法】50只C57BL/6J雄性小鼠随机平均分成10组,分别给予正常饲料、高脂饲料以及高脂饲料加8种不同配方的益生菌产品(50亿CFU/只),所有动物连续喂养9周,每周测量小鼠体重1次。最后一周测定空腹血糖、葡萄糖耐量试验(glucose tolerance test,GTT)、血脂相关指标,称取内脏重量,并留取小鼠盲肠内容物,提取小鼠肠道菌群总DNA,利用16S rDNA测序检测相关细菌含量。【结果】部分益生菌可引起小鼠体重增速加快,而部分益生菌可减缓小鼠肥胖和降低内脏脂肪重量,同时缓解高血脂症。丹尼斯克品牌益生菌配方组小鼠肠道中厚壁菌/拟杆菌比例(F/B)是正常饮食组的22.8倍,Akkermansia muciniphila(Akkermansia)细菌含量几乎为0;而菌拉丁品牌益生菌配方组小鼠F/B比例与正常饲料饮食组类似,Akkermansia含量为0.5%,为正常饮食对照组小鼠的一半左右。【结论】益生菌可影响小鼠体重和代谢,但不同配方的益生菌效果截然相反。特定的益生菌配方对肥胖和高血脂的改善可能是由于其选用的菌株本身的特性以及菌株之间的相互配比能够降低小鼠肠道中F/B比例以及升高Akkermansia的含量所带来的。此研究为进一步开发可改善代谢的益生菌产品提供了参考。     

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.     

基于肠道菌群和短链脂肪酸代谢探讨不同饮食条件下高脂血症大鼠发病机制

目的 本研究拟对比两种不同高脂饮食方式诱导的高脂血症大鼠肠道菌群变化与短链脂肪酸代谢特征,以宿主-肠道菌群-代谢角度探讨高脂血症可能的微观机制。方法 SPF级SD大鼠分为：正常饮食组(CG组):饲喂大鼠维持饲料;高脂饮食组(HFD1组):每天足量饲喂高脂饲料;限饲高脂饮食组(HFD2组):每天限量饲喂高脂饲料80 g,不限量饲喂维持饲料。8周后检测血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平;苏木精-伊红(HE)染色观察大鼠肝组织和肾周脂肪病理学变化;取结肠内容物进行16S rDNA高通量测序,观察肠道菌群结构与功能的变化,并检测结肠内容物中短链脂肪酸的含量。结果 与CG组相比,HFD1组和HFD2组大鼠摄食量下降,体重升高;血清中TC、TG、LDL-C均显著升高;肝组织发生明显脂肪变性,肾周脂肪出现炎性病变;高脂干预后大鼠肠道菌群相对丰度显著变化,其中乳杆菌属相对丰度明显降低,菌群结构和功能变化明显,总短链脂肪酸、乙酸、丁酸、异丁酸下降显著。结论 两种高脂饮食方式均能引起大鼠高脂血症,且发病机制基本一致,均与脂质代谢以...     

实验性2型糖尿病心肌病大鼠模型的建立与评价

目的建立和评价2型糖尿病心肌病（DC）大鼠模型,探究高糖脂饮食在模型建立中的作用。方法将雄性Wistar大鼠随机分成正常对照组、高糖脂饮食组和高糖脂负荷小剂量STZ组。高糖高脂膳食诱导11周负荷小剂量链脲佐菌素（STZ）（30 mg/kg）腹腔注射建立DC模型,并观察糖代谢、脂代谢和心功能的变化。结果①大鼠经高糖高脂饲料诱导4周后,与正常对照组相比,胆固醇（TCH）和甘油三酯（TG）均显著增高（P〈0.05）,血糖值没有明显变化（P〉0.05）。②大鼠注射30 mg/kg STZ后72 h,血糖水平开始升高,继续以高糖高脂饲料喂养6周后,与正常对照组比较,高糖脂饮食组和高糖脂负荷小剂量STZ组大鼠TG、TCH维持高水平,差异有显著性（P〈0.05）;高糖脂负荷小剂量STZ组大鼠血糖值持续高水平,与正常对照组差异有显著性（P〈0.001）。③心功能测量结果显示,高糖脂饮食组大鼠出现温和的心脏功能异常（左心室收缩压降低,左心室舒张末压升高）;高糖脂负荷小剂量STZ组大鼠左心室收缩和舒张功能均出现异常（LVSP、每搏输出量、心排量降低,LVEDP、左心室最大舒张速率升高）,但以舒张功能异常为主。结论大鼠高糖脂饮食诱导负荷小剂量STZ可建立类似临床症状的2型DC模型,高糖脂饮食在糖脂代谢紊乱和心脏功能损伤过程中有重要作用,结合糖、脂代谢指标和心脏功能指标可以有效简便评价糖尿病心肌病模型。     

肠道菌群与肥胖关系的研究进展

西方化的高脂饮食方式造成了越来越多的肥胖人群。高脂饮食在一定程度上可以改变肠道菌群的结构组成和功能,促进宿主对食物营养的吸收,从而增加体重形成肥胖。高脂饮食诱导的肥胖者肠道菌群的改变会导致宿主能量吸收增加,肠道通透性和炎症增加,而有减肥功能的短链脂肪酸合成能力下降。最近研究发现肠道菌群也可以通过影响中枢神经系统,尤其是下丘脑相关基因的表达来控制食欲,从而调控肥胖的形成。本文系统介绍了最近几年高脂饮食诱导肥胖的研究,总结了一些与肥胖形成有密切关系的肠道菌群以及其在肥胖形成中的作用机制,为进一步研究肠道菌群与肥胖之间的调控作用奠定了基础。最后总结了肠道菌群可以作为一个预防和治疗肥胖的有效靶点,可以通过在食物中添加有益菌或者通过菌群移植来治疗肥胖。     

母鼠营养不良导致子代在生命早期出现糖脂代谢紊乱及其机制探讨

为了探讨母鼠孕期和哺乳期营养不良对子代生命早期糖脂代谢的影响及其机制,文章对孕期和哺乳期母鼠分别喂养高脂饮食、低蛋白饮食和正常饮食,观察其子鼠断乳时(3周龄)糖脂代谢指标,并采用荧光定量PCR方法检测子鼠肝组织氧化物酶增殖物激活受体γ(PPARγ)基因的表达情况。结果表明：子鼠在3周龄时,与正常饮食组相比,低蛋白饮食组子鼠出生体重(7.36±0.91 vs 8.94±1.39,P<0.0001)较低,体长较短(12.27±0.53 vs 13.44±0.36,P<0.0001);高脂饮食组子鼠体重(9.53±0.68 vs 7.36±0.91,P<0.0001)和体长(13.22±0.35 vs 12.27±0.53,P<0.0001)均高于低蛋白饮食组;另外,高脂饮食组子鼠腹腔糖耐量实验30 min和60 min血糖明显高于正常饮食组(P<0.001),且高脂饮食组30 min血糖水平也明显高于低蛋白饮食组(P<0.001),高脂饮食组子鼠糖耐量曲线下面积明显大于正常饮食组(P<0.001)。另外,与正常饮食组相比,高脂饮食组子鼠空腹胆固醇水平明显升高(1.64±0.21 vs 1.18±0.16,P<0.01),低蛋白饮食组空腹胆固醇水平明显下降(0.96±0.09 vs 1.18±0.16,P<0.05)。荧光定量PCR结果显示,在低蛋白饮食组和高脂饮食组,其子鼠肝组织PPARγ基因表达量均明显高于正常饮食组(P<0.05)。结果显示,母鼠妊娠期和哺乳期高脂饮食与低蛋白饮食均可以诱导子鼠在发育早期出现糖脂代谢紊乱,PPARγ基因可能在其中参与了重要的调控作用。     

Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism

Gut microbiota dysbiosis has been implicated in a variety of systemic disorders, notably metabolic diseases including obesity and impaired liver function, but the underlying mechanisms are uncertain. To investigate this question, we transferred caecal microbiota from either obese or lean mice to antibiotic‐free, conventional wild‐type mice. We found that transferring obese‐mouse gut microbiota to mice on normal chow (NC) acutely reduces markers of hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non‐inoculated mice, a phenotypic trait blunted in conventional NOD2 KO mice. Furthermore, transferring of obese‐mouse microbiota changes both the gut microbiota and the microbiome of recipient mice. We also found that transferring obese gut microbiota to NC‐fed mice then fed with a high‐fat diet (HFD) acutely impacts hepatic metabolism and prevents HFD‐increased hepatic gluconeogenesis compared to non‐inoculated mice. Moreover, the recipient mice exhibit reduced hepatic PEPCK and G6Pase activity, fed glycaemia and adiposity. Conversely, transfer of lean‐mouse microbiota does not affect markers of hepatic gluconeogenesis. Our findings provide a new perspective on gut microbiota dysbiosis, potentially useful to better understand the aetiology of metabolic diseases.     

Dietary modulation of clostridial cluster XIVa gut bacteria (Roseburia spp.) by chitin-glucan fiber improves host metabolic alterations induced by high-fat diet in mice

Recent studies have provided new evidence that alterations in the composition of the gut microbiota — known as dysbiosis — participate in the development of obesity. The aim of the present study was to investigate the ability of chitin-glucan (CG) from a fungal source to modulate both the gut microbiota and glucose and lipid metabolism in high-fat (HF) diet-induced obese mice. Supplementation of the HF diet with fungal CG (10% w/w) induced caecal enlargement with prominent changes in gut microbiota: it restored the number of bacteria from clostridial cluster XIVa including Roseburia spp., which were decreased due to HF feeding. Furthermore, CG treatment significantly decreased HF-induced body weight gain, fat mass development, fasting hyperglycemia, glucose intolerance, hepatic triglyceride accumulation and hypercholesterolemia, independently of the caloric intake. All those parameters were negatively correlated with specific bacteria of clostridial cluster XIVa, i.e., Roseburia spp. (Pearson's correlations analysis). In contrast to prebiotics that more specifically target the bifidobacteria species, CG effects on obesity appear to be independent of the incretin glucagon-like peptide 1 (GLP-1) production, since portal GLP-1 and proglucagon (its precursor) expression were not modified by the dietary intervention. In conclusion, our findings support the view that chronic consumption of CG has potential beneficial effects with respect to the development of obesity and associated metabolic diabetes and hepatic steatosis, through a mechanism related to the restoration of the composition and/or the activity of gut bacteria, namely, bacteria from clostridial cluster XIVa.     

Targeting the Microbiota to Address Diet-Induced Obesity: A Time Dependent Challenge

Links between the gut microbiota and host metabolism have provided new perspectives on obesity. We previously showed that the link between the microbiota and fat deposition is age- and time-dependent subject to microbial adaptation to diet over time. We also demonstrated reduced weight gain in diet-induced obese (DIO) mice through manipulation of the gut microbiota with vancomycin or with the bacteriocin-producing probiotic Lactobacillus salivarius UCC118 (Bac⁺), with metabolic improvement achieved in DIO mice in receipt of vancomycin. However, two phases of weight gain were observed with effects most marked early in the intervention phase. Here, we compare the gut microbial populations at the early relative to the late stages of intervention using a high throughput sequencing-based analysis to understand the temporal relationship between the gut microbiota and obesity. This reveals several differences in microbiota composition over the intervening period. Vancomycin dramatically altered the gut microbiota composition, relative to controls, at the early stages of intervention after which time some recovery was evident. It was also revealed that Bac⁺ treatment initially resulted in the presence of significantly higher proportions of Peptococcaceae and significantly lower proportions of Rikenellaceae and Porphyromonadaceae relative to the gut microbiota of L. salivarius UCC118 bacteriocin negative (Bac^-) administered controls. These differences were no longer evident at the later time. The results highlight the resilience of the gut microbiota and suggest that interventions may need to be monitored and continually adjusted to ensure sustained modification of the gut microbiota.     

Increased maternal fat consumption during pregnancy alters body composition in neonatal mice

Maternal overnutrition prior to and during gestation causes pronounced metabolic dysfunction in the adult offspring. However, less is known about metabolic adaptations in the offspring that occur independently of postnatal growth and nutrition. Therefore, we evaluated the impact of excess maternal dietary lipid intake on the in utero programming of body composition, hepatic function, and hypothalamic development in newborn (P0) offspring. Female mice were fed a low-fat (LF) or high-fat (HF) diet and were mated after 4, 12, and 23 wk. A subset of the obese HF dams was switched to the LF diet during the second (DR2) or third (DR3) pregnancies. The HF offspring accrued more fat mass than the LF pups, regardless of duration of maternal HF diet consumption or prepregnancy maternal adiposity. Increased neonatal adiposity was not observed in the DR3 pups. Liver weights were reduced in the HF offspring but not in the DR2 or DR3 pups. Offspring hepatic triglyceride content was reduced in the HF pups, but hepatic inflammation and expression of lipid metabolism genes were largely unaffected by maternal diet. Maternal diet did not alter the hypothalamic expression of orexigenic and anorexigenic neuropeptides in the offspring. Thus, the intrauterine programming of increased neonatal adiposity and reduced liver size by maternal overnutrition is evident in mice at birth and occurs prior to the development of maternal obesity. These observations demonstrate that dietary intervention during pregnancy minimizes the deleterious effects of maternal obesity on offspring body composition, potentially reducing the offsprings' risk of developing obesity and related diseases later in life.     

儿童单纯性肥胖小鼠模型的制作

目的通过调整窝仔数的方法建立幼儿单纯性肥胖模型,并与高脂饲料制备模型进行比较。方法48只雌性KM小鼠产仔鼠后,一半仔鼠数目为14～16只,一半仔鼠调整为6只（雌雄各3只）。仔鼠离乳时或第9周时仔鼠分别饲喂普通饲料或高脂饲料。仔鼠在15周后处死,称重,测量体长、腰围,生殖器重、脂肪重（肾周和生殖器周脂肪）,计算体脂比。结果①BD2组常规饲料饲喂至15周结束后,无论雌雄仔鼠,其体重与BDl组比较差异均有显著性（P〈0．05）,且BD2组体重超过BD1组体重雌性为26．3％,雄性为20．0％。同一处理方式,雌性仔鼠体脂比均高于雄性。②不同时间饲喂高脂饲料,无论调整窝仔数与否,高脂饲料各组仔鼠,无论雌雄,其各组仔鼠体重均比BD1组高（P均〈0．05）;HFD4组雌性和雄性仔鼠体重与BD2组相比差异均存在显著性（P〈0．05）。结论通过调整窝仔数的方法可以成功制备儿童单纯性肥胖模型。在儿童早期肥胖的情况下,成年后过度高脂饮食会导致机体储存更多的脂肪。     

Effects of Maternal Diet and Exercise during Pregnancy on Glucose Metabolism in Skeletal Muscle and Fat of Weanling Rats

Obesity during pregnancy contributes to the development of metabolic disorders in offspring. Maternal exercise may limit gestational weight gain and ameliorate these programming effects. We previously showed benefits of post-weaning voluntary exercise in offspring from obese dams. Here we examined whether voluntary exercise during pregnancy influences lipid and glucose homeostasis in muscle and fat in offspring of both lean and obese dams. Female Sprague-Dawley rats were fed chow (C) or high fat (F) diet for 6 weeks before mating. Half underwent voluntary exercise (CE/FE) with a running wheel introduced 10 days prior to mating and available until the dams delivered; others remained sedentary (CS/FS). Male and female pups were killed at postnatal day (PND)19 and retroperitoneal fat and gastrocnemius muscle were collected for gene expression. Lean and obese dams achieved similar modest levels of exercise. At PND1, both male and female pups from exercised lean dams were significantly lighter (CE versus CS), with no effect in those from obese dams. At PND19, maternal obesity significantly increased offspring body weight and adiposity, with no effect of maternal exercise. Exercise significantly reduced insulin concentrations in males (CE/FE versus CS/FS), with reduced glucose in male FE pups. In males, maternal obesity significantly decreased muscle myogenic differentiation 1 (MYOD1) and glucose transporter type 4 (GLUT4) mRNA expressions (FS vs CS); these were normalized by exercise. Maternal exercise upregulated adipose GLUT4, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1α) mRNA expression in offspring of dams consuming chow. Modest voluntary exercise during pregnancy was associated with lower birth weight in pups from lean dams. Maternal exercise appeared to decrease the metabolic risk induced by maternal obesity, improving insulin/glucose metabolism, with greater effects in male than female offspring.     

Stronger anti-obesity effect of white ginseng over red ginseng and the potential mechanisms involving chemically structural/compositional specificity to gut microbiota

BackgroundGinseng has therapeutic potential for treating obesity and the associated gut microbiota dysbiosis. However, whether white ginseng and red ginseng, the two kinds of commonly used processed ginseng, possess different anti-obesity effects remains unknown.PurposeAnti-obesity effects of water extracts of white ginseng and red ginseng (WEWG and WERG) were compared, and the potential mechanisms were discussed.MethodsChemical profiles of WEWG and WERG were characterized by ultra-high performance liquid chromatography-tandem triple quadrupole mass spectrometry (UHPLC-QqQ-MS/MS) and high performance liquid chromatography coupled with evaporative light scattering detector (HPLC-ELSD). Anti-obesity effects of WEWG/WERG were examined by determining fat accumulation, systemic inflammation, enteric metabolic disorders and gut microbiota dysbiosis in high-fat diet (HFD)-fed obese mice.ResultsBoth WEWG and WERG exerted anti-obesity effects, with WEWG stronger than WERG. Compared to WERG, WEWG contained less contents of carbohydrates (polysaccharides, oligosaccharides, free monosaccharides) and ginsenosides, but chemical structures or compositions of these components in WEWG were characteristic, i.e. narrower molecular weight distribution and higher molar ratios of glucose residues of polysaccharides; higher content ratios of oligosaccharides DP2–3 (di-/tri-saccharides)-to-oligosaccharides DP4–7 (tetra-/penta-/hexa-/hepta-saccharides), sucrose-to-melibiose, maltose-to-trehalose and high-polar-to-low-polar ginsenosides. WEWG better ameliorated fat accumulation, enteric metabolic disorders and gut microbiota dysbiosis in HFD-fed obese mice than WERG.ConclusionThe stronger anti-obesity effect of white ginseng appears to correlate with differences in its chemical profile as compared to red ginseng. The carbohydrates and ginsenosides in WEWG potentially present more structural and compositional specificity to the obesity-associated gut bacteria, allowing more beneficial effects of WEWG on the gut microbiota dysbiosis. This consequently better alleviates the enteric metabolic disorders and systemic inflammation, thereby contributing to the stronger anti-obesity effect of WEWG as compared to WERG.     

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

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.