重度肥胖症患者膳食干预前后肠道内硫酸盐还原菌的定量检测

目的检测重度肥胖症患者膳食干预过程中,肠道内硫酸盐还原菌（SRB）的数量变化,为进一步研究SRB与肥胖的关系提供参考。方法以SRB基因组中的重要功能基因一腺苷酰硫酸（APS）还原酶基因作为指示基因,通过实时定量PCR的方法检测了12名重度肥胖症患者在进行膳食干预过程中随着体重的降低,肠道内SRB的数量变化,同时以16SrRNA基因对肠道内总菌进行定量来计算SRB占总菌的相对比例。结果膳食干预过程中,随着患者体重的显著降低,其肠道内SRB占总菌的比例也显著下降。在维持期,患者体重仍和干预前有显著差异,但较干预期有所回升;其体内SRB含量也显著低于干预前,但相比干预期,有所上升。结论研究结果提示肠道菌群中SRB细菌与肥胖的发展有密切关系,为后续研究SRB细菌的功能和作用机理奠定了基础。     

哺乳期过度喂养对幼鼠肥胖和肠道菌群结构的影响

目的 研究哺乳期过度喂养对幼鼠肠道细菌组成的影响以及肠道细菌与哺乳期过度喂养导致的幼年肥胖的相关性.方法 将正常出生体重的4日龄雄性ICR仔鼠分为正常喂养组(NF组,每8只由1只母鼠喂养)和哺乳期过度喂养组(OF组,每4只由1只母鼠喂养),哺乳至3周龄时,对仔鼠进行口服糖耐量试验(OGTT),称量体重、各种器官和脂肪组织的重量,用基于细菌16S rRNA基因的变性梯度凝胶电泳(DGGE)和实时定量PCR分析仔鼠的粪便细菌组成,对细菌类群数量与表型数据进行相关分析.结果 OF组仔鼠从10日龄起体重显著高于NF组,3周龄时附睾和肾周脂肪垫重量显著高于NF组,两组仔鼠的空腹血糖以及OGTT血糖曲线下面积比较差异无统计学意义.对DGGE图谱的主成分分析表明两组仔鼠的菌群结构比较差异有统计学意义.定量PCR显示,OF组仔鼠粪便中产生内毒素的肠杆菌科细菌和产生破坏肠屏障功能的H2S的硫酸盐还原菌的数量显著高于NF组,而双歧杆菌、乳杆菌和丁酸盐产生菌的数量在两组仔鼠之间差异无统计学意义.粪便硫酸盐还原菌的数量与内脏脂肪的重量显著正相关.结论 哺乳期过度喂养增加了肠道中肠杆菌科细菌和硫酸盐还原菌的数量,这些细菌的增加与仔鼠幼年期肥胖相关.     

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...     

高脂饮食对雄性SD大鼠肠道菌群的影响

目的探讨通过膳食饲喂高脂饲料诱发的高脂血症大鼠肠道菌群结构的变化。方法 24只SD（Spra-gue Dawley,SD）雄性大鼠随机分为A、B两组,分别连续饲喂基础饲料和高脂饲料42 d,并于第0、9、18、30和42天采集大鼠粪便,应用DGGE（Denaturing gradient gel electrophoresis）和q-PCR技术对肠道菌群进行定性定量分析。结果第42天时A、B组大鼠血清总胆固醇值（TC）分别为（2.01±0.14）mmol/L、（5.16±0.22）mmol/L,B组TC水平较A组明显增高（P〈0.05）。DGGE电泳图谱显示B组42 d时肠道菌群构成较0 d时变化显著,而A组不同时期肠道菌落构成无明显差异。q-PCR定量结果显示,随着饲喂高脂饲料天数的增加,B组小鼠肠道内乳杆菌属和双歧杆菌属较0 d明显降低（P〈0.01）,而拟杆菌门数量呈递减趋势且趋势比较平缓;梭菌属呈递增趋势且增幅相对拟杆菌门的变化较大。结论高脂饮食可导致肠道菌群结构的改变,这种改变会进一步促进高脂血症的形成。     

小鼠对于高脂诱导的肥胖的易感性与肠道菌群的关系

目的探究肠道菌群与小鼠在高脂膳食下形成的不同肥胖表型的关系。方法高脂饲料构建肥胖抵抗(DIO-R)和肥胖易感(DIO-P)模型,正常饲料组为对照(NC),使用末端限制性片段长度多态性(T-RFLP)和荧光实时定量PCR(RT-PCR)技术分析小鼠初始(0周)和干预后(7周)的肠道菌群。结果不仅在表型差异形成后,DIO-R和DIO-P两组小鼠的肠道菌群差异具有统计学意义,而且在初始时刻,不同肥胖表型小鼠的肠道菌群就存在不同:0周和7周时,DIO-P组和DIO-R组在酶切片段的主成分分析图上均可以明显区分,且两组小鼠肠道中Lactobacillus、Bifidobacterium、Akkermansia muciniphila、Desulfovibrio、Staphylococcus aureus、Enterobacter cloacae六种细菌的定量结果也具有明显的差别。结论肠道菌群初始状态的差异可能引导小鼠摄入高脂后对于肥胖的易感性。     

抗生素和高脂饮食对大鼠肠道乳杆菌多样性的影响

【目的】对正常、高脂、抗生素处理大鼠肠道内乳杆菌进行定性和定量分析,比较不同处理组大鼠肠道乳杆菌的多样性。【方法】应用纯培养和非培养技术(16S r RNA基因序列分析、变性梯度凝胶电泳、实时荧光定量PCR)对大鼠肠道乳杆菌进行分离鉴定和多样性分析。【结果】16S r RNA基因序列同源性分析结果显示,正常组大鼠肠道内分离出的乳杆菌包括约氏乳杆菌(Lactobacillus johnsonii)、鼠乳杆菌(Lactobacillus murinus)、嗜酸乳杆菌(Lactobacillus acidophilus)、罗伊氏乳杆菌(Lactobacillus reuteri)、植物乳杆菌(Lactobacillus plantarum)、肠道乳杆菌(Lactobacillus intestinals)、动物乳杆菌(Lactobacillus animalis)和阴道乳杆菌(Lactobacillus vaginalis);但L.animalis在高脂处理组大鼠肠道内未分离到,L.intestinals和L.vaginalis在抗生素处理组大鼠中未分离到。DGGE结果显示3个组别大鼠肠道中乳杆菌构成差异明显,同一组内样品间相似性较高;相较于正常组和高脂组,抗生素组的丰度较差;且正常组大鼠肠道内乳杆菌的多样性高于高脂组和抗生素组。q-PCR结果显示正常组大鼠肠道乳杆菌的数量明显高于高脂组和抗生素组,高脂组的数量也明显高于抗生素组,且3个组别之间存在显著差异(P0.01)。【结论】高脂饮食及抗生素的使用会减少肠道内乳杆菌多样性。     

降胆固醇乳酸菌对高脂日粮大鼠肠道代谢产物及胆汁酸代谢的研究

通过对肥胖大鼠肠道代谢物改变的研究,揭示乳酸菌降低肥胖大鼠血清胆固醇的机制及对各代谢途径产生的影响。选取健康雄性5周龄SD大鼠并分为3组:饲喂低脂日粮的对照组(C),饲喂高脂日粮的高脂组(H),饲喂高脂日粮同时灌胃乳酸菌BX-1的乳酸菌组(BX-1)。通过气相色谱-质谱联用(GC-MS)非靶向的方式测定各处理组大鼠粪便代谢产物的变化。灌胃乳酸菌BX-1可影响肥胖大鼠肠道代谢物,尤其可促进肥胖大鼠体内泛酸及多种糖代谢中间产物(醛糖、木糖、乳糖、核糖、鼠李糖、果糖)含量的增加。同时影响氨基酸代谢产物脯氨酸的大量增加,伴随焦谷氨酸和鸟氨酸的降低。BX-1还能促进高脂日粮大鼠肠道内不饱和脂肪酸十八烯酸的增加。BX-1对胆汁酸代谢物的影响较大,促进肥胖大鼠肠道内游离胆汁酸以及牛磺类结合胆汁酸的大量生成。胆固醇作为胆汁酸合成的前体物质,有助于血清胆固醇的降低。BX-1主要通过调节肥胖大鼠体内糖代谢、氨基酸代谢以及胆汁酸代谢来降低血清胆固醇含量。     

高脂饮食诱导肥胖与肥胖抵抗型非酒精性脂肪肝大鼠模型的建立

目的:利用高脂饲料复制肥胖与肥胖抵抗型非酒精性脂肪肝SD大鼠模型。方法:体质量100±10g的雄性SD大鼠140只,按照体重随机抽取120只用于模型建立,喂食高脂、高能饲料。连续8周后,将体质量大于正常对照组平均体质量+1.96倍标准差的模型大鼠作为肥胖型非酒精性脂肪肝组(NO组),体质量小于正常对照组平均体质量+1.0倍标准差的作为肥胖抵抗型非酒精性脂肪肝组(NOR组)。8周内动态观察大鼠的一般情况、体质量变化,8周末每组随机取8只处死,比较血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、胆固醇(TC)、甘油三脂(TG)水平变化及肝指数、脂体比,观察肝脏形态学改变。剩余20只作为正常对照组,喂食普通饲料。结果:NO与NOR组大鼠体重增长差距逐渐增大,至8w末,NO组体重显著高于NOR组及正常对照组(P0.01),脂肪重量和脂体比均显著升高,NO组脂肪重量显著高于NOR组(P0.05,0.01),但脂体比间未见显著差异;NO与NOR组TG、ALT显著升高(P0.05),其中NO组大鼠血清TG、TC显著高于NOR组(P0.05);两组肝重量和肝指数均显著升高,NO组肝重量显著高于NOR组(P0.05,0.01),但肝指数间未见显著差异,两组肝细胞内均弥散大量脂肪空泡。结论:利用高脂饲料成功建立肥胖与肥胖抵抗型非酒精性脂肪肝SD大鼠模型,与人类发病特征相似,为肥胖与非酒精性脂肪的研究提供更有针对性的动物模型。     

茶籽皂苷对高脂血症大鼠肠道菌群的影响研究

本实验旨在研究茶籽皂苷对高脂血症大鼠肠道菌群的影响。60只雄性Wistar大鼠适应性喂养1周后随机分为正常组(10只,C组)和造模组(50只)。C组饲喂基础饲料,造模组饲喂高脂饲料。造模成功后,将造模组大鼠按体重随机分为模型对照组(H组)、阳性对照组(P组)、茶籽皂苷高、中、低剂量组(TSH组、TSM组、TSL组),并进行灌胃。灌胃4周后,用16S rRNA测序技术检测茶籽皂苷对肠道菌群的影响。结果显示:与C组相比,H组大鼠肠道菌群的丰度和多样性显著降低,其群落结构从门到属均发生显著变化。灌胃茶籽皂苷后,肠道菌群的丰度以及从门到属的群落结构也均得到有效调节,有益菌群相对丰度提升,致病菌群得到抑制。结果表明茶籽皂苷对由高脂饲料诱发的高脂血症大鼠的肠道菌群起到正向调节作用。     

健康成年人肠道硫酸盐还原菌和丁酸盐产生菌的性别差异

探究人体肠道内重要的功能菌——硫酸盐还原菌和丁酸盐产生菌在健康成年个体中的数量,并分析其与年龄、性别的关系。采集40名健康成年志愿者(男性:女性=1:1,年龄23~53岁)的粪便样品,采用试剂盒Invi Mag誖Stool DNA Kit联合Bead beating的方法提取粪便中细菌总DNA。通过定量PCR技术对总菌、硫酸盐还原菌以及丁酸盐产生菌的拷贝数进行定量检测。结果显示,40名健康成年人每纳克粪便DNA中含有的细菌总量为(9.22×106±7.35×106)个拷贝,硫酸盐还原菌拷贝数为(9.21×103±9.87×103),而丁酸盐产生菌拷贝数稍高于硫酸盐还原菌,为(2.68×104±3.08×104)。硫酸盐还原菌和丁酸盐产生菌的数量在不同个体间存在较大差异。Spearman相关分析显示三类基因的拷贝数与志愿者年龄无显著相关关系。硫酸盐还原菌和丁酸盐产生菌的拷贝数及其相对丰度存在显著的性别差异,表现在男性个体含有更少的硫酸盐还原菌(p0.05)和更多的丁酸盐产生菌(p0.01)。本研究揭示了硫酸盐还原菌和丁酸盐产生菌在健康成年人肠道内的数量,为进一步探究肠道菌群的性别差异提供了新的思路。     

野生蓝莓和花青素提取物对高脂饮食小鼠肠道菌群的影响

【目的】研究野生蓝莓和花青素提取物对高脂饮食小鼠肠道菌群的影响。【方法】采用高脂饲料喂养C57BL/6小鼠,同时膳食补充野生蓝莓或花青素提取物,将25只无菌小鼠分为5组:正常对照组(Normal chow diet,NCD),普通饲料+10 g/100 g蓝莓组(NCD+BB),高脂饲料组(High-fat diet,HFD),高脂饲料+10 g/100 g蓝莓组(HFD+BB),高脂饲料+20 mg/100 g花青素组(HFD+ACN),饲养10周,每周对其食物摄入量、能量摄入量以及体重进行测定,并运用DGGE方法对小鼠肠道菌群结构变化进行动态监测。【结果】各实验组食物摄入量无显著性差异,HFD+BB组和HFD+ACN组能量摄入量均明显高于NCD+BB组。虽然HFD+BB组体重增加最为明显,但10周末时HFD+BB组体重与其他各组无显著差异。随着实验的进行,HFD组、HFD+BB组和HFD+ACN组肠道微生物多样性发生明显变化。HFD+BB组与NCD组菌群差异最大,HFD+ACN组与NCD组肠道菌群DGGE图谱相似性系数明显高于HFD组,对优势条带测序结果显示膳食补充蓝莓或花青素提取物可明显降低肥胖相关细菌Firmicutes的数量。【结论】蓝莓和花青素提取物可改善由高脂饮食引起的肠道微生态失调,调节肠道菌群结构,具有潜在的减肥消脂功能。     

Postweaning low-calcium diet promotes later-life obesity induced by a high-fat diet

The aim of this study was to investigate the effects of a postweaning low-calcium diet on later obesity and explore the underlying mechanisms. Ninety-six male rats were weaned at 3 weeks of age, fed standard (STD: 0.50% calcium, n=48) and low-calcium (LC: 0.15% calcium, n=48) diets for 3 weeks, and then fed the standard diet for a 3-week washout period successively. Finally, the STD rats were divided into STD control and high-fat diet (HFD) groups, and the LC ones into LC control and LC+HFD (LCHF) groups. The STD and LC rats were fed the standard diet, while the HFD control and LCFD ones were fed a high-fat diet for 6 weeks to induce obesity. During the three feeding periods, adenosine-monophosphate-activated protein kinase (AMPK) and its responsive proteins phospho-acetyl-coA carboxylase, carnitine palmitoyltransferase 1 and uncoupling protein 3 were persistently down-regulated in the LC group (decreased by 18%, 24%, 18% and 20%, respectively) versus the STD group, and these effects were significantly more pronounced in the LCHFD group (decreased by 21%, 30%, 23% and 25%, respectively) than the HFD group by a later high-fat stimuli, causing more fat and body weight in adulthood. However, lipolysis enzymes, serum leptin, insulin and lipids were not significantly affected until the body weight and fat content changed at 15 weeks of age. The results suggest that the low-calcium diet after weaning promotes rat adult-onset obesity induced by high-fat diet, which might be achieved by programming expressions of genes involved in AMPK pathway.     

Changes in Gut Microbiota in Rats Fed a High Fat Diet Correlate with Obesity-Associated Metabolic Parameters

The gut microbiota is emerging as a new factor in the development of obesity. Many studies have described changes in microbiota composition in response to obesity and high fat diet (HFD) at the phylum level. In this study we used 16s RNA high throughput sequencing on faecal samples from rats chronically fed HFD or control chow (n = 10 per group, 16 weeks) to investigate changes in gut microbiota composition at the species level. 53.17% dissimilarity between groups was observed at the species level. Lactobacillus intestinalis dominated the microbiota in rats under the chow diet. However this species was considerably less abundant in rats fed HFD (P<0.0001), this being compensated by an increase in abundance of propionate/acetate producing species. To further understand the influence of these species on the development of the obese phenotype, we correlated their abundance with metabolic parameters associated with obesity. Of the taxa contributing the most to dissimilarity between groups, 10 presented significant correlations with at least one of the tested parameters, three of them correlated positively with all metabolic parameters: Phascolarctobacterium, Proteus mirabilis and Veillonellaceae, all propionate/acetate producers. Lactobacillus intestinalis was the only species whose abundance was negatively correlated with change in body weight and fat mass. This species decreased drastically in response to HFD, favouring propionate/acetate producing bacterial species whose abundance was strongly correlated with adiposity and deterioration of metabolic factors. Our observations suggest that these species may play a key role in the development of obesity in response to a HFD.     

小檗碱对大鼠肠道菌群结构的体外影响

目的研究小檗碱在体外对高脂饮食诱导的肥胖、胰岛素抵抗大鼠(HFD)肠道菌群和正常饮食对照大鼠(NCD)肠道菌群结构的体外影响。方法采用体外厌氧培养、PCR-DGGE和454焦磷酸测序技术研究小檗碱对肠道菌群结构和多样性的影响。结果 DGGE指纹图谱和454焦磷酸测序结果都表明,小檗碱可以改变肠道菌群的结构,高剂量的小檗碱可以减少肠道微生物的多样性。应用偏最小二乘法判别模型分析(PLS-DA)挑选与小檗碱相关的细菌类群(OTU),在HFD组中挑选了55个关键OTUs,其中53个被明显抑制或消除,剩余2个分别属于Proteus和Escherichia/Shigella属的OTUs则被小檗碱富集。在NCD组中挑选的51个关键OTUs中,32个被小檗碱抑制,17个被小檗碱富集。被富集的除了属于Klebsielal属的OTU外,还包括可以产生短链脂肪酸的Lactobacillus、Blautia属的OTUs。结论小檗碱可以直接调节肠道菌群的结构,对不同结构的肠道菌群其作用也不相同,不同浓度的小檗碱对肠道菌群的影响有较大差异。高浓度的小檗碱可以抑制大部分细菌的生长(其中有很多为肠道条件致病菌),减少肠道微生物的多样性,富集Enterobacteriaceae科的细菌(Proteus、Escherichia/Shigella、Klebsielal)。相较于HFD组,小檗碱可以显著富集NCD组大鼠肠道菌群中的短链脂肪酸产生菌。     

Alterations and structural resilience of the gut microbiota under dietary fat perturbations

Disequilibrium of the gut microbiota by dietary fat has been implicated in the incidence of overweight or obesity. However, it remains to be elucidated whether dietary fat perturbations in early life have long-lasting impacts on the gut microbiota and to what extent unbalanced diet-induced alterations in childhood are reversible. Accordingly, three groups of 1-day-old hens were used. They were fed with a low-fat diet (LFD), basal diet (BD) and high-fat diet (HFD), respectively, for 6 weeks and then switched to the same normal diets (NDs) for another 19 weeks. At week 6, hens in the LFD and HFD groups were found to have higher body weight, plasma glucose, total cholesterol, triglycerides and low-density lipoprotein cholesterol levels than their counterparts in the BD group, whereas upon switching to NDs, the metabolic deteriorations observed during the LFD consumption were alleviated. Principal component analysis revealed a shift of the gut microbiota structure in the LFD and HFD groups away from that of the BD group at week 6, while the gut microbiota structure of the LFD group was moved back to that of the BD group after reverting to NDs. Additionally, abnormal alterations of obesity-related phylotypes were observed in the LFD and HFD groups, whereas the abundance of these phylotypes in the LFD group was almost reverted to the BD levels over time. Collectively, dietary fat perturbations in early life have long-term impacts on hosts, and the structural resilience of the gut microbiota in hens fed with HFD was lower than that in their LFD counterparts.     

高脂食物诱导的肥胖小鼠不同脑区即刻早期蛋白和酪氨酸羟化酶的变化

目的：在高脂食物诱导肥胖的小鼠中检测多巴胺神经元的表达。方法：10只雄性小鼠饲喂高脂膳食作为高脂食物组（HFD）,10只雄性小鼠饲喂10%脂肪膳食作为对照组（NCD）。实验第10周,小鼠禁食12 h后称重,尾静脉取血测定基础血糖水平;实验11周进行葡萄糖耐受（GTT）测试和胰岛素抵抗实验（ITT）;实验12周,动物禁食4 h后处死,测定血清胰岛素和瘦素（leptin）浓度,免疫组织化学法检测即刻早期蛋白（c-Fos-ir）和酪氨酸羟化酶（TH-ir）的表达。结果：饲喂12周高脂食物后,HFD组体重明显增加。GTT测试显示HFD组在15 min和30 min血糖浓度均明显高于NCD组（P<0.05）。ITT测试显示HFD组在15 min和30 min血糖浓度均显著高于NCD组（P<0.05）。同时,禁食后,HFD组的胰岛素浓度和leptin浓度显著高于NCD组（P<0.01）。免疫组化结果表明HFD组在伏隔核、下丘脑室旁核、腹侧背盖区和黑质的c-Fos-ir细胞数均明显多于NCD组（P<0.01）,且腹侧被盖区和黑质的TH-ir和共表达TH/Fos-ir细胞也显著多于NCD组（P<0.01）。而且HFD组VTA区和SN区TH-ir的细胞数与HFD组小鼠的终体重呈正相关（P<0.05）。结论：长期饲喂高脂食物导致的肥胖与奖赏系统多巴胺神经元的可塑性有关。     

High dietary intake of medium-chain fatty acids during pregnancy in rats prevents later-life obesity in their offspring

We investigated the effects of dietary fatty acids of different chain lengths during pregnancy in the rat on the susceptibility of offspring to later-life obesity and the underlying mechanisms. Pregnant rats were fed three different diets: standard (STD), high medium-chain fatty acids (MCFA); and high long-chain fatty acids (LCFA). The male offspring were assigned to three groups: STD control, MCFA and LCFA according to the maternal diets and suckled by dams fed with STD during pregnancy and lactation. After weaning, the offspring were fed with STD from 3 to 8 weeks of age. At the age of 8 weeks, rats in three groups: high-fat diet (HFD) control, MCFA and LCFA were fed with HFD until 14 weeks of age in an attempt to induce obesity, and rats in the HFD control group were selected randomly from the STD control group. Body weight and body fat content were decreased in the MCFA group accompanied by down-regulated mRNA expression of fatty acid synthase and acetyl-coA carboxylase 1, and increased mRNA and protein expression of adenosine monophosphate (AMP)-activated protein kinase (AMPK), carnitine palmitoyltransferase 1 and uncoupling protein 3 compared with the corresponding controls at 3, 8 and 14 weeks of age. The results suggested that the MCFA diet during pregnancy prevented later-life obesity in the offspring when they were exposed to HFD in later life, which might be related to programming of the expression of genes involved in fatty acid metabolism.     

Hypolipidemic effects of crude extract of adlay seed (Coix lachrymajobi var. mayuen) in obesity rat fed high fat diet: relations of TNF-alpha and leptin mRNA expressions and serum lipid levels

To find out whether the expressions of these adipocyte markers are influenced by oriental medicine, obesity rats induced by high fat diet (HFD) for 8 weeks were injected with 50 mg/100 g body weight adlay seed crude extract (ACE), daily for 4 weeks. The results are summarized as follows: HFD + ACE group significantly reduced food intakes and body weights. Weights of epididymal and peritoneal fat were dramatically increased in HFD groups compared with those of normal diet (ND) group but significantly decreased more in HFD + ACE group than those of HFD + saline group (sham). Those of brown adipocytes were increased in HFD + ACE group compared to ND and sham groups but there was no significant difference. The sizes in white adipose tissue (WAT) by microscope were markedly larger in HFD groups than ND group but considerably reduced in HFD + ACE group compared with sham group. The levels of triglyceride, total-cholesterol and leptin in blood serum were significantly decreased in HFD + ACE group compared to those of sham group. Leptin and TNF-alpha mRNA expressions in WAT of rats were remarkably increased more in sham group than in those of ND group. Those of HFD + ACE group were significantly decreased compared with those of sham group, especially. TNF-alpha mRNA expression in HFD + ACE group was declined more than that of ND group. In conclusion, treatments of ACE modulated expressions of leptin and TNF-alpha and reduced body weights, food intake, fat size, adipose tissue mass and serum hyperlipidemia in obesity rat fed HFD. Accordingly, the oriental medicine extract, adlay seed crude extract, can be considered for obesity therapies controlling.     

Colonic aberrant crypt formation accompanies an increase of opportunistic pathogenic bacteria in C57BL/6 mice fed a high-fat diet

The increasing worldwide incidence of colon cancer has been linked to obesity and consumption of a high-fat Western diet. To test the hypothesis that a high-fat diet (HFD) promotes colonic aberrant crypt (AC) formation in a manner associated with gut bacterial dysbiosis, we examined the susceptibility to azoxymethane (AOM)-induced colonic AC and microbiome composition in C57/BL6 mice fed a modified AIN93G diet (AIN, 16% fat, energy) or an HFD (45% fat, energy) for 14 weeks. Mice receiving the HFD exhibited increased plasma leptin, body weight, body fat composition and inflammatory cell infiltration in the ileum compared with those in the AIN group. Consistent with the gut inflammatory phenotype, we observed an increase in colonic AC, plasma interleukin-6, tumor necrosis factor-α, monocyte chemoattractant protein-1 and inducible nitric oxide synthase in the ileum of the HFD-AOM group compared with the AIN-AOM group. Although the HFD and AIN groups did not differ in bacterial species number, the HFD and AIN diets resulted in different bacterial community structures in the colon. The abundance of certain short-chain fatty acid (SCFA) producing bacteria (e.g., Barnesiella) and fecal SCFA (e.g., acetic acid) content were lower in the HFD-AOM group compared with the AIN and AIN-AOM groups. Furthermore, we identified a high abundance of Anaeroplasma bacteria, an opportunistic pathogen in the HFD-AOM group. Collectively, we demonstrate that an HFD promotes AC formation concurrent with an increase of opportunistic pathogenic bacteria in the colon of C57BL/6 mice.     

Structural resilience of the gut microbiota in adult mice under high-fat dietary perturbations

Disruption of the gut microbiota by high-fat diet (HFD) has been implicated in the development of obesity. It remains to be elucidated whether the HFD-induced shifts occur at the phylum level or whether they can be attributed to specific phylotypes; additionally, it is unclear to what extent the changes are reversible under normal chow (NC) feeding. One group (diet-induced obesity, DIO) of adult C57BL/6J mice was fed a HFD for 12 weeks until significant obesity and insulin resistance were observed, and then these mice were switched to NC feeding for 10 weeks. Upon switching to NC feeding, the metabolic deteriorations observed during HFD consumption were significantly alleviated. The second group (control, CHO) remained healthy under continuous NC feeding. UniFrac analysis of bar-coded pyrosequencing data showed continued structural segregation of DIO from CHO on HFD. At 4 weeks after switching back to NC, the gut microbiota in the DIO group had already moved back to the CHO space, and continued to progress along the same age trajectory and completely converged with CHO after 10 weeks. Redundancy analysis identified 77 key phylotypes responding to the dietary perturbations. HFD-induced shifts of these phylotypes all reverted to CHO levels over time. Some of these phylotypes exhibited robust age-related changes despite the dramatic abundance variations in response to dietary alternations. These findings suggest that HFD-induced structural changes of the gut microbiota can be attributed to reversible elevation or diminution of specific phylotypes, indicating the significant structural resilience of the gut microbiota of adult mice to dietary perturbations.