苦瓜-人参预防给药对高脂诱导肥胖小鼠胰岛素抵抗的影响

[目的]考察苦瓜、人参、苦瓜-人参预防给药对高脂诱导肥胖小鼠糖脂代谢及胰岛素抵抗的影响,为"一补一泄、一寒一热"苦瓜-人参对药改善肥胖、胰岛素抵抗,预防2型糖尿病提供实验证据。[方法]采用高脂饲料喂养法诱导肥胖胰岛素抵抗小鼠模型,并给予苦瓜、人参、苦瓜-人参对药分别进行预防性干预,以二甲双胍作为阳性对照。给药干预16周后,测摄食量、体质量、脂肪指数、空腹血糖(FPG)、空腹血清胰岛素(FINS)、血脂水平,计算稳态模型胰岛素抵抗指数、胰岛素敏感指数,评价胰岛素抵抗与分泌水平,口服葡萄糖耐量实验考察血糖调节能力。苏木精-伊红(HE)染色观察睾周脂肪细胞形态。[结果]高脂饲料诱导小鼠的体质量、皮下脂肪指数、FPG、FINS水平明显升高,并发生明显胰岛素抵抗,而人参可以显著改善胰岛素抵抗,苦瓜可明显降低FPG、体质量和皮下脂肪含量,苦瓜-人参对药则可明显降低FINS及皮下脂肪含量,并且各给药干预组在不同程度上改善了肥胖小鼠的脂肪细胞形态。[结论]人参能明显改善肥胖小鼠胰岛素抵抗,苦瓜可以有效减轻其FPG及体质量,苦瓜-人参对药降低FINS更有优势。     

五仁丸加减方对高脂饲料诱导小鼠肥胖的预防作用

目的 探讨五仁丸加减方对高脂饲料诱导小鼠肥胖的预防作用。方法 将60只昆明小鼠随机分为对照组、模型组、阳性组(27.3 mg/kg奥利司他)和五仁丸加减方低、中、高剂量组(0.75、1.50、2.25 g/kg),每组10只,给予60%纯化的高脂饲料造模,同时分别灌胃给予相应药物,连续60 d。记录小鼠体质量、腰围和进食量,CT扫描内脏脂肪和总脂肪蓄积程度,记录肾周脂肪和附睾脂肪含量,检测血清TC、TG、LDL-C、HDL-C水平,观察肾周脂肪和附睾脂肪病理学变化。结果 与模型组比较,五仁丸加减方组小鼠体质量和腰围降低(P<0.01),但不影响进食量(P>0.05);内脏脂肪、总脂肪蓄积程度及肾周脂肪、附睾脂肪含量降低(P<0.05,P<0.01);血清TC、TG、LDL-C水平降低(P<0.05,P<0.01),HDL-C水平升高(P<0.05,P<0.01);脂肪细胞体积和形态得到改善。结论 五仁丸加减方可通过促进肥胖小鼠脂肪消耗来发挥对肥胖的预防作用。     

肥儿调理液对营养性肥胖大鼠脂质代谢的影响

目的观察肥儿调理液对营养性肥胖大鼠脂质代谢及脂肪重量、细胞形态的影响。方法取幼年大白鼠，连续喂饲高营养饲料6周制备营养性肥胖模型，并于第3周开始给药，4周后，取血测量胆固醇（TC）、三酰甘油（TG）、高密度脂蛋白胆固醇（HDL-C）含量；并取脂肪称重和镜下观察脂肪细胞的个数和直径大小变化。结果63．0g／kg肥儿调理液能明显降低营养性肥胖大鼠脂肪湿重，降低血清TC及TG含量，提高HDL-C含量。组织学观察发现，63．0g／kg肥儿调理液还能明显减小脂肪细胞的直径，对单位视野下脂肪细胞个数有增高趋势。结论肥儿调理液对营养性肥胖大鼠脂质代谢有明显促进作用。     

紫花毕岱提取物对肥胖大鼠血脂及瘦素水平的影响

目的通过紫花毕岱提取物对肥胖大鼠的干预,观察大鼠体重、血脂、血浆瘦素水平的变化及血浆中肝酯酶和脂蛋白酯酶活性的变化,探讨紫花毕岱提取物对肥胖大鼠的减肥作用及机制。方法用高能量饲料造成雄性大鼠肥胖模型,按体重将其随机分为4组,各组均继续给予高能量饲料。肥胖对照组灌胃生理盐水;阳性西药组灌胃盐酸西布曲明;另外2组灌胃紫花毕岱提取物,剂量分别为6、12g／kg。给药6周后,观察紫花毕岱提取物治疗前后大鼠体重、肥胖指数、内脏脂肪重量、血脂、血浆中肝酯酶和脂蛋白酯酶、血浆中瘦素水平的变化。结果给予紫花毕岱提取物治疗后,营养性肥胖大鼠体重、肥胖指数、内脏脂肪重量均明显低于肥胖对照组（P〈0．05）;血浆瘦素水平明显降低（P〈0．01）;紫花毕岱提取物高、低剂量组血三酰甘油、总胆固醇明显降低（P〈0．05）,血浆中肝酯酶和脂蛋白酯酶活性明显升高。结论紫花毕岱提取物灌服6周后对营养性肥胖大鼠有明显减肥作用,该作用未显示与促进血浆瘦素分泌有关,机制可能与紫花毕岱提取物降血脂作用有关。     

针刺对肥胖大鼠脂肪组织M1型巨噬细胞及IL-6表达的影响研究

目的:观察针刺对肥胖大鼠脂肪组织M1型巨噬细胞及IL-6表达的影响,探讨针刺治疗肥胖的分子作用机制。方法:将24只SD雄性大鼠随机分为正常组、模型组和针刺组,每组8只。予"双侧足三里、阴陵泉、丰隆、天枢、中脘及关元"等穴位针刺,30 min/次/d,每5 d暂停1次,共30 d,并记录每周体质量。治疗结束后,分离各组大鼠的肾周脂肪、肠周脂肪及附睾脂肪等内脏脂肪,并记录其湿重。采用蛋白质免疫印迹(Western Blot)技术检测各组大鼠脂肪组织中M1型巨噬细胞标志物诱导型一氧化氮合酶(inducible nitric oxide synthase, iNOS)及IL-6蛋白的表达;HE染色观察各组大鼠附睾脂肪组织形态。结果:与正常组比较,模型组大鼠的体质量、内脏脂肪湿重、iNOS及IL-6蛋白的表达均显著升高,脂肪细胞平均面积增大,差异具有统计学意义(P<0.05或P<0.01)。与模型组比较,针刺组大鼠的体质量、内脏脂肪湿重、iNOS及IL-6蛋白的表达均显著降低,脂肪细胞平均面积减小,差异具有统计学意义(P<0.05或P<0.01)。结论:针刺能降低肥胖大鼠...     

槐花提取物降血糖活性研究

目的研究槐花Sophora japonica L.(Leguminosae)提取物对2型糖尿病小鼠降血糖活性。方法通过超声提取法获得槐花乙醇提取物。使用腹腔注射烟碱和链脲霉素诱导的2型糖尿病小鼠模型和3T3-L1前脂肪细胞分化模型,检测槐花乙醇提取物对小鼠血糖的影响和对3T3-L1前脂肪细胞分化的影响。结果槐花乙醇提取物灌胃剂量每日100μg/g,连续灌胃给药3周,降低了2型糖尿病小鼠的血糖,改善口服葡萄糖耐受试验OGTT过程中的糖耐量。0.4 mg/L和0.8 mg/L的槐花乙醇提取物均能促进3T3-L1前脂肪细胞分化。结论槐花乙醇提取物降低2型糖尿病小鼠血糖,促进3T3-L1前脂肪细胞分化,具体作用机制有待进一步研究。     

健脾化痰方对肥胖胰岛素抵抗大鼠糖脂代谢的作用

目的观察健脾化痰方对肥胖胰岛素抵抗大鼠糖脂代谢的作用。方法 60只大鼠中随机取10只作为空白组,采用普通饲料喂养,另外50只采用高脂饲料喂养以建立肥胖胰岛素抵抗模型,8周后造模大鼠随机均分为模型组和健脾化痰方低、中、高剂量组(5.4、10.8、21.6 g/kg),除了空白组给予标准饲料外,其余各组继续给予高脂饲料,干预时间为8周。16周后,观察空腹血糖、胰岛素、胰岛素抵抗指数,内脏脂肪组织HE染色后采用real-time PCR、Western blot法测定Wnt10b、β-catenin、PPARγ、ap2、LPL、FAS mRNA及蛋白表达水平。结果与空白组比较,模型组TG、TC、LDL-C水平均显著升高(P0.05);与模型组比较,健脾化痰方组能显著降低三者水平(P0.05)。模型组大鼠内脏脂肪组织以大脂肪细胞为主,经健脾化痰方处理后以小脂肪细胞为主。与模型组比较,健脾化痰方中、高剂量组均能明显降低大鼠内脏脂肪颗粒面积;与空白组比较,模型组大鼠Wnt10b、β-catenin mRNA表达下降,蛋白水平下调,PARγ、ap2、LPL、FAS mRNA及蛋白表达水平升高,经健脾化痰方处理后有所改善。结论健脾化痰方可改善肥胖胰岛素抵抗大鼠脂肪组织的胰岛素敏感性,明显减轻大鼠体质量(以减少内脏脂肪为主),其作用机制可能与激活经典wnt信号通路有关。     

普洱茶精粉对营养性肥胖大鼠减肥作用的初步实验观察

目的:观察普洱茶精粉对营养性肥胖大鼠的减肥作用.方法:高脂营养饲料饲养大鼠,建立营养性肥胖大鼠模型后分别给予低、中、高剂量(0.83g/kg·bw、1.66g/kg·bw、2.5g/kg·bw)的普洱茶精粉溶液连续灌胃35d,称量各组大鼠的体重和脂肪湿重,统计分析各组数据.结果:中、高剂量组具有显著降低肥胖大鼠体重及内脏脂肪的作用(P＜0.05).结论:普洱茶精粉对营养性肥胖人鼠有一定的减肥作用.     

菩人丹对ob/ob小鼠糖脂代谢及胰岛素抵抗的影响

[目的]考察菩人丹对肥胖小鼠糖脂代谢及胰岛素抵抗的影响,为中药复方菩人丹调节糖脂代谢的临床应用提供实验依据。[方法]将ob/ob小鼠随机分为模型组和菩人丹组,后者给予菩人丹干预15周,以C57BL/6J为空白组。测定小鼠空腹体质量、内脏脂肪指数、空腹血糖(FPG)、空腹血清胰岛素(FINS)及血脂水平,计算稳态模型胰岛素抵抗指数(HOMA-IR)及胰岛素敏感指数(ISI),评价胰岛素抵抗与分泌水平,口服葡萄糖耐量试验(OGTT)考察ob/ob小鼠对葡萄糖的耐受性;苏木精-伊红(HE)染色观察睾周脂肪细胞形态。[结果]模型组ob/ob小鼠的空腹体质量、内脏脂肪指数、OGTT曲线下面积、血脂水平与HOMA-IR均显著升高,ISI显著下降;菩人丹对ob/ob小鼠空腹体质量、内脏脂肪指数及糖耐量的影响无统计学意义;菩人丹能够降低ob/ob小鼠血清中总胆固醇(TC)、低密度脂蛋白(LDL)及HOMA-IR,升高ISI,同时使ob/ob小鼠睾周脂肪细胞排列相对规则有序。[结论]经15周观测,模型组ob/ob小鼠已形成肥胖、血脂紊乱、糖耐量损伤以及胰岛素抵抗,糖尿病前期模型复制成功;菩人丹有效改善了ob/ob小鼠糖脂代谢紊乱,增强了胰岛素敏感性,降低了胰岛素抵抗程度,表明菩人丹对糖尿病前期向2型糖尿病发展有确切的干预效果。     

降脂减肥胶囊的主要药效学研究

目的:研究降脂减肥胶囊的主要药效学,为临床应用提供实验依据。方法:采用营养性肥胖模型,除空白组外(普通饲料),其余大鼠均喂饲高脂饲料,连续5周造模。5周后,将造模动物分为6组,每组10只。分别口服给予相应药物:千姿美0.22 g.kg-1,曲美1.38 mg.kg-1,降脂减肥胶囊高,中,低剂量组分别为1.48,0.74,0.37 g.kg-1,空白组和模型组给同体积的水,并记录各组动物每天的进食量,连续5周。各组动物末次给药后,检测血清TC,TG,LDL-C,HDL-C的含量;计算Lee’s指数、脂肪指数、全视野中的脂肪细胞个数,并用测微器测量脂肪细胞的大小。结果:降脂减肥胶囊口服给药,可使高脂饲料引起的营养性肥胖模型大鼠的体重明显减轻,血清TC、LDL含量明显降低,血清HDL含量明显升高,显著降低大鼠脂肪指数,增加全视野的脂肪细胞数量,缩小脂肪细胞体积。结论:该药可对抗高脂饲料所致的营养性肥胖的发生。     

Lutein ameliorates high-fat diet-induced obesity,fatty liver,and glucose intolerance in C57BL/6J mice

Obesity is a multi-factorial metabolic syndrome that increases the risk of cardiovascular diseases, diabetes, and cancer. We recently demonstrated the antiadipogenic efficacy of lutein using a 3 T3-L1 cell culture model. This study aimed to examine the antiobesity efficacy of lutein on high-fat (60% kcal fat) diet-induced C57BL/6J obese mice model. Lutein (300 and 500 μM), Orlistat (30 mg/kg body weight - positive control), and its combination (orlistat, 15 mg/kg body weight+lutein, 300 μM) were administered in high-fat diet (HFD)-fed mice every other day for 24 weeks. The effect on serum and hepatic lipid parameters was estimated using biochemical assay kits. The adipose tissue expression of adipocyte differentiation markers at gene and protein levels was analyzed by RT-PCR and western blotting, respectively. The results showed that lutein administration and drug significantly reduced epididymal and abdominal adipose tissue weights. Further, lutein reduced the serum cholesterol and LDL-C concentration compared to the HFD group. The HFD-induced elevation in the hepatic triglycerides and cholesterol levels were significantly blocked by lutein and its combination with the drug. Similarly, lutein and its drug combination efficiently lowered the HFD-mediated elevated blood glucose levels. Lutein downregulated the expression of CEBP-α, PPAR-γ, and FAS in the epididymal adipose tissue. Thus, supplementation of lutein may control diet-induced obesity and associated complications in the human population.     

Effect of the Capsicoside G‐rich Fraction from Pepper (Capsicum annuum L.) Seeds on High‐fat Diet‐induced Obesity in Mice

Obesity is one of the most common metabolic syndromes and is a major threat to human health worldwide. Given the size of this problem, there is growing interest in natural agents that may decrease obesity. In this study, we investigated the anti‐obesity effect of a capsicoside G‐rich fraction (CRF; 13.35% capsicoside G) isolated from pepper seeds in diet‐induced obese mice. C57BL/6J mice were fed either a normal diet or a high‐fat diet (HFD), with or without CRF (HFD + CRF; 10 and 100 mg/kg body weight). The body weight and food efficiency ratio of mice fed HFD + CRF were lower in comparison to that of mice fed only an HFD. Epididymal adipose tissue weight and adipocyte hypertrophy were significantly lower in HFD + CRF mice than in HFD mice. The fat deposition in the liver of mice fed HFD + CRF was lower compared to that of mice fed only an HFD. CRF significantly reversed the HFD‐induced elevation of the expression of key adipocyte differentiation regulators, including peroxisome proliferator‐activated receptor γ, CCAAT/enhancer‐binding protein α, sterol regulatory element binding protein 1c, and their target genes. These results suggest that CRF could be used as dietary therapy for the prevention of obesity and obesity‐related metabolic diseases. Copyright © 2016 John Wiley & Sons, Ltd.     

Regulation of obesity and lipid disorders by extracts from Angelica acutiloba root in high-fat diet-induced obese rats

The aim of this study was to investigate the antiobesity and antihyperlipidemic effects of Angelica acutiloba root (Japanese Dong Quai). High‐fat diet (HFD)‐induced obese rats were treated orally with the polyphenolic‐rich extract of Angelica acutiloba root (AARE) once daily for 8 weeks. The AARE (300 mg/kg per day) supplementation significantly lowered body weight gain, visceral fat‐pad weights and plasma lipid levels, as well as the coronary artery risk index and the atherogenic index of HFD‐fed rats. The AARE caused dose related reductions in the hepatic triglyceride and cholesterol contents, as well as lowered hepatic lipid droplet accumulation and epididymal adipocyte size in the HFD‐fed rats. The AARE reversed the HFD‐induced down‐regulation of the hepatic peroxisome proliferator activated receptor‐α (PPARα). The HFD‐induced decreases of the hepatic protein level of acyl‐CoA oxidase (ACO), and the cytochrome P450 isoform 4A1 (CYP4A1) was up‐regulated by AARE. The elevated expressions of hepatic sterol regulatory element binding proteins (SREBPs) of HFD‐fed rats were lowered by AARE. These results suggest that AARE attenuated visceral fat accumulation and improved hyperlipidemia in HFD‐induced obesity by increasing lipid metabolism through the down‐regulation of SREBPs and enhanced the expression of ACO and CYP4A1 in the liver, which was likely mediated by up‐regulation of the expression of hepatic PPARα. Copyright © 2011 John Wiley & Sons, Ltd.     

The Anti‐Obesity Effects of the Dietary Combination of Fermented Red Ginseng with Levan in High Fat Diet Mouse Model

In this study, to evaluate the anti‐obesity effects of fermented red ginseng (FG), levan (L), and their combination (FGL), we investigated their effects on the weights of body, liver and white adipose tissue, lipid profiles, and biomarkers for insulin resistance in high fat diet (HFD)‐induced obese C57BL/6J male mice. Furthermore, the levels of leptin in the serum were measured. FG (150 mg/kg/d), L (100 mg/kg/d), and FGL (150 mg/kg/d of FG plus 100 mg/kg/d of L) were administered orally to mice daily for 11 weeks. After 11 weeks feeding, FGL showed significantly lower body weight and fat mass with decreasing food efficiency ratio than the HFD control mice. In addition, the FGL group was significantly lower in the levels of total cholesterol and fasting blood glucose and score of the homeostatic model assessment of insulin resistance. Furthermore, FGL decreased serum leptin levels compared to the HFD control group. Taken together, FGL showed a significant anti‐obesity effect in HFD‐induced obese mice and prevent insulin and leptin resistance. FGL may be potentially useful for the prevention of obesity. Copyright © 2013 John Wiley & Sons, Ltd.     

Fucoidan Prevents High‐Fat Diet‐Induced Obesity in Animals by Suppression of Fat Accumulation

This study examines the antiobesity effects of fucoidan in an animal model of diet‐induced obesity. Mice were fed a standard diet or high‐fat diet (HFD) for 5 weeks. After that, the mice were divided into four experimental groups, with 10 mice per group, including a standard diet group, HFD group, HFD containing 1% fucoidan (HFD + FUCO 1%) group and HFD containing 2% fucoidan (HFD + FUCO 2%) group. The fucoidan supplementation group had significantly decreased body‐weight gain, food efficiency ratio and relative liver and epididymal fat mass compared with the HFD group. The mice supplemented with fucoidan showed significantly reduced triglyceride, total cholesterol and low‐density lipoprotein levels in the plasma. Liver steatosis induced by the HFD improved in the fucoidan‐supplemented group. Furthermore, fucoidan affected the down‐regulation expression patterns of epididymal adipose tissue genes such as peroxisome proliferator‐activated receptor γ, adipose‐specific fatty acid binding protein and acetyl CoA carboxylase. Therefore, fucoidan may be considered for use in improving obesity. Copyright © 2013 John Wiley & Sons, Ltd.     

Effect of Sutherlandia frutescens on the Lipid Metabolism in an Insulin Resistant Rat Model and 3T3‐L1 Adipocytes

High fat diet induced insulin resistance correlates with dyslipidaemia and ectopic fat deposits in skeletal muscle and liver. The effects of Sutherlandia frutescens, an antidiabetic medicinal plant, on lipid metabolism were evaluated in an insulin resistant (IR) rat model and in 3 T3‐preadipocytes. Wistar rats received normal diet (ND) or high fat diet (HFD). After the onset of IR in the HFD group, the rats were subdivided into two subgroups, which either continued with HFD or were treated with 50 mg S. frutescens/kg BW/day and HFD (HFD + SF). After 4 weeks, the HFD + SF rats had a significantly lower body weight than the HFD rats (p < 0.05). Blood plasma analysis showed a decrease in insulin, free fatty acids and triglycerides. Related changes in lipid parameters were observed in the liver, skeletal muscle and adipose tissue. To investigate the effects of S. frutescens on adipose tissue, 3 T3‐L1 cells were used as a model. Treatment with S. frutescens led to a decrease in triglyceride accumulation, whilst glucose consumption and lactate production were increased (p < 0.05). These results indicate that S. frutescens directly affects mitochondrial activity and lipid biosynthesis in adipose tissue and provide a mechanism by which S. frutescens can restore insulin sensitivity by modulating fatty acid biosynthesis. Copyright © 2012 John Wiley & Sons, Ltd.     

The Korean traditional medicine Gyeongshingangjeehwan inhibits adipocyte hypertrophy and visceral adipose tissue accumulation by activating PPARα actions in rat white adipose tissues

Aim of the study

Gyeongshingangjeehwan (GGEx), which is a polyherbal drug composed of four medicinal plants, has traditionally been used as anti-obesity drug in Korean local clinics. Thus, we investigated the effects of GGEx on visceral adiposity and examined whether adipose peroxisome proliferator-activated receptor α (PPARα) activation is involved in this process.

Materials and methods

After Obese Otsuka Long-Evans Tokushima Fatty (OLETF) rats and differentiated 3T3-L1 adipocytes were treated with GGEx, we studied the effects of GGEx on not only visceral white adipose tissue (WAT) mass and adipocyte size, but also the expression of adipocyte marker and PPARα target genes.

Results

Administration of GGEx to obese rats for 8 weeks decreased visceral WAT weight by 30% and the size of adipocytes in mesenteric WAT by 31% without weight changes of other organs. Concomitantly, GGEx increased mRNA levels of PPARα target genes responsible for fatty acid β-oxidation in mesenteric WAT whereas decreased mRNA expression of adipocyte markers, such as PPARγ, aP2 and leptin. Serological studies demonstrated that plasma levels of free fatty acids and triglycerides as well as insulin and glucose were decreased following GGEx treatment. Consistent with the in vivo data, GGEx increased PPARα reporter gene activity and induced the mRNA expression of PPARα target genes involved in mitochondrial fatty acid β-oxidation in 3T3-L1 cells. GGEx also inhibited triglyceride accumulation in these cells.

Conclusion

These results suggest that GGEx promotes the reductions in visceral fat mass and adipocyte size in obese animals, and that this event may be mediated by adipose PPARα activation.