Green coffee bean extract improves obesity by decreasing body fat in high-fat diet-induced obese mice

Objective:To evaluate possible lipid catabolism and body fat regulation effects of 3-caffeoylquinic acid in Green coffee bean extract(GCBE) in high-fat diet(HFD)-induced obese mice.Methods:Obesity was induced in mice using a HFD for four weeks.Then,mice were fed only HFD or HFD with GCBE at 50,100,and 200 mg/kg.Fatty acid synthesis mechanism regulation of body fat was investigated through real-time PCR and Western blot assay.Body fat reduction was measured through dual-energy X-ray absorptiometry.Results:In HFD-induced obese mice,GCBE treatment significantly decreased body weight gain,liver weight and white adipose tissue weights with regulation of adipose tissue lipolysis hormones,like adiponectin and leptin.GCBE treatment decreased mR NA expression levels of adipogenesis and adipocyte metabolism related genes in adipose tissues and the liver,and decreased the corresponding protein expression.Dual energy X-ray absorptiometry measurements were used to compare body fat between mice on high-fat and those treated with GCBE.GCBE treated mice had a lower fat mass compared to HFD alone fed mice and relative body weight and fat mass were markedly decreased.Conclusions:GCBE has a potential anti-obesity effect with lowering body fat accumulation by regulating adipogenesis and lipid metabolism-related genes and proteins in WAT and liver.

Monascus pilosus-fermented black soybean inhibits lipid accumulation in adipocytes and in high-fat diet-induced obese mice

Objective:To explore the anti-obesity effects and the mechanism of action of Monascus pilosus(M.pilosus)-fermented black soybean(MFBS)extracts(MFBSE)and MFBS powders(MFBSP)in adipocytes and high-fat diet(HFD)-induced obese mice,respectively.Methods:Black soybean was fermented with M.pilosus,and the main constituents in MFBS were analyzed by HPLC analysis.In vitro,MFBSE were examined for anti-adipogenic effects using Oil-Red O staining.In vivo,mice were fed a normal-fat diet(NFD)control,HFD control or HFD containing 1 g/kg MFBSP for 12 weeks,and then body weight gain and tissues weight measured.Real-time PCR and western blot assay were used to determine the mechanism of anti-adipogenic effects.Results:MFBSE inhibited lipid accumulation in 3T3-L1 adipocytes without exerting cell cytotoxicity.MFBSP treatment in HFD-fed mice significantly decreased the body weight gain compared with the HFD control mice.MFBSE and MFBSP treatment resulted in significantly lower mRNA levels of adipogenesis-related genes,such as peroxisome proliferator-activated receptorγ(PPARγ),fatty acid-binding protein 4(FABP4),and fatty acid synthase(FAS),in adipocytes and in white adipose tissue(WAT)of HFD-induced obese mice.Conclusions:These results suggest that the anti-obesity effects of MFBS are elicited by regulating the expression of adipogenesis-related genes in adipocytes and WAT of HFDinduced obese mice.

High-fat diet and oral infection induced type 2 diabetes and obesity development under different genetic backgrounds

Background:Type 2 diabetes(T2D)is an adult-onset and obese form of diabetes caused by an interplay between genetic,epigenetic,and environmental components.Here,we have assessed a cohort of 11 genetically different collaborative cross(CC)mouse lines comprised of both sexes for T2D and obesity developments in response to oral infection and high-fat diet(HFD)challenges.Methods:Mice were fed with either the HFD or the standard chow diet(control group)for 12 weeks starting at the age of 8 weeks.At week 5 of the experiment,half of the mice of each diet group were infected with Porphyromonas gingivalis and Fusobacterium nucleatum bacteria strains.Throughout the 12-week experimental period,body weight(BW)was recorded biweekly,and intraperitoneal glucose tolerance tests were performed at weeks 6 and 12 of the experiment to evaluate the glucose tolerance status of mice.Results:Statistical analysis has shown the significance of phenotypic variations between the CC lines,which have different genetic backgrounds and sex effects in different experimental groups.The heritability of the studied phenotypes was estimated and ranged between 0.45 and 0.85.We applied machine learning methods to make an early call for T2D and its prognosis.The results showed that classification with random forest could reach the highest accuracy classification(ACC=0.91)when all the attributes were used.Conclusion:Using sex,diet,infection status,initial BW,and area under the curve(AUC)at week 6,we could classify the final phenotypes/outcomes at the end stage of the experiment(at 12 weeks).

The Effects of Xylitol on Body Weight Loss Management and Lipid Profile on Diet-Induced Obesity Mice

Xylitol is an alternative sweetener which has been previously reported to have many beneficial effects such as prevention from dental caries, reduction of visceral fat and increased synthesis of collagen. However, its role in body weight loss management has not been uncovered before. This study sought to investigate the effects of xylitol on body weight loss management, blood glucose and lipid profile on diet-induced obesity (DOI) mice. Fifteen male mice were subjected to high fat diet (60 kcal%) and normal drinking water for 28 days and then randomly divided into three (control, glucose and xylitol) groups. Each group of mice was then fed with normal diet for another 28 days with supplied normal drinking water (control);glucose solution 10% and xylitol solution 10%. Body weight loss was found to be significantly high in xylitol mice (2.56 ± 0.21, p = 0.003) compared to the other two groups. Lowest blood glucose level was found in the control group mice with the mean 7.65 ± 0.10 (p = 0.001). Xylitol mice had also showed the lowest total cholesterol level (4.20 ± 0.90, p = 0.000) than the other groups, but highest in HDL level (2.72 ± 0.14, p = 0.000). In conclusion, these findings proved that xylitol has the potential to reduce body weight, lowering the blood glucose but yet increase the HDL level.

Comparative study on the difference of obesity model induced by two kinds of high fat diet in Sprague-Dawley rats

Objective: To explore the differences of obese Sprague-Dawley(SD)rats model induced by lard oil high-fat(HF)diet or purified HF diet. Methods: SD weanling rats were randomly divided into three groups: D1 group,where rats were fed by lard oil HF diet;D2 group,where rats were fed by purified HF diet;C group,where rats were fed on chow. After 12 weeks,diet-induced obesity rat(stop 33% based on weight)were selected for further study,and the rest rats from group D1 and D2 were excluded. The food intake and weight were weighted daily and weekly,respectively. The subcutaneous,visceral and total fat contents of rats was measured by 256-row CT scan and the Lee index was calculated accordingly. The kidney,liver,testis,spleen and heart were weighted respectively. Serum leptin and insulin levels were quantified. The pathology in liver and adipose tissues were analyzed by HE staining. Oral glucose tolerance test(OGTT)was used to compare the glucose tolerance ability. Serum total cholestero(lT-CHO),high density lipoprotein(HDL-C),low density lipoprotein(LDL-C),triglyceride(TG)and inflammatory cytokines IL-6,TNF-α were detected as well. Results: After 12 weeks,the body weight,subcutaneous fat,visceral fat,total fat mass,wet weight of liver,kidney and heart,area under blood glucose curve and the levels of serum insulin,leptin,T-CHO,LDL-C,TG,IL-6 and TNF-α in group D2 were significantly increased compared to those of group C and group D1. HDL-C of group D2 was markedly lower than that in group C(P<0. 05). The visceral fat,total fat content and HDL-C in group D1 were significantly different from those of group C(P<0. 05). Steatosis and enlarged adipocyte were found in the livers of rats in group D1 and D2,and the lesions were more significant in group D2. Conclusion: Purified HF diet was more effective in inducing metabolic abnormalities,steatosis,peripheral chronic inflammation in obese SD rat models. But lard oil HF diet was more economical when only inducing visceral steatosis was required.

Assessing the host genetic background effects on type 2 diabetes and obesity development in response to mixed–oral bacteria and high-fat diet using the collaborative cross mouse model

Background: Host genetic background and sex, play central roles in defining the pathogenesis of type 2 diabetes(T2 D), obesity and infectious diseases. Our previous studies demonstrated the utilization of genetically highly diverse inbred mouse lines, namely collaborative cross(CC), for dissecting host susceptibility for the development of T2 D and obesity, showing significant variations following high-fat(42% fat) diet(HFD). Here, we aimed to assessing the host genetic background and sex effects on T2 D and obesity development in response to oral-mixed bacterial infection and HFD using the CC lines.Materials and Methods: Study cohort consists of 97 mice from 2 CC lines(both sexes), maintained on either HFD or Standard diet(CHD) for 12 weeks. At week 5 a group of mice from each diet were infected with Porphyromonas gingivalis(Pg) and Fusobacterium nucleatum(Fn) bacteria(control groups without infection). Body weight(BW) and glucose tolerance ability were assessed at the end time point of the experiment.Results: The CC lines varied(P <.05) at their BW gain and glucose tolerance ability(with sex effect) in response to diets and/or infection, showing opposite responses despite sharing the same environmental conditions. The combination of diet and infection enhances BW accumulation for IL1912, while restraints it for IL72. As for glucose tolerance ability, only females(both lines) were deteriorated in response to infection.Conclusions: This study emphasizes the power of the CC mouse population for the characterization of host genetic makeup for defining the susceptibility of the individual to development of obesity and/or impaired glucose tolerance.

Impact of age on host responses to diet-induced obesity:Development of joint damage and metabolic set points

Background:Osteoarthritis is one of the leading causes of pain and disability worldwide,and a large percentage of patients with osteoarthritis are individuals who are also obese.In recent years,a series of animal models have demonstrated that obesity-inducing diets can result in synovial joint damage(both with and without the superimposition of trauma),which may be related to changes in percentage of body fat and a series of low-level systemic inflammatory mediators.Of note,there is a disparity between whether the dietary challenges commence at weaning,representing a weanling onset,or at skeletal maturity,representing an adult onset of obesity.We wished to evaluate the effect ofthe dietary exposure time and the age at which animals are exposed to a high-fat and high-sucrose(HFS) diet to determine whether these factors may result in disparate outcomes,as there is evidence suggesting that these factors result in differential metabolic disturbances.Based on dietary exposure time,we hypothesized that rats fed an HFS diet for 14 weeks from weaning(HFS Weanling) would demonstrate an increase in knee joint damage scores,whereas rats exposed to the HFS diet for 4 weeks,starting at 12 weeks of age(HFS Adult) and rats exposed to a standard chow diet(Chow)would not display an increase in knee joint damage scores.Methods:Male Sprague-Dawley rats were fed either an HFS diet for 14 weeks from weaning(HFS Weanling) or an HFS diet for 4 weeks,starting at 12 weeks of age(HFS Adult).At sacrifice,joints were scored using the modified Mankin Criteria,and serum was analyzed for a defined subset of inflammatory markers(Interleukin-6,leptin,monocyte chemoattractant protein-1,and tumor necrosis factorα).Results:When the HFS Weanling and HFS Adult groups were compared,both groups had a similar percent of body fat,although the HFS Weanling group had a significantly greater body mass than the HFS Adult group.The HFS Weanling and HFS Adult animals had a significant increase in body mass and percentage of body fat when compared to the Chow group.Although knee joint damage scores were low in all 3 groups,we found,contrary to our hypothesis,that the HFS Adult group had statistically significant greater knee joint damage scores than the Chow and HFS Weanling groups.Furthermore,we observed that the HFS Weanling group did not have significant differences in knee joint damage scores relative to the Chow group.Conclusion:These findings indicate that the HFS Weanling animals were better able to cope with the dietary challenge of an HFS diet than the HFS Adult group.Interestingly,when assessing various serum proinflammatory markers,no significant differences were detected between the HTS Adult and HFS Weanling groups.Although details regarding the mechanisms underlying an increase in knee joint damage scores in the HFS Adult group remain to be elucidated,these findings indicate that dietary exposure time maybe less important than the age at which an HFS diet is introduced.Moreover,increases in serum proinflammatory mediators do not appear to be directly linked to knee joint damage scores in the HFS Weanling group animals but may be partially responsible for the observed knee joint damage in the adults over the very short time of exposure to the HFS diet.

Construction of Mouse Nutritional Obesity Model

[ Objective] The aim of this study is to construct the model for simple obesity induced by high-fat diet, which is closest to human obesity, laying a foundation for the studies of obesity related theories. [Method[ ICR and KM mice, half male and half female, were randomly divided into the high-fat diet experimental group and the normal diet control group based on body weights, and certain days later, body weight, Lee＇ s index, wet weight of adipose tissue, quantity of adipose cell in the same visual field and blood indices were measured. [Result]All indices mentioned a- bove of the female I CR mouse had significant statistical differences with those of the control group （P 〈 0.01 or P 〈 0.05）. [ Conclusion] To con- struct mouse nutritional obesity model successfully, different high-fat diets are required by different lines as well as different sexes in the same line.

Hepatic transcriptome signatures in mice and humans with nonalcoholic fatty liver disease

Background:Nonalcoholic fatty liver disease(NAFLD)is the main reason for cirrhosis and hepatocellular carcinoma.As a starting point for NAFLD,the treatment of nonalcoholic fatty liver(NAFL)is receiving increasing attention.Mice fed a high-fat diet(HFD)and hereditary leptin deficiency(ob/ob)mice are important NAFL animal models.However,the comparison of these mouse models with human NAFL is still unclear.Methods:In this study,HFD-fed mice and ob/ob mice were used as NAFL animal models.Liver histopathological characteristics were compared,and liver transcriptome from both mouse models was performed using RNA sequencing(RNA-seq).RNAseq data obtained from the livers of NAFL patients was downloaded from the GEO database.Global gene expression profiles in the livers were further analyzed using functional enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway.Results:Our results showed that the biochemical parameters of both mouse models and human NAFL were similar.Compared with HFD-fed mice,ob/ob mice were more similar in histologic appearance to NAFL patients.The liver transcriptome characteristics partly overlapped in mice and humans.Furthermore,in the NAFL pathway,most genes showed similar trends in mice and humans,thus demonstrating that both types of mice can be used as models for basic research on NAFL,considering the differences.Conclusion:Our findings show that HFD-fed mice and ob/ob mice can mimic human NAFL partly in pathophysiological process.The comparative analysis of liver transcriptome profile in mouse models and human NAFL presented here provides insights into the molecular characteristics across these NAFL models.

Effect of mango seed kernel extract on the adipogenesis in 3T3-L1 adipocytes and in rats fed a high fat diet

Mangoes (Mangifera indica L.) are one of the most important tropical foods. The seed is one of the main by-products of mango processing. Therefore, it is important to find an economically viable use for this waste (e.g., as a food additive or supplement with high nutraceutical value). We investigated the anti-obesity effects of mango seed kernel extract with hot water (MSKE-W) in 3T3-L1 adipocytes and in a high fat diet (HFD)-induced obesity rat model. MSKE-W caused a significant decrease in the activity of glycerol 2-phosphate dehydrogenase in 3T3-L1 adipocytes without eliciting cell cytotoxicity and inhibited cellular lipid accumulation through down-regulation of transcription factors such as PPARγ and C/EBPα. In the animal model, rats fed an HFD containing 1% MSKE-W gained less weight than rats fed an HFD alone. The visceral fat mass in rats fed an HFD containing 1% MSKE-W tended to be lower than that in rats fed an HFD alone. Furthermore, histological examination of rat livers from an HFD showed steatohepatitis. However, rats on an HFD containning 1% MSKE-W showed no histopathological changes in liver tissue. Our results indicate that MSKE-W influences anti-obesity effects, both in vitro and in vivo, and suggest that MSKE-W provides a novel preventive potential against obesity.

高强度耐力运动对食源性肥胖小鼠肝脏CLK2、PGC-1α和PPARα表达的影响

目的:研究高强度耐力运动对食源性肥胖小鼠肝脏蛋白CLK2、PGC-1α和PPARα的影响。方法:雄性4周龄C57BL/6J小鼠,先常规饲料适应性喂养1周,再通过8周高脂饲料喂养建立食源性肥胖小鼠模型,对照小鼠使用常规饲料喂养。肥胖小鼠经1周适应性跑台运动后进行高强度耐力跑台运动,对照小鼠不进行运动训练。运动训练进行8周后获取各组小鼠肝脏并称量肝脏质量;取部分肝脏组织进行HE染色,观察肝脏细胞形态,剩余肝脏组织通过Western Blot方法检测CLK2、PGC-1α和PPARα的表达情况并进行组间比较。结果:①食源性肥胖小鼠肝脏质量明显增加,肝细胞正常形态受到破坏;②高脂诱导能明显增加肝脏CLK2和PGC-1α表达,明显减少PPARα表达;③高强度耐力运动能有效减轻肥胖小鼠肝脏质量并恢复肝细胞正常形态;④高强度耐力运动能明显减少肥胖小鼠肝脏CLK2和PGC-1α表达,明显增加PPARα表达。结论:高强度耐力运动能够明显减少肝脏的脂质积累,改善肝脏脂质代谢情况。

营养性肥胖动物模型的实验研究

目的 观察高脂饲料配方对制造营养性肥胖动物模型成功率的影响。方法 用改进的高脂饲料喂养大鼠 16wk ,观察体重及肥胖指标 ,并与普食组进行比较。结果 高脂饲料和普通饲料喂养的大鼠体重分别为 (491 6 2± 4 6 89)g、(394 2 0± 5 0 78) g ,Lees指数分别为 319 0 4± 9 4 9、30 4 6 3± 5 99,经统计学处理 ,高脂组优于普食组 (P <0 0 1,P <0 0 5 )。造模成功后 ,高脂组大鼠的附睾脂肪量、肾周脂肪量、心包脂肪量及肝、肾重量均大于普食组 ,两组比较差异有显著性。 (P <0 0 1)。结论 含 12 %猪油、总油脂量为 18%的高脂饲料致肥效果较好 ,配方组成较为合理 ,致肥率达 5 8 9% 。

营养性肥胖动物模型的建立

目的观察高脂饲料配方对制造营养性肥胖大鼠动物模型的影响。方法用改进的高脂饲料喂养大鼠6周,观察体重及Lees指数、身长、尾长、及肥胖指标,并与普食组进行比较。结果喂养6周后,高脂组大鼠体重为305·50±21·21g,普食组大鼠体重为235·00±17·86g,两者比较差异有显著性意义(P<0·05);另外,高脂组腹腔各部位脂肪重量及肝脏重量与普食组比较也有显著性差异(P<0·05)。结论高脂饮食可以引起大鼠营养性肥胖;总油脂含量18%,猪油含量12%配制的高脂饲料配方组成较为合理,致肥效果明显。

肥胖大鼠模型的建立及其脂代谢相关分子机制研究

目的建立饮食诱导的肥胖(diet-induced obesity,DIO)大鼠模型并初步探讨其发病的分子机制。方法用脂肪含量30%的高脂饲料饲喂雄性SD大鼠25周,观察大鼠体重、Lee's指数、肝组织病理改变,检测大鼠空腹血糖及空腹血清胰岛素水平,并通过real-time PCR,检测成模大鼠肝脏中乙酰辅酶A羧化酶(ACC)、脂肪酸合酶(FAS)、激素敏感酯酶(HSL)以及固醇调节元件结合蛋白-1c(SREBP-1c)的表达变化。结果高脂饲料饲喂6周后,DIO组大鼠体重、Lee's指数均显著增加;25周后肝脏脂肪异常蓄积,出现中重度脂肪肝,空腹血糖及胰岛素水平显著升高,出现明显的胰岛素抵抗。肝脏中ACC、FAS和HSL表达显著增加,SREBP-1c表达水平达到正常组的2.56倍,两组间差异极其显著。结论成功建立了DIO大鼠模型,通过检测脂代谢相关基因的表达水平,初步阐释了营养性肥胖的发生与脂代谢变化之间的关系,SREBP-1c,ACC,FAS和HSL参与了DIO的形成,从而初步揭示了脂代谢变化与营养性肥胖的发生的关系。

有氧运动对高脂膳食诱导雄性大鼠生殖机能的干预作用

目的探讨有氧运动干预高脂膳食诱导肥胖大鼠生殖机能的作用。方法 5周龄雄性SD大鼠40只,随机分为C组(普通膳食)、HF组(高脂膳食)、CE组(运动)、HE组(高脂膳食+运动)。CE组和HE组进行为期10周(6次/周,60 min/次)的游泳训练。测量大鼠睾周脂、体质量、Lees指数、血液总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C);测定精子总数、活动率、畸形率。结果 CE组体质量显著低于对照组(P<0.01),HF组显著高于C组、CE组、HE组(P<0.01);HF组Lees指数显著高于C组和CE组(P<0.01),显著高于HE组(P<0.05);CE组睾周脂显著低于C组(P<0.05),HF组显著高于C组、CE组、HE组(P<0.01)。相比于C组,HF组、HE组TC浓度显著增高(P<0.01),CE组TG浓度显著低于C组(P<0.05),CE组HDL浓度显著增高(P<0.01),HF组、HE组LDL浓度显著增高(P<0.01)。相比于HF组,CE组TC浓度、TG浓度、LDL浓度显著降低(P<0.01),CE组HDL浓度显著升高(P<0.01)。HF组精子总数显著低于C组(P<0.05);HE组畸形率显著高于C组(P<0.05),HF组显著高于C组、CE组、HE组(P<0.01);HF组活动率显著低于C组(P<0.01),显著低于CE组、HE组(P<0.05)。结论有氧运动可改善高脂饮食诱导的体质量增加、睾丸周脂增加、脂代谢异常及大鼠的精子质量,但10周的连续游泳运动并不能完全抵消高脂膳食对大鼠的负面影响。

苦瓜提取物对营养性肥胖小鼠的减肥作用

建立小鼠营养性肥胖模型,研究苦瓜醇提物(MCE)的减肥作用。10只ICR小鼠饲喂普通饲料(ND),其余50只小鼠饲喂营养饲料(HFD),阳性药为赛尼可(50mg/kg),MCE高、中、低剂量分别为500、250和100mg/kg。6周后测定小鼠体重、Lee’s指数、附睾和肾周脂肪垫湿重、血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)浓度和丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)活性。结果表明,MCE各剂量组及阳性药组均可以降低肥胖小鼠的Lee’s指数,脂肪湿重、体脂比、血清TC、TG、LDL-C浓度和ALT、ALP活性,升高HDL-C浓度,且高、中剂量MCE组和赛尼可组数据具有显著差异(P<0.05),提示MCE具有良好的减肥作用,其机制可能是通过抑制脂肪生成、调节血脂和保护肝脏功能。

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。

雄性SD大鼠性成熟期营养性肥胖模型的建立

目的:建立雄性SD营养性肥胖大鼠动物模型。方法:选用出生后21天雄性SD大鼠,随机分为对照组(8只,普通饲料喂养)和营养组(15只,用自制的营养性饲料喂养),分别于喂养后第一至五周末,观察大鼠体重、体长,计算Lee's指数,喂养5周后打击头部处死,取附睾脂肪垫称重,睾丸、肝脏做石蜡切片、HE染色,并与普食组进行比较分析。结果:喂养5周后,营养组大鼠体重达到(307.38±18.26)g,而普食组大鼠仅为(265.00±22.00)g,Lee's指数前者也明显高于后者(P<0.01);营养组附睾脂肪垫重量为(1.22±0.19)g,高于普食组(0.86±0.14)g(P<0.01),在体重、Lee's和附睾脂肪垫三者中,Lee's指数和附睾脂肪垫更具有显著性差异(P<0.01);切片行HE染色,发现营养组肝脏呈现严重肝脂变(对照组肝细胞形态正常),与对照组相比营养组睾丸生精小管壁呈现区域性变薄,生精上皮细胞结构紊乱。结论:成功建立了雄性SD大鼠肥胖动物模型,肥胖对雄性SD大鼠的生殖活动造成影响,为男性肥胖以及由此所引发的各种相关病症的研究提供了研究平台和理论基础。

BVT.2733影响饮食诱导肥胖小鼠中Visfatin表达的研究

目的:构建高脂饮食诱导肥胖小鼠模型,观察BVT.2733在改善胰岛素抵抗中的作用及对Visfatin表达的影响。方法:构建高脂饮食诱导的肥胖小鼠模型,分为肥胖对照组和BVT.2733治疗组,肥胖对照组给予安慰剂、治疗组给予BVT.2733灌胃2周,同时设正常饮食的小鼠为正常对照组。放射免疫法测小鼠空腹胰岛素水平,生化法检测血糖,实时定量RT-PCR检测内脏脂肪组织Visfatin的mRNA表达。观察各组小鼠脂肪组织的形态学变化。结果:与正常对照组相比,肥胖对照组小鼠脂肪细胞明显增大,体重增加,空腹血糖、血清胰岛素水平升高(P<0.05)。与肥胖对照组相比,BVT.2733治疗组小鼠脂肪细胞体积减小,空腹血清胰岛素水平明显下降(P<0.01),脂肪组织Visfatin mRNA表达显著降低(P<0.05)。结论:BVT.2733能够降低体重,减少脂肪组织,并且降低Visfatin的表达水平。

BVT.2733与肥胖小鼠中MCP-1表达的相关性研究

目的:研究BVT.2733对MCP-1表达的影响以及探讨其改善胰岛素抵抗的作用机制。方法:建立高脂饮食诱导的肥胖小鼠模型,随机分为三组:正常对照组、肥胖对照组、BVT.2733治疗组。分别给予安慰剂、BVT.2733灌胃14天,采用生化法检测血糖,放免法检测小鼠空腹胰岛素水平,Real-time PCR检测内脏脂肪中MCP-1的mRNA表达。观察各组胰岛素抵抗相关指标表达差异情况。结果:肥胖组小鼠体重明显增加,空腹血糖及胰岛素水平升高(P<0.05),形态学上发现小鼠脂肪细胞体积增大。与肥胖对照组相比较,治疗组小鼠脂肪细胞体积减小,空腹胰岛素水平下降明显(P<0.01),脂肪组织MCP-1 mRNA表达明显降低(P<0.05)。结论:BVT.2733能够降低MCP-1的表达水平,其可能通过抑制炎症来改善胰岛素抵抗。