高脂饮食和地塞米松联合诱导胰岛素抵抗大鼠模型

目的用高脂饲料＋地塞米松（dexamethasone,DEX）隔日腹腔注射建立实验性胰岛素抵抗大鼠模型,研究该模型糖代谢、脂代谢和激素水平等方面的变化。方法采用Wistar雄性大鼠,分为正常对照组、高脂组、DEX组（1mg/kg,i.p.）和高脂＋DEX组（1mg/kg,i.p.）,连续观察8周,每周测定大鼠空腹血糖,分别于造模第2周和第8周测糖耐量,8周后处死大鼠,测定胸腺、脾脏、肝脏等脏器重量。结果高脂饲料能加重腹腔注射DEX造成的空腹血糖升高,造模第8周空腹血糖（7.7±0.7）较空白组（6.5±0.6）显著升高。使模型动物糖耐量明显异常,肝糖原、肌糖原含量显著增加,血浆胰岛素及游离脂肪酸水平显著升高,各脏器指数明显增加。结论高脂＋DEX隔日腹腔注射能成功诱导胰岛素抵抗大鼠模型,这种造模方法较单纯注射DEX或单纯高脂饲养成模率高,造模周期短。     

高脂饮食诱导肥胖易感和肥胖抵抗的表型差异

超重与肥胖是许多代谢相关疾病的危险因素,严重威胁人类健康和生命。通常认为肥胖的发生是遗传因素与环境因素相互作用的结果。在构建饮食性肥胖模型过程中,动物常出现两种截然不同的表型,即肥胖易感和肥胖抵抗。既往研究主要基于体重、体成分、物质与能量代谢、行为学（如摄食偏好）等探讨肥胖易感型和肥胖抵抗型表型差异,然而其内部调控机制,仍没有较为明确而系统的阐述。本文在综述表型特征的基础上,从脂质代谢、胃肠道激素水平和肠道炎症、肠道微生物群和肠-脑轴信号通路、下丘脑-垂体-甲状腺轴、下丘脑弓状核食欲调节系统功能改变以及表观遗传学等方面探讨高脂饮食诱导肥胖表型差异的可能机制。     

不同脂肪高脂日粮诱发胰岛素抵抗综合征大鼠模型的比较

目的分析猪油、豆油、氢化椰子油、乳脂四种不同脂肪的高脂日粮分别诱发胰岛素抵抗综合征（IRS）大鼠的血液生化指标差异,为此类模型的建立及实验研究提供参考。方法雄性SD大鼠随机分为5组,对照组给予普通日粮,高脂组给予脂肪热量比相同的高脂日粮。喂养6周,每两周测定空腹血糖、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-c）、总胆固醇（TC）、胰岛素,根据胰岛素敏感性指数（ISI）=ln1/（FPG×FINS）评定大鼠的胰岛素敏感性。结果6周后,猪油组、乳脂组、豆油组血清胰岛素均显著高于对照组（P〈0.05）;乳脂组血清TG显著高于其它高脂组（P〈0.05）;高脂组血清HDL-c均显著低于对照组（P〈0.05）并以豆油组下降幅度最大;猪油组、乳脂组ISI显著低于对照组（P〈0.05）;而各组间血清总胆固醇、血糖及体重无明显差异（P〉0.05）。结论4种高脂日粮诱发IRS大鼠模型的综合效果依次为乳脂、猪油、豆油、氢化椰子油。     

燕麦纤维改善高脂饮食诱导的肥胖小鼠胰岛素抵抗的机制研究

目的：研究燕麦纤维对高脂饮食诱导小鼠胰岛素抵抗的影响。方法：采用8w龄C57BL/6J雄性小鼠高脂喂养16w,同时预防性给药,监测血液生化指标,进行糖耐量实验,ELISA法测胰岛素并计算HOMR-IR指数,解剖分离小鼠的内脏脂肪组织并称重,以及取部分组织做HE染色进行形态学观察,研究燕麦纤维对高脂诱导小鼠肥胖和胰岛素抵抗的影响。结果：与模型组比较,阳性药小檗碱组与燕麦纤维组的血糖（GLU）、甘油三酯（TG）、游离脂肪酸（FFA）、总胆固醇（TC）均能显著降低;燕麦纤维组低密度脂蛋白胆固醇（LDL-C）也显著降低,血浆胰岛素水平极显著降低,能增强胰岛素敏感性,改善胰岛素抵抗;血浆中炎症因子TNF-α、IL-6、L-1β及MCP-1显著降低,分别降低了27%、81%、31%、50%。小鼠体质量和内脏脂肪显著减少。脂肪细胞面积减小。结论：燕麦纤维通过减少小鼠内脏脂肪,减少FFA和炎症因子的分泌,改善由高脂饮食诱导的胰岛素抵抗,增加胰岛素敏感性。     

乳双歧杆菌V9对高脂饮食诱导的NAFLD大鼠的改善作用

研究乳双歧杆菌V9(V9)对高脂饮食诱导的非酒精性脂肪肝疾病(NAFLD)大鼠脂代谢、肠道损伤的改善作用,并探讨其作用机制。雄性Wistar大鼠随机分为5组：空白对照组(Control)、高脂饮食模型组(HFD)、黄连素阳性药物组(Berberine)、乳双歧杆菌V9治疗组(HFD/V9)和乳双歧杆菌V9对照组(V9)。除Control和V9给予普通维持饲料外,其他给予高脂饮食6周构建NAFLD模型。6周后,将高脂饮食替换为普通维持饲料,大鼠灌胃给予乳双歧杆菌V9(1×10⁹ CFU/mL)或黄连素(50 mg/kg)。4周后,收集血液、肝脏以及结肠组织用于后续试验检测。与Control组相比,HFD组中肝脏非酯化脂肪酸(NEFA)、甘油三酯(TG)、肝脏脂肪酸合成酶(FAS)和肝脏脂肪酸结合蛋白1(Fabp1)mRNA的表达明显增高(P<0.01);同时,肠道细胞因子白介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)、Toll-样受体2(TLR2)和Toll-样受体9(TLR9)的mRNA表达在HFD模型组中也明显升高(P<0.01);相反地,紧...     

Orexin-A对高脂饮食诱导肥胖大鼠摄食和体重的影响

目的:探讨Orexin-A对高脂饮食诱导的肥胖大鼠摄食和体重的影响。方法:通过检测SD大鼠24 h动态SPA的分布情况来定义HA大鼠和LA大鼠,创建饮食诱导肥胖(DIO)大鼠模型,向HA和LA大鼠延髓外侧下丘脑(rLH)和黑质多巴胺致密部(SN))微量注射orexin-A,观察orexin-A对能量消耗、自发动态运动(SPA)的作用,以及动态SPA对饮食诱导肥胖(DIO)的抵抗作用。结果:雄性SD大鼠在标准饮食情况下,24 h动态SPA呈正偏态分布,非固定SPA(ambulatory SPA)与瘦体重(lean mass,LM)(P0.05)以及总体重(P0.05)显著相关。HA和LA大鼠(high and low activity rats)间的固有SPA(intrinsic SPA)差异有显著统计学意义(P0.05)。与LA大鼠相比,HA大鼠延髓外侧下丘脑(rLH)和黑质多巴胺致密部(SN)的orexin-A反应性更高。在r LH和SN注射orexin-A能显著增加动态SPA(r LH:P0.05;SN:P0.05)。在HA和LA大鼠的r LH注射orexin-A,每种剂量与注射相同剂量的a CSF的大鼠相比效果有显著差异。而对于SN注射OXA,只有注射高剂量OXA的HA大鼠,与对照组相比,才出现著差异。在r LH注射OXA后,对HA/LA大鼠动态SPA均有显著影响(P0.05)。HA大鼠比LA大鼠能量消耗更高。不同的饮食对于HA和LA大鼠转化为SPA有不同的影响,HA大鼠对DIO敏感性低于LA大鼠。与LA大鼠相比,在LF(Low Fat)饮食条件下,转化为脂肪量的热量更少。结论:Orexin-A可通过增加大鼠活动量,使高脂饮食诱导的肥胖大鼠体重减轻。     

木犀草素预防高脂膳食诱导的小鼠胰岛素抵抗的实验研究

目的:探讨黄酮类成分木犀草素对高脂饮食诱导的肥胖小鼠模型的胰岛素抵抗的影响。方法:30只C57BL/6J小鼠分正常饮食对照组(10只),高脂膳食组(对照组,10只)和高脂膳食加2%木犀草素组(木犀草素组,10只),干预16周,观察体重、血脂水平、血糖、胰岛素敏感性及胰岛素水平的变化。结果:小鼠在给予高脂膳食16周后,体重水平、血脂水平、血糖水平、胰岛素水平显著高于木犀草素组,胰岛素敏感性显著下降,与木犀草素组比较,P<0.05或P<0.01。而木犀草素组则可显著抑制体重、血脂、血糖及胰岛素水平的升高,与胰岛素敏感性未见明显下降,与正常对照组比较,P>0.05。结论:木犀草素可预防高脂膳食诱导的胰岛素抵抗。     

高脂饮食对动物生理行为影响的实验研究

给予大鼠高脂饮食,观察对大鼠体重、日饮水量、血糖、血脂水平的影响。结果发现,给予高脂饮食后,大鼠的血糖和TG、TC、LDL、HDL 分别升高了140.89%和25.77%、275.52%、105.54%、31.25%,与实验前比,差异有显著性意义（P<0.01）;给予实验组大鼠二苯乙烯20 d,大鼠日饮水量显著减少（P<0.05～0.001）,体重明显增加（P<0.05～0.001）,血糖和血脂水平比给药前显著降低（P<0.05-0.01）。     

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。     

大鼠胰岛素抵抗形成中脂联素受体基因表达及运动的影响

目的:检测SD大鼠脂联素受体的分布,观察大鼠胰岛素抵抗(IR)形成中脂联素受体(Adipok)基因表达及运动的影响。方法:46只雄性SD大鼠随机分为4组(n=12),以高脂膳食喂养诱导IR,同时运动组实施10周游泳运动干预。结果:AdipoR1/R2mRNA分别在骨骼肌和肝脏高表达(P<0.05);H组骨骼肌AdipoR1和肝脏AdipoR2mRNA表达显著低于C组(P<0.05)。结论:骨骼肌和肝脏AdipoR1/R2mRNA表达的下调可能是高脂大鼠IR形成的机制之一,未观察到运动干预的显著影响。     

Histopathological changes in rat pancreas and skeletal muscle associated with high fat diet induced insulin resistance

The effects of a high fat diet on the development of diabetes mellitus, insulin resistance and secretion have been widely investigated. We investigated the effects of a high fat diet on the pancreas and skeletal muscle of normal rats to explore diet-induced insulin resistance mechanisms. Forty-four male Wistar rats were divided into six groups: a control group fed standard chow, a group fed a 45% fat diet and a group fed a 60% fat diet for 3 weeks to measure acute effects; an additional three groups were fed the same diet regimens for 8 weeks to measure chronic effects. The morphological effects of the two high fat diets were examined by light microscopy. Insulin in pancreatic islets was detected using immunohistochemistry. The homeostasis model assessment of insulin resistance index and insulin staining intensity in islets increased significantly with acute administration of high fat diets, whereas staining intensity decreased with chronic administration of the 45% fat diet. Islet areas increased significantly with chronic administration. High fat diet administration led to islet degeneration, interlobular adipocyte accumulation and vacuolization in the pancreatic tissue, as well as degeneration and lipid droplet accumulation in the skeletal muscle tissue. Vacuolization in the pancreas and lipid droplets in skeletal muscle tissue increased significantly with chronic high fat diet administration. We suggest that the glucolipotoxic effects of high fat diet administration depend on the ratio of saturated to unsaturated fatty acid content in the diet and to the total fat content of the diet.     

Effect of β-Caryophyllene on insulin resistance in skeletal muscle of high fat diet and fructose-induced type-2 diabetic rats

High fat diet feeding results in hyperglycemia and insulin resistance, which is a major pathological feature of type-2 diabetes mellitus. The use of oral hypoglycaemic drugs is limited due to its deleterious side effects and there is a need to find more efficacious agents for diabetes management. Hence, it is of interest to show the mechanism of action of β-Caryophyllene on insulin signalling molecules in gastrocnemius muscle of high fat diet - induced type-2 diabetic rats. An oral effective dose of with β-Caryophyllene (200 mg/kg b.wt) was given for 30 days to high fat diet (comprising 2% cholesterol, 1% cholic acid, 30% coconut oil, 67% conventional rat feed) and fructose fed type-2 diabetic rats to find out whether β-Caryophyllene regulates IRS-1/Akt pathway of insulin signalling. The data shows that, β-Caryophyllene treatment significantly increased the mRNA and protein expression of insulin receptor (IR) in diabetic rats whereas there is no significant difference in mRNA expression of insulin receptor-substrate-1 (IRS-1) was observed among groups. The Akt mRNAand GLUT-4mRNA and protein level were also improved in gastrocnemius muscle of type-2 diabetic rats. Thus, we concluded that β-Caryophyllene could be used as potential phyto medicine for type-2 diabetes management.     

SOCS-1 deficiency does not prevent diet-induced insulin resistance

Obesity is associated with inflammation and increased expression of suppressor of cytokine signaling (SOCS) proteins, which inhibit cytokine and insulin signaling. Thus, reducing SOCS expression could prevent the development of obesity-induced insulin resistance. Using SOCS-1 knockout mice, we investigated the contribution of SOCS-1 in the development of insulin resistance induced by a high-fat diet (HFD). SOCS-1 knockout mice on HFD gained 70% more weight, displayed a 2.3-fold increase in epididymal fat pads mass and increased hepatic lipid content. This was accompanied by increased mRNA expression of leptin and the macrophage marker CD68 in white adipose tissue and of SREBP1c and FAS in liver. HFD also induced hyperglycemia in SOCS-1 deficient mice with impairment of glucose and insulin tolerance tests. Thus, despite the role of SOCS proteins in obesity-related insulin resistance, SOCS-1 deficiency alone is not able to prevent insulin resistance induced by a diet rich in fat.     

Grape seed proanthocyanidins and metformin act by different mechanisms to promote insulin signaling in rats fed high calorie diet

Key pathways like insulin signaling, AMP activated kinase (AMPK) activation and inflammatory signaling are involved in the complex pathological network of hepatic insulin resistance. Our aim is to investigate whether grape seed proanthocyanidins (GSP) and metformin (MET) target any of these pathways in insulin resistant rat liver. Albino Wistar rats were rendered insulin resistant by feeding a high fat-fructose diet (HFFD). Either GSP (100 mg/kg b.w), MET(50 mg/kg b.w) or both were administered to insulin resistant rats as therapeutic options. HFFD-feeding caused hyperglycemia, hyperinsulinemia, increased gluconeogenesis, decreased tyrosine phosphorylation of insulin receptor-β(IR-β) and insulin receptor substrate-1 (IRS-1) and increased serine phosphorylation of IRS-1. The association of p85α subunit of phosphotidyl inositol 3 kinase(PI3K) with IRS-1 and subsequent Akt phosphorylation were reduced while the expression of mitogen activated protein kinases (MAPK) were increased in HFFD rats. Both MET and GSP reduced hyperglycemia and hyperinsulinemia and improved glycolysis, tyrosine phosphorylation of IR-β and IRS-1, IRS-1-PI3K association and Akt activation. However, activation of tumor necrosis factor-α, interleukin-6, leptin and suppressor of cytokine signaling-3 and reduction in adiponectin caused by chronic HFFD feeding were reversed by GSP better than by MET. Activation of AMPK by GSP was much less compared to that by MET. These findings suggest that GSP might activate PI3K pathway and promote insulin action by reducing serine kinase activation and cytokine signaling and MET by targeting AMPK. The beneficial effects were enhanced during combination therapy. Thus, combination therapy with MET and GSP may be considered for the management of metabolic syndrome.     

Isocaloric intake of a high‐fat diet promotes insulin resistance and inflammation in Wistar rats

The aim of this study was to investigate the effect of isocaloric intake from a high‐fat diet (HFD) on insulin resistance and inflammation in rats. Male Wistar rats were fed on an HFD (n = 12) or control diet (n = 12) for 12 weeks. Subsequently, all animals were euthanized, and blood glucose, insulin, free fatty acids, C‐reactive protein, lipid profile, cytokines and hepatic‐enzyme activity were determined. Carcass chemical composition was also analyzed. During the first and the twelfth weeks of the experimental protocol, the oral glucose tolerance test and insulin tolerance test were performed and demonstrated insulin resistance (P < 0.05) in the HFD group. Although food intake (g) was lower (P < 0.05) in the HFD group compared with the control group, the concentration of total cholesterol, low‐density lipoprotein, C‐reactive protein and liver weight were all significantly higher. The kinase inhibitor of κB, c‐Jun N‐terminal kinase and protein kinase B expressions were determined in the liver and skeletal muscle. After an insulin stimulus, the HFD group demonstrated decreased (P = 0.05) hepatic protein kinase B expression, whereas the kinase inhibitor of κB phospho/total ratio was elevated in the HFD muscle (P = 0.02). In conclusion, the isocaloric intake from the HFD induced insulin resistance, associated with impaired insulin signalling in the liver and an inflammatory response in the muscle. Copyright © 2012 John Wiley & Sons, Ltd.     

应用高脂饮食联合维生素D3建立慢性系膜增殖性肾炎血管病变大鼠模型

目的 探讨应用高脂饮食建立慢性系膜增殖性肾炎血管病变模型的方法.方法 雄性Wistar大鼠行单侧肾切除后随机分为单纯肾切除组、单纯肾炎组、单纯高脂组、肾炎高脂组.单纯肾炎组、肾炎高脂组在单侧肾切除后3d尾静脉注射OX7抗体(100 mg/kg),1周后尾静脉连续注射OX7抗体(每次100 mg/kg,1次/周,共3次),单纯肾切除组和单纯高脂组在同一时间尾静脉注射PBS,注射抗体后第2天单纯高脂组、肾炎高脂组腹腔注射维生素D3(6万U/kg,1次/4周),同时给予高脂饲料.分别于第4、8、10周观察各组大鼠的一般情况、体重、血压、尿蛋白、血浆白蛋白、血脂、血钙、肾功能以及肾脏病理改变.结果 模型组(肾炎高脂组)大鼠第8周肾小球外的小动脉出现管壁增厚,管腔变小,平滑肌细胞减少,细胞排列紊乱,纤维组织增生.第10周单纯肾炎组和单纯高脂组肾小球外小动脉管壁轻度增厚,管腔变化不明显,模型组血管病变积分明显高于单纯肾炎组和单纯高脂组(P＜0.05).结论 通过对慢性抗Thy1肾炎大鼠加用高脂饲料并腹腔注射维生素D3的方法,可以成功建立慢性系膜增殖性肾炎血管病变模型.     

链脲佐菌素制备糖尿病大鼠模型探讨

目的探讨链脲佐菌素(STZ)配合不同饮食建立糖尿病模型的方法,并对模型大鼠学习记忆能力进行考察,为糖尿病的深入研究及药物开发提供可靠的模型。方法雄性SD大鼠70只,随机分为7组,分别为空白对照组(Ⅰ);高糖高脂膳食组(Ⅱ);0周STZ(30 mg/kg)+高糖高脂膳食组(Ⅲ);0周STZ(30 mg/kg)+常规膳食组(Ⅳ);6周STZ(20 mg/kg)+高糖高脂膳食组(Ⅴ);6周STZ(25 mg/kg)+高糖高脂膳食组(Ⅵ);6周STZ(30 mg/kg)+高糖高脂膳食组(Ⅶ)。采用尾静脉注射STZ配合不同饮食制备糖尿病模型,动态监测模型大鼠血糖的变化,生化方法检测大鼠血脂的改变,放免法检测模型大鼠血清胰岛素、胰高血糖素。Morris水迷宫检测不同造模型条件对大鼠空间学习记忆能力的影响。结果与对照组比较,Ⅲ组大鼠于注射72 h后血糖升高明显(P<0.01),至注射第2周血糖升高达顶点(P<0.01),以后逐渐降低,至观察第10周,血糖维持在15 mmol/L(P<0.05)。IV组大鼠于注射72 h后血糖升高,以后迅速降低,至观察第10周,血糖降低至正常水平。Ⅴ、Ⅵ、Ⅶ组大鼠于注射72 h后显著升高,此后呈波浪式变化;随着注射剂量增加,降低程度减慢。高糖高脂饲料喂养10周后,各组大鼠CHO,TG,LDL-C均增加;Ⅲ、Ⅳ、Ⅴ组大鼠血清INS水平较对照组增高,除IV外,各组胰高血糖素均高于对照组。水迷宫试验结果显示,Ⅶ组潜伏期延长,与对照组比较,具有统计学意义。结论 STZ(30 mg/kg)配合高糖高脂膳食能够快速、稳定的建立糖尿病大鼠模型,高糖高脂膳食组6周后尾静脉注射STZ(30 mg/kg)制备模型,血糖升高显著,血清胰岛素水平降低明显,倾向于1型糖尿病模型。     

高脂喂养合并小剂量链脲佐菌素建立2型糖尿病大鼠模型

目的 观察不同配方的高脂饲料,以及不同周龄的大鼠对于该模型的造模成功率和模型病变特点的影响.方法 将26只3周龄SD大鼠分为正常一组(N1组)、模型一组(M1组)和模型二组(M2组);26只5周龄SD大鼠分为正常二组(N2组)、模型三组(M3组)和模型四组(M4组).M1组和M3组给予高脂饲料配方一喂养,M2组和M4组给予高脂饲料配方二喂养.4周后,各模型组大鼠腹腔注射STZ溶液35 mg/kg.连续观察大鼠的空腹血糖(FBG)、空腹胰岛素(FIN)、总胆固醇(TG)、甘油三酯(TC)水平.结果 5周龄SD大鼠的FBG水平在注射STZ后两周即可达到稳定状态,并维持在较高的水平;高脂饲料配方二使大鼠的进食量和体重增加明显,并且成功诱导出胰岛素抵抗( insulin resistance,IR).结论 选取5周龄SD大鼠作为模型动物,并给予配方二高脂饲料喂养,所建立的大鼠模型具备2型糖尿病的主要特征,是值得推广的2型糖尿病动物模型.     

Post-natal diet determines insulin resistance in fetally malnourished, low birthweight rats (F1) but diet does not modify the insulin resistance of their offspring (F2)

We examined the effects of prenatal and postnatal nutrition on birthweight and insulin sensitivity, indicated by the glucose/insulin (G/I) ratio, in adult rats (F1 generation) and in their adult offspring (F2 generation). Rat pups (F1) whose dams consumed low-protein diets during gestation (malnourished) consumed either nutritionally adequate (control) or high-fat diets ad libitum post-weaning. The offspring of these rats (F2) were maintained on the same diets as their respective dams. Separate pups (F1) whose dams consumed high-fat diets during gestation (over-nourished) were maintained on high-fat diets post-weaning, as were their offspring (F2). Birthweights were significantly reduced in all fetally malnourished F1 animals. At approximately 70 d of age, fasting insulin sensitivity in over-nourished F1 rats was significantly reduced compared to controls regardless of whether they were malnourished or over-nourished in utero; however, fetally malnourished F1 rats consuming control diets post-natally had significantly greater fasting insulin sensitivity than control animals. At 30 and 120 min post-glucose load, insulin sensitivity was reduced 12-65% in both groups of over-nourished F1 rats as compared to the fetally malnourished F1 rats consuming the control diet. Birthweights were significantly lower in F2 animals whose dams (F1) were fetally malnourished and weaned to high fat diets. Insulin sensitivity was significantly reduced in all F2 animals versus control animals, regardless of dietary treatment. Thus, post-natal diets alter insulin sensitivity in fetally malnourished, adult rats; and maternal malnutrition during gestation results in insulin resistance in offspring, irrespective of offsprings' birthweight or diet.     

Sodium Pentaborate Pentahydrate ameliorates lipid accumulation and pathological damage caused by high fat diet induced obesity in BALB/c mice

BackgroundObesity is one of the most popular topic in the field of research. In order to defeat this highly widespread disease, the mechanism of fat accumulation at the molecular level and its elimination are crucial. The use of boron has been showing promising results during the recent years.MethodsIn this study, anti-obesity potential of Sodium Pentaborate Pentahydrate (SPP) used as a dietary supplement on BALB/c mice fed with a high-fat diet was evaluated. Mice were divided into four groups with different diets, consisting of a normal diet, a high-fat diet (HFD) (containing 60 % fat), a HFD-supplemented with 0.5 mg/g body weight (BW) of SPP and a HFD-supplemented with 1.5 mg/g body weight (BW) of SPP. The animals were then observed for 10 weeks and physically monitored, and were sacrificed at the end of the experiment for physical and physicochemical evaluation.ResultsAccording to the physical parameters measured -body weight, food and water intake ratios-, the results indicate that SPP decreased weight gain in a dose dependent manner. Measurement of the hormone levels in the blood and fat accumulation in organs of mice also supported the anti-obesity effects of SPP. Expressions of adipogenesis related genes were also negatively regulated by SPP administration in white adipose tissue (WAT) tissue.ConclusionThese findings promise a treatment approach and drug development that can be used against obesity when SPP is used in the right doses. As a future aspect, clinical studies with SPP will reveal the effect of boron derivatives on obesity.