孕哺期高脂膳食对子代SD大鼠空间学习记忆能力的影响

目的 研究孕哺期高脂膳食对子代SD大鼠空间学习记忆能力的影响。 方法 成年雌性SD孕鼠10只随机分为对照组和高脂组,分别喂以标准鼠粮和含20%猪油的高脂饲料。仔鼠4周龄断乳,对照组雄性仔鼠10只维持原饲料,10只转饲以高脂饲料;高脂组雄性仔鼠10只维持原饲料,10只转饲以标准鼠粮。12周龄,进行Morris水迷宫测试其空间学习记忆能力,称量体重、内脏脂肪和全脑质量,测试血浆瘦素水平。 结果 持续高脂膳食的仔鼠空间学习能力低于其它仔鼠(P＜0.05),但空间记忆能力各组仔鼠无差异(P>0.05);断乳后高脂膳食可造成仔鼠体重(P＜0.05)和内脏脂肪质量(P＜0.05)增加;孕哺期高脂膳食造成仔鼠全脑质量降低(P＜0.05)和血浆瘦素水平下降(P＜0.05)。 结论 孕哺期高脂膳食造成子代脑发育障碍和血浆瘦素水平降低,这可能与子代空间学习能力损伤有关。     

SD大鼠孕哺期喂养高能量饲料对子代脂代谢的影响

目的 探索SD大鼠孕哺期给予高能量饲料对子代脂代谢的影响。 方法 成年SD孕鼠15只随机分为对照组、高脂组、高脂高糖组,在孕哺期分别给予标准鼠粮、高脂饲料(含20%猪油)和高脂高糖饲料(含20%猪油和10%蔗糖)。仔鼠4周处死,称量体重、肝脏和肾周脂肪质量,并检测血浆甘油三酯、胆固醇、高密度脂蛋白和瘦素水平。结果 体重、肝脏和肾周脂肪质量,高脂组[(90.05±6.71)、(3.73±0.18)和(0.41±0.12)g]和高脂高糖组[(89.82±5.08)、(3.82±0.27)和(0.41±0.13)g]均高于对照组[(70.60±17.30)、(2.87±0.83)和(0.22±0.07)g](P＜0.05);高脂高糖组总胆固醇水平(1.72±0.10)高于高脂组(0.9±0.33)和对照组(0.8±0.3)(P＜0.05);高脂组(0.83±0.54)和高脂高糖组(1.02±0.22)的甘油三脂水平高于对照组(0.45±0.21)(P＜0.05);高密度脂蛋白和瘦素,高脂组(0.23±0.08,1.16±0.06)和高脂高糖组(0.26±0.09,1.15±0.04)的低于对照组(0.50±0.03,1.26±0.08)(P＜0.05)。 结论SD大鼠孕哺期摄入高能量饲料造成子代肥胖、血脂异常和血浆瘦素水平下降等脂代谢紊乱。     

孕哺期铅暴露对雄性子代大鼠海马组织中沉默信息调节因子表达的影响

目的探讨大鼠孕期及哺乳期铅暴露对雄性仔鼠海马组织中沉默信息调节因子(silent information regulator1,SIRT1)表达的影响。方法将12只健康SPF级雌性SD孕鼠随机分为3组,分别为对照组(去离子水)、低剂量铅暴露组(0.5 g/L乙酸铅)和高剂量铅暴露组(2.0 g/L乙酸铅),每组4只。采取自由饮水的方式进行染毒,自妊娠第1天开始至仔鼠21 d断乳为止。在仔鼠断乳后,采用电感耦合等离子体原子发射光谱法(ICP-AES)检测6只雄性仔鼠全血和海马组织中铅的含量,采用RT-PCR检测6只雄性仔鼠海马组织SIRT1 mRNA水平的变化,采用Western blot和免疫荧光组织化学法检测6只雄性仔鼠海马组织SIRT1蛋白水平的变化。结果孕哺期不同剂量铅暴露后,雄性仔鼠血铅和海马组织中铅含量均高于对照组,海马中SIRT1 mRNA和蛋白水平的表达均低于对照组,且高剂量铅暴露组仔鼠海马中SIRT1mRNA和蛋白水平低于低剂量组,差异均有统计学意义(P0.05)。结论孕哺期铅暴露可下调仔鼠海马中SIRT1基因表达,从而可能影响海马神经元功能及仔鼠学习记忆能力。     

孕哺期氧化乳蛋白饮食对子代小鼠学习记忆能力的影响

目的 探索孕哺期氧化乳蛋白饮食对子代小鼠脑部氧化还原状态及学习记忆能力的影响。方法 通过不同处理方法[加热、次氯酸(HClO)、过氧化氢-铜(H2O2-Cu)]对全脂乳进行氧化修饰。雌雄鼠合笼成功即开始饲喂氧化乳蛋白日粮3w,产后母乳喂养,仔鼠3w断乳后,随机分为三批,第一批立即测定仔鼠脑部的氧化损伤指标,第二、三批分别饲以原来氧化乳蛋白日粮和普通饲料至6w,进行Morris水迷宫测试空间学习记忆能力;测定6w仔鼠脑部的抗氧化及氧化损伤指标。结果 孕哺期饲喂氧化乳蛋白日粮,子代小鼠脑部氧化还原状态失衡,与空白对照组相比,氧化修饰组子代小鼠脑部抗氧化酶活力(CAT、SOD)和总抗氧化能力(T-AOC)均呈现不同程度的下降(P<0.05),水迷宫实验中,与空白对照组相比,氧化乳蛋白组潜伏期明显上升,穿越平台次数低于空白对照组(P<0.05)。结论 孕哺期饲喂氧化乳蛋白日粮,引起子代小鼠脑部氧化应激,降低其抗氧化防御能力,同时影响其空间学习记忆能力。     

燃煤型氟中毒对仔鼠学习记忆及海马区胶质纤维酸性蛋白表达的影响

目的观察母鼠青春期及孕哺期燃煤型氟中毒对仔鼠学习记忆及海马区胶质纤维酸性蛋白(GFAP)表达的影响。方法 48只断乳两周的健康清洁级SD大鼠(雌鼠32只、雄鼠16只),按体重将雌鼠随机分为对照组、低氟组、中氟组、高氟组,每组8只,其中低、中、高氟组饲料含氟量分别为24.4、47.8、106.0 mg/kg;染氟组以燃煤型氟中毒重病区原煤烘干的玉米为主要饲料喂养3个月,对照组及雄鼠食用正常饲料。染氟3个月后雌雄大鼠按2∶1合笼交配,雌鼠妊娠后继续染毒,直至仔鼠断乳,仔鼠断乳后食用正常饲料。计算仔鼠脑脏器系数,以氟离子选择电极法检测仔鼠脑氟含量,以Morris水迷宫检测30 d龄仔鼠学习记忆能力,以Western blot检测仔鼠海马区GFAP的表达水平。结果与对照组比较,各染氟组仔鼠脑脏器系数无明显差异(P0.05);中氟组和高氟组仔鼠脑氟含量升高,差异有统计学意义(P0.05)。与对照组比较,定位航行实验第3、4天的中氟组及高氟组仔鼠平均逃避潜伏期延长,高氟组仔鼠首次到达平台时间延长,且穿越平台次数减少,差异均有统计学意义(P0.05)。与对照组相比,高氟组仔鼠海马区GFAP表达水平增加,差异有统计学意义(P0.05)。结论母鼠燃煤型氟暴露可影响仔鼠学习记忆能力,其机制可能与仔鼠海马区GFAP表达水平增加有关。     

孕期高脂喂养对胎鼠心肌细胞的影响

目的 探讨Sprague-Dawley(SD)大鼠妊娠期高脂喂养对胎鼠心肌细胞的影响。方法 选择清洁级SD大鼠,雄性10只、雌性20只,鼠龄96～103 d,体重240~260 g。适应性喂养3 d后SD雌性大鼠与雄性大鼠按2∶1比例合笼过夜,次日早上检查,以阴道涂片发现精子为妊娠第0天。将孕鼠随机分为A、B两组,每组10只。A组予普通饲料喂养,B组予高脂饲料喂养,分别喂养至孕期的第21天。禁食16 h采集血标本测定血脂。取胎鼠心肌组织,分别于光镜和电镜下观察心肌细胞结构的改变。结果 孕第21天,与A组孕鼠比较,B组孕鼠血总胆固醇及低密度脂蛋白胆固醇明显升高(P=0.000),而高密度脂蛋白胆固醇明显下降(P=0.001)。在光镜下观察两组胎鼠心肌细胞HE染色切片,B组细胞结构欠清晰,细胞存在水肿,细胞胞核形态不规则,细胞核内染色加深。两组胎鼠心肌组织超微结构观察提示:与A组比较,B组细胞内细胞器模糊,线粒体嵴断裂,数量减少等。结论 高脂喂养的SD大鼠孕期存在脂代谢异常(高胆固醇血症、高低密度脂蛋白胆固醇血症及低高密度脂蛋白胆固醇血症),其胎鼠存在心肌细胞损害。     

孕哺期大鼠全氟辛烷磺酸暴露对子代糖代谢的影响

[目的]探讨孕哺期全氟辛烷磺酸(PFOS)暴露对子代大鼠糖代谢的影响. [方法]将Wistar孕鼠自孕0天(GD0)随机分为对照组(0mg/kg)、低剂量组(0.6 mg/kg)和高剂量组(2mg/kg),每组10只;PFOS灌胃染毒至仔鼠出生后21天(PND21)断乳为止.采用高效液相/质谱法检测PND0、PND21时仔鼠血清PFOS含量;观察仔鼠体重变化趋势;比较9周龄和15周龄仔鼠空腹血糖、空腹胰岛素水平;检测仔鼠瘦素和抵抗素基因表达水平变化. [结果] PND21时低剂量组和高剂量组仔鼠血清中PFOS浓度分别为(16.00±1.27)mg/L和(80.54±6.55) mg/L(P＜0.05).低剂量组雌性仔鼠出生后8、9周龄和高剂量7～9周龄,低剂量组雄性仔鼠出生8～12周龄、高剂量7、8、10周龄的体重均明显低于对照组(均P＜ 0.05).高剂量组9周龄和低剂量组15周龄雌性仔鼠的胰岛素水平分别为(10.85±1.37)mU/L和(13.62±1.87) mU/L,均高于对照组(P＜0.05);高剂量组9周龄雄性仔鼠的空腹血糖和胰岛素水平分别为(5.43±0.77) mmol/L和(13.23±1.81)mU/L,15周龄雄性仔鼠低剂量组分别为(4.99±0.54) mmol/L和(13.57±1.22)mU/L,15周龄高剂量组分别为(5.71±0.56) mmol/L和(13.44±2.97)mU/L,均高于对照组(P＜0.05).高剂量组15周龄雄性仔鼠的抵抗素基因表达上调1.25±0.03(P＜ 0.05),瘦素基因表达下调0.67±0.08(P＜0.05). [结论]PFOS孕哺期暴露可能引起子代大鼠糖代谢异常,增加糖尿病患病风险.     

初断乳大鼠锌补充对成年高脂诱导肥胖后胰岛素的影响

目的 探讨初断乳大鼠锌补充对成年期高脂饮食下胰岛素水平的影响,为阐明生命早期适量补锌预防成年后胰岛素抵抗的机制提供重要依据。方法 初断乳雄性SD大鼠85只随机分为基础饲料组和高、中、低锌补充组。锌补充4周后各组均以基础饲料喂养1周,于第5周末检测大鼠血糖、胰岛素水平并计算胰岛素抵抗指数。随后将基础饲料组大鼠随机分为肥胖组和正常对照组,肥胖诱导组及3个锌补充组均喂以高脂饲料。高脂干预8周后处死所有大鼠并检测上述指标。结果 大鼠成年高脂干预后,1)3个锌补充组分别较肥胖诱导组体重明显降低(P＜0.05),高脂饲料喂养后锌补充组体重正常,而肥胖诱导组发生肥胖;2)3个锌补充组分别较肥胖诱导组血糖、胰岛素明显降低(P＜0.05),而胰岛素抵抗指数明显升高(P＜0.05),高脂饲料喂养后锌补充组胰岛素水平正常,而肥胖诱导组产生胰岛素抵抗。结论 生命早期适量补锌可持续发挥作用,在一定程度上维持成年后高脂膳食下血糖和胰岛素处于正常水平,预防胰岛素抵抗发生。     

孕鼠补充二十二碳六烯酸对仔鼠肝脏肉碱棕榈酰转移酶-I mRNA表达的影响

目的 研究孕鼠补充二十二碳六稀酸(DHA)对仔鼠脂肪代谢及肉碱棕榈酰转移酶-I(CPT-I)mRNA水平的影响.方法 成年SD雌鼠随机分成A、B、C三组,待其妊娠后A组给予基础饲料、B组补充低剂量的DHA(1g/kg bw),C组补充高剂量的DHA(2g/kg bw).所有雄性仔鼠出生后均由A组母鼠哺乳,断乳后给予基础饲料喂饲至出生后第8周.每组8只,动态观察仔鼠的体重、体脂含量、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白(HDL-C)7L CPT-I mRNA水平.结果 三组仔鼠的出生体重差异无显著性(P>0.05);仔鼠出生后的第8周时,C组的体重显著低于A组(P<0.05),B、C组的体脂含量、TG水平显著低于A组(P<0.05).而C组HDL-C水平显著高于A组(P<0.05),但三组TC水平差异无显著性(P>0.05).动态观察表明,肝脏CPT-I mRNA水平持续性出现B、C高于A组,C组高于B组.结论 孕期补充DHA可能通过持续性上调仔鼠肝脏CPT-I基因表达来增强脂肪酸的氧化,降低血脂水平,但孕期摄入过量的DHA可能对子代产生不利影响.     

孕哺期至成年反式脂肪酸摄入对小鼠学习记忆能力的影响

目的探讨孕哺期至成年反式脂肪酸(TFA)摄入对子代小鼠学习记忆能力的影响。方法将30只SPF级妊娠昆明小鼠随机分为3组,分别为对照组和低剂量(4%TFA占供能比)组、高剂量(8%TFA占供能比)组,每组10只。自妊娠第0天至仔鼠出生后第21天(断乳),采用饲喂方法进行染毒;断乳后,雄性仔鼠继续染毒,方法同母鼠,直至出生第24周。采用Morris水迷宫定位航行实验和平台探索实验测定仔鼠学习记忆功能。结果在定位航行实验中,与对照组比较,训练第5天高剂量TFA组雄性仔鼠到达平台的总路径延长,训练第4天和第5天高剂量TFA组仔鼠逃避潜伏期延长,差异均有统计学意义(P0.05)。在空间探索实验中,与对照组比较,高剂量TFA组和低剂量TFA组雄性仔鼠的穿越平台次数较少,高剂量TFA组雄性仔鼠在目标象限停留时间较短,差异有统计学意义(P0.05);各剂量TFA组雄性仔鼠在其他象限的停留时间均无明显变化。结论孕哺期至成年高剂量的TFA摄入可影响仔鼠脑组织发育,损害学习记忆能力。     

生命早期使用抗生素对生命后期喂饲高脂饲料大鼠炎症因子的影响

目的 探索哺乳期使用抗生素对断乳后喂饲高脂饲料大鼠的影响。方法 将24只出生7天的SD大鼠仔鼠,随机分为高脂抗生素组（ATHF组）和高脂对照组（HF组）,分别灌胃剂量为150mg/kg·d的阿莫西林溶液和生理盐水,持续10天。断乳后两组仔鼠均喂饲高脂饲料。观察两组仔鼠体重、脏器系数、空腹血糖、血脂、血清炎症因子水平等的变化。结果 两组仔鼠间体重、脏器系数、空腹血糖及血脂均没有统计学差异。研究结束时,ATHF组与HF组相比仔鼠血清瘦素浓度升高,但差异没有统计学意义（2033.09±822.7 vs 1746.23±556.7,P＞0.05）;血清脂联素（5791.35±932.3 vs 4755.55±536.6,P＜0.05）、IL-6（449.93±85.4 vs 353.94±72.2,P＜0.05）、C反应蛋白水平（7556.52±746.7 vs 6678.84±869.2,P＜0.05）均增加,差异有统计学意义。结论 生命早期使用抗生素可以加重生命后期使用高脂饮食所引发的成年期大鼠全身慢性炎症反应。     

同等剂量槲皮素、芹菜素对高尿酸血症大鼠的影响及其机制研究

目的研究同等剂量槲皮素(Quercetin,Que)和芹菜素(Apigenin,Api)对腺嘌呤+盐酸乙胺丁醇诱导大鼠高尿酸血症的影响及其机制。方法利用腺嘌呤+盐酸乙胺丁醇片灌胃法诱导SD大鼠制备高尿酸血症模型,槲皮素、芹菜素预防治疗3周,测定血清尿酸(SerumUricAcid,SUA)、血清以及肝脏中的黄嘌呤氧化酶(Xanthine Oxidase,XOD)、腺苷脱氨酶(adenosine deaminase,ADA)的活性。结果槲皮素和芹菜素均可显著降低SUA水平,抑制血清和肝脏中的ADA水平,槲皮素能够显著抑制血清和肝脏中的XOD的活性,但是芹菜素对肝脏XOD活性影响不大。结论槲皮素、芹菜素均有干预腺嘌呤+盐酸乙胺丁醇诱导高尿酸血症的作用。可能的机制是槲皮素通过抑制机体XOD和ADA的活性,减少血尿酸的生成量,从而降低血清尿酸水平;而芹菜素可能通过抑制体内ADA的活性,或许还有别的途径来降低SUA水平,但是具体机制有待于进一步研究。     

孕期高中链脂肪膳食对后代UCP3基因的影响

目的:探讨孕期膳食对子代肥胖和肥胖相关基因解偶联蛋白3(UCP3)表达的影响,寻找肥胖预防和治疗的靶标。方法:W istar孕鼠分别食用标准膳食和高中链脂肪膳食,所产雄性子鼠分别为对照组和高中链脂肪酸组(HMCFA),3周断乳后大鼠均食用标准膳食至成年,将对照组的大鼠随机分为两组:一组继续食用标准膳食;另一组为高脂对照组(HFCON),HFCON和HMCFA组的大鼠均高脂膳食诱导肥胖6周。分别在大鼠出生、断乳、成年、高脂诱导肥胖后各处死一批大鼠,取褐色脂肪检测UCP3 mRNA的表达。结果:与孕期标准膳食的子代相比,孕期高中链脂肪膳食可持续降低子代大鼠的体重和肥胖率(P<0.05),同时也可持续升高UCP3 mRNA的表达。结论:孕期高中链脂肪膳食可降低子代成年高脂诱导肥胖的发生;其机制为通过程序性升高子代UCP3基因的表达增加脂肪氧化和热能散失。     

Effect of palatable diet on growth, caloric intake and endocrine-metabolic profile in weanling rats with dorsomedial hypothalamic lesions

Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated rats served as controls. All animals were fed lab chow for 15 postoperative days. At that time they were subdivided into two groups each. One DMNL and one control group continued to be fed lab chow until the termination of the experiment on postoperative day 116. A second DMNL and control group were fed a high-fat diet and 32% sucrose solution (HF/SS diet). All DMNL rats showed reduced body weight and linear growth, but the HF/SS diet depressed these parameters further below the levels of the chow-fed groups. Both DMNL and control rats fed HF/SS had more carcass fat, heavier epididymal fat pads, more carcass fat per calories eaten, higher plasma levels of glucose, glycerol and free fatty acids but lower insulin levels than chow-fed DMNL rats and controls. This occurred in the face of lower body weights and caloric intake. Neither growth hormone nor insulin showed lesion effects. Rats with DMNL exhibited the same inverse relationship between plasma insulin and free fatty acids as controls. The data indicate that DMNL rats respond to the HF/SS diet essentially like sham-operated controls, i.e., they develop dietary obesity. Although they do show some small deficits, their lipogenic capacity is actually significantly greater than that of HF/SS-diet fed controls.     

A maternal high-fat diet represses the expression of antioxidant defense genes and induces the cellular senescence pathway in the liver of male offspring rats

Maternal high-fat (HF) diet feeding is associated with increased risk of developing metabolism-related diseases in adult offspring, including chronic liver disease. The present study tested the hypothesis that maternal HF diet leads to a decreased antioxidant defense capacity and causes cellular senescence in liver of adult offspring rats, which might increase risk of developing chronic liver disease. Timed-pregnant Sprague Dawley rats were fed a HF diet (45% of energy from fat) or a control (C) diet (16% of energy from fat) during gestation and lactation. The resulting offspring were fed a C diet after weaning to generate 2 offspring groups: C diet-fed offspring of dams fed C diet (C/C) and C diet-fed offspring of dams fed a HF diet (HF/C). At 12 wk of age, male rats were killed and samples were collected for analysis. Maternal HF diet significantly increased plasma TG and hepatic TBARS concentrations and the size of hepatic lipid droplets in offspring rats. The expression of antioxidant defense genes, such as glutathione peroxidase-1, Cu/Zn superoxide dismutase (Sod1), paraoxonase enzymes (Pon1, Pon2, and Pon3), were significantly lower in the liver of HF/C pups than in C/C pups. The expression of Inhibitor of cyclin dependent Kinase 4a (p16INK4a), a marker of cellular senescence, and cyclooxygenase-2 (Cox2), a proinflammatory marker, was significantly higher in the HF/C offspring group than in the C/C offspring group. Western-blot analysis shows that cyclin D1 and phosphorylated retinoblastoma protein were significantly lower in HF/C offspring than in C/C offspring. The results provide the first evidence to our knowledge that maternal HF diet might alter antioxidant defense capacity and program the p16INK4a-dependent cellular senescence in the liver of adult offspring.     

Sex Differences in Early Programming by Maternal High Fat Diet Induced-Obesity and Fish Oil Supplementation in Mice

Pre-pregnancy obesity is a contributing factor for impairments in offspring metabolic health. Interventional strategies during pregnancy are a potential approach to alleviate and/or prevent obesity and obesity related metabolic alterations in the offspring. Fish oil (FO), rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs) exerts metabolic health benefits. However, the role of FO in early life remains still unknown. Hence, this study objective was to determine the effect of FO supplementation in mice from pre-pregnancy through lactation, and to study the post-natal metabolic health effects in gonadal fat and liver of offspring fed high fat (HF) diet with or without FO. Female C57BL6J mice aged 4–5 weeks were fed a HF (45% fat) diet supplemented with or without FO (30 g/kg of diet) and low fat (LF; 10% fat) pre-pregnancy through lactation. After weaning, offspring (male and female) from HF or FO dams either continued the same diet (HF-HF and FO-FO) or switched to the other diet (HF-FO and FO-HF) for 13 weeks, creating four groups of treatment, and LF-LF was used as a control group. Serum, gonadal fat and liver tissue were collected at termination for metabolic analyses. Offspring of both sexes fed HF with or without fish oil gained (p < 0.05) more weight post weaning, compared to LF-LF-fed mice. All the female offspring groups supplemented with FO had reduced body weight compared to the respective male groups. Further, FO-FO supplementation in both sexes (p < 0.05) improved glucose clearance and insulin sensitivity compared to HF-HF. All FO-FO fed mice had significantly reduced adipocyte size compared to HF-HF group in both male and females. Inflammation, measured by mRNA levels of monocyte chemoattractant protein 1 (Mcp1), was reduced (p < 0.05) with FO supplementation in both sexes in gonadal fat and in the liver. Markers of fatty acid synthesis, fatty acid synthase (Fasn) showed no sex specific differences in gonadal fat and liver of mice supplemented with HF. Female mice had lower liver triglycerides than male counterparts. Supplementation of FO in mice improved metabolic health of offspring by lowering markers of lipid synthesis and inflammation.     

腹型肥胖、血脂谱异常与高尿酸血症并存鹌鹑模型的病理机制

目的 观察高脂饮食诱导的腹型肥胖鹌鹑的血清尿酸含量、脂质谱、脂代谢及尿酸代谢相关酶活性,探讨腹型肥胖伴脂质谱异常、高尿酸血症的可能机制。方法 采用高脂饲料诱导腹型肥胖鹌鹑模型,分别于高脂饮食的第7和14天检测正常(n=12)和腹型肥胖鹌鹑模型(n=12)的血清尿酸及血糖水平、脂质谱、脂代谢及尿酸代谢相关酶活性以及体重、腹部脂肪重量、腹脂率。结果 研究第7天模型组鹌鹑的体重、腹部脂肪重量及腹脂率与正常组的差异无统计学意义（P均＞0.05）。第14天两组鹌鹑体重的差异无统计学意义(P＞0.05),模型组的腹部脂肪重量[(3.91±2.13)比(2.40±0.96)g,P=0.0468]及腹脂率（1.92％±0.97％比1.22％±0.45％,P=0.0447）均显著高于正常组。研究第7及14天模型组鹌鹑血清总胆固醇（P值分别为0.0042和0.0006）和低密度脂蛋白胆固醇（P值分别为0.0045和0.0010）水平均显著高于正常组;甘油三酯水平显著低于正常组（P值分别为0.0006和0.0024）;尿酸代谢相关酶腺苷脱氨酶（P值分别为0.0237和0.0060）及黄嘌呤氧化酶活性（P值分别为0.0142和0.0071）均显著高于正常组。第14天模型组的尿酸水平显著高于正常组(P=0.0320);高密度脂蛋白胆固醇水平显著低于正常组(P=0.0197);模型组脂代谢相关酶脂蛋白脂酶活性显著高于正常组（P=0.0419）。结论 高脂饮食不但可诱发鹌鹑血脂谱异常,并随造模时间的延长而伴发腹型肥胖与高尿酸血症。脂代谢及尿酸代谢相关酶活性改变可能是腹型肥胖伴发血脂谱异常、高尿酸血症的病理机制。