铅暴露对大鼠心脏功能的影响及槲皮素保护作用的研究

目的探讨铅暴露对大鼠心脏功能的影响及槲皮素的保护作用。方法成年雄性SD大鼠30只,随机分为对照组、醋酸铅组(1 g/L)和醋酸铅(1 g/L)加槲皮素(30 mg/kg)组,每组10只,通过饮水方式染毒8周。应用试剂盒检测心脏组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、钠钾ATP酶(Na+-K+-ATPase)、钙镁ATP酶(Ca2+-Mg2+-ATPase)、乳酸脱氢酶(LDH)、肌酸激酶(CK)的水平变化,并进行心电图和病理形态学检查。结果铅染毒组大鼠心脏组织中MDA、Ca2+-Mg2+-ATPase水平和CK、LDH活力较对照组显著升高,而SOD和Na+-K+-ATPase水平显著下降;槲皮素组MDA、Ca2+-Mg2+-ATPase水平和CK、LDH活力较铅染毒组均显著下降,而SOD和Na+-K+-ATPase水平显著上升,心电图检查显示铅染毒组大鼠心率(HP)对照组显著下降,而P-R间期、Q-T间期较铅染毒组显著升高;槲皮素组心率较染毒组显著上升,P-R间期、Q-T间期较铅染毒组显著下降。病理学检查结果显示铅染毒组大鼠心肌组织内可见较多量炎细胞浸润,而槲皮素组有显著缓解。结论铅暴露可以导致实验大鼠心脏功能紊乱,而槲皮素对其有一定的保护作用。     

原花青素对大鼠亚硒酸钠性白内障的初步研究

[目的]研究原花青素预防大鼠硒性白内障的作用机理并初步探讨其量效关系.[方法]将40只12日龄雄性SD大鼠随机分为正常对照组、模型组、原花青素低剂量组和原花青素高剂量组,模型组参照张家萍等人亚硒酸 钠性白内障大鼠模型制作方法进行造模,原花青素低、高剂量组为在给予亚硒酸钠的同时给予原花青素,剂量分别为20 rag/kg体重和100mg/kg体重.在实验d 16处死全部大鼠.采用化学比色法测定晶状体中丙二醛(MDA)、超氧化物歧化酶(SOD)、以及谷胱甘肽过氧化物酶(GSH-Px)含量.[结果]与模型组相比,原花青素高剂量组晶状体中MDA含量有显著性降低(P<0.05),SOD、GSH-Px含量有显著性增高(P<0.05).[结论]原花青素具有抑制大鼠晶状体白内障发生发展作用,其作用机制与其良好的抗氧化作用有关.     

大豆硒蛋白对糖尿病大鼠心肌损伤的保护作用

目的探讨大豆硒蛋白对糖尿病大鼠心肌损伤的保护作用。方法 Wistar大鼠50只,,随机分为正常对照组(NC)、糖尿病对照组(DM)、低剂量Se治疗组(L-Se)、中剂量Se治疗组(M-Se)、高剂量Se治疗组(H-Se)。后4组腹腔注射链脲佐菌素55 mg/kg制备DM模型。第7w起,NC、DM组予0.5%CMC-Na 10ml/(kg.d),L-Se、M-Se、H-Se组分别予大豆硒蛋白2,4,8g/(kg.d)灌胃。第12w末处死大鼠,检测血糖、血清及心肌组织中SOD、GSH-Px、NOS活性和MDA、NO含量以及心肌组织中Na+-K+-ATPase、Ca2+-ATPase活性。结果与模型组比较,补充外源性大豆硒蛋白后,M-Se、H-Se组可明显降低糖尿病大鼠血糖及MDA含量(均P<0.001),显著增加血清GSH-Px、NOS活性(P<0.001),同时使心肌线粒GSH-Px活性、NO含量明显增加(均P<0.001),并且使心肌组织Na+-K+-ATPase、Ca2+-ATPase活性显著增加(P<0.01,P<0.001)。结论大豆硒蛋白对糖尿病大鼠心肌损伤具有保护作用。     

吡格列酮对高脂饮食大鼠心肌PPAR γ-AP-1信号途径及抗氧化作用的研究

[目的]观察吡格列酮(pioglitazone,PI)对高脂饮食大鼠心肌PPARγ-AP-1信号途径的影响及抗氧化作用.[方法]随机选取雄性SD大鼠24只,随机分为对照组(C)、高脂组(HF)、吡格列酮处理组(HF+PI)3组,每组8只.对照组饲喂基础饲料,其他两组饲喂高脂饲料.各组同时做灌胃处理分别饲以干预剂.于0周、3周、6周尾静脉采血测TG、TC、HDL-C含量及6周末脂质过氧化产物MDA含量及抗氧化SOD、GPx活性变化.6周末留取心肌组织.RT-PCR分析各组PPARγ mRNA表达水平.Western blot检测心肌PPARγ、AP-1蛋白质水平.[结果](1)吡格列酮能降低高脂饮食大鼠血清TG、TC含量;(2)吡格列酮能显著降低血清MDA含量,增加血清SOD、全血GPx活性;(3)高脂饮食大鼠心肌PPARγmRNA表达水平明显降低;而吡格列酮能显著增加心肌PPARγmRNA表达水平;(4)高脂组心肌PPARγ蛋白表达水平降低,核转录因子AP-1呈高表达水平;而吡格列酮组心肌PPARγ蛋白表达水平较高脂组呈高水平表达,核转录因子AP-1表达水平较高脂组降低.[结论]吡格列酮能拮抗高脂饮食大鼠心肌PPARγ表达水平降低,并由此途径阻止心肌核转录因子AP-1表达水平的升高,并具有降血脂、抗氧化作用.     

Oncolyn对衰老小鼠脑组织中ATP酶活性和神经生长因子的表达的影响

目的探讨衰老过程神经生长因子的表达和ATP酶的变化以及Oncolyn的调节作用。方法90只昆明种小鼠随机分为对照组、衰老组和Oncolyn组。应用D-半乳糖颈部皮肤注射复制衰老小鼠模型,同时经口给入Oncolyn70天,检测脑组织Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶的水平,应用免疫组化的方法检测海马中NGF、BDNF的表达情况。结果与对照组比较,衰老组小鼠脑组织中Ca2+-Mg2+-ATPase和Na+-K+-ATPase由0.27,0.046(U/mg prot)下降到0.022和0.021(U/mg prot),差异有显著性(P<0.05),尤其以Ca2+-Mg2+-ATPase降低严重。而Oncolyn组的Ca2+-Mg2+-ATPase和Na+-K+-ATPase均高于衰老组(分别为0.056,0.117U/mg prot),以Na+-K+-ATPase提高较大。衰老小鼠海马组织中NGF、BDNF表达与对照组比较分别下降了48.28%和43.25%(P<0.05)。而应用Oncolyn干预后组NGF、BDNF表达均增加(分别增加了46.67%和163.64%)。结论Oncolyn在一定程度上可以通过增加ATP酶活性和提高神经生长因子表达来延缓衰老。     

苯并[a]芘对大鼠海马组织氧化应激及ATP酶的影响

目的 通过研究苯并[a]芘(B[a]P)对大鼠行为学、海马氧化应激及ATP酶的影响,探讨B[a]P的神经行为毒性分子机制.方法 将120只21d龄雄性SD大鼠,随机分为空白对照组、植物油组(溶剂对照组),2.5、5.0、10.0 mg/kg B[a]P染毒组,每组24只.腹腔注射给药,每天1次,连续4周.染毒结束后,用Morris水迷宫和穿梭箱检测学习记忆能力;用化学比色法测定海马超氧化物歧化酶(SOD)、Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶的活力及丙二醛(MDA)含量;用荧光标记方法测定海马Ca2+浓度.结果 各染毒组大鼠的水迷宫逃避潜伏期、穿梭箱主动回避反应潜伏期(AARL)和被动回避反应潜伏期(RARL)均明显高于空白对照组和溶剂对照组,水迷宫末次跨平台次数和穿梭箱主动回避反应次数(AARF)均明显低于空白对照组和溶剂对照组,差异均有统计学意义(P＜0.05);且呈剂量-效应关系.与空白对照组和溶剂对照组比较,染毒组大鼠海马组织SOD活力、Na+-K+-ATP酶和ca2+-Mg2+-ATP酶活力明显下降,且呈剂量-效应关系,差异均有统计学意义(P＜0.05).染毒组大鼠海马组织MDA含量、Ca2+浓度均明显高于空白对照组和溶剂对照组,且呈剂量-效应关系,差异均有统计学意义(P＜0.05).结论 B[a]P所致神经行为毒性,可能与染毒后大鼠海马组织氧化应激受损,Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活力下降有关.     

魔芋多糖对小鼠瘦素和Na~+-K~+-ATP酶水平的影响

目的探讨魔芋多糖对高脂饮食小鼠血清瘦素和小肠粘膜Na+-K+-ATP酶水平的影响。方法将实验动物分为正常对照组、高脂对照组和高、中、低剂量魔芋多糖与高脂联合处理组共5个组,连续喂饲20天,用ELISA法测定血清瘦素水平,分光光度法测定小肠粘膜Na+-K+-ATP酶活性以及体重、体脂、血糖等指标。结果第10天高脂对照组的体重和餐后血糖为(31.3±2.11)g和(7.5±1.15)mmol/L,魔芋多糖高剂量组则为(28.0±2.06)g和(4.8±0.73)mmol/L。第20天高脂对照组的血清瘦素浓度和小肠粘膜Na+-K+与高脂联合处理-ATP酶活性为(1078.5±61.69)pg/ml和(16.2±1.48)μmolPi/(mg pro·h),魔芋多糖高剂量与高脂联合处理组则为(820.5±58.52)pg/ml和(11.2±1.10)μmolPi/(mgpro·h)。两组间各项指标差别均有显著性意义(P<0.05)。结论魔芋多糖能够降低高脂饮食小鼠餐后血糖、血清瘦素水平和小肠粘膜Na+-K+-ATP酶活性,抑制体重和体脂的增加。     

bFGF对慢性酒精中毒大鼠脑和肝组织ATP酶活力的影响

[目的]观察碱性成纤维细胞生长因子(bFGF)对慢性酒精中毒大鼠脑组织及肝组织Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力,探讨bFGF对慢性酒精中毒所致的脑损伤、肝损伤的保护作用。[方法]选择成年Wistar雄性大鼠,采用白酒灌胃建立慢性酒精中毒模型,慢性酒精中毒模型建立成功的大鼠随机抽签法分为酒精中毒对照组、生理盐水(NS)对照组和bFGF治疗组,每组10只。另10只不灌白酒作为正常对照组。bFGF治疗组大鼠白酒灌胃的同时,1 h后按12μg/kg剂量肌肉注射,共14 d。各组大鼠到相对应的时间点取出各组大鼠脑组织、肝组织制成匀浆,测定脑组织、肝组织匀浆中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力。[结果]与正常对照组相比,慢性酒精中毒后大鼠脑组织及肝组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显降低(P﹤0.01);经bFGF治疗后脑组织及肝组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于酒精中毒对照组及NS对照组(P﹤0.05)。[结论bFGF能提高慢性酒精中毒脑组织和肝组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,提示bFGF对慢性酒精中毒所致的脑损伤和和肝损伤具有保护作用。     

补充烟酰胺与硫胺素对肥胖大鼠体重和能量代谢的影响

目的观察硫胺素和烟酰胺对高脂饲料诱导的肥胖大鼠能量代谢酶活性的影响。方法采用预防肥胖模型法,2×2析因设计分为4组:高脂对照组(F0),高脂+硫胺素(F1),高脂+烟酰胺(F2),高脂+硫胺素+烟酰胺(F3),每组大鼠12只,高脂饲料喂养;同时每天给予硫胺素100mg/kg bw、烟酰胺250mg/kg bw灌胃,F0组自来水灌胃;设正常对照组(C)12只,普通饲料喂养,自来水灌胃,15w后处死大鼠,检测干预前后红细胞能量代谢酶活性。结果经15w喂养后,F0组大鼠体重比C组平均增加了15.7%;而F2及F3组与F0相比,体重分别降低了35.0%和30.0%(P<0.05);比C组大鼠平均体重分别下降了22.8%和17.0%(P<0.05);而F组大鼠体重未见明显降低(P>0.05)。红细胞能量代谢酶结果显示:与F0组大鼠相比,C组红细胞转酮醇酶活力系数(ETKAC)降低了86.55%,Na+-K+-ATPase活性升高了40.54%;F1、F2及F3组,ETKAC分别降低了87.89%、95.07%和86.25%,转酮醇酶(TK)活性显著升高(P<0.05);Na+-K+-ATPase活性分别升高了49.55%、122.17%和57.84%(P<0.05)。结论烟酰胺补充可抑制大鼠体重增长,而硫胺素作用不明显;但二者均可使TK、Na+-K+-ATPase的活性增强,影响机体能量代谢。     

鱼油饮食对肥胖模型大鼠胰岛素敏感性的影响因素分析

[目的]探讨鱼油饮食对高脂诱导肥胖模型大鼠胰岛素敏感性的影响及其与血清瘦素、TNF-α、IL-6水平变化的关系.[方法]高脂诱导肥胖模型大鼠,按体重分为两组：高脂组和鱼油组,分别饲以相应饲料,共4周,检测各项指标.[结果]与对照组相比,高脂组血清瘦素、IL-6、I/G比值显著增高,I/G比值与血清瘦素、IL-6密切相关,血清TNF-α无增高;鱼油饮食显著降低血清IL-6水平,一定程度上降低了血糖（15%,P=0.067）,但血清瘦素、胰岛素、TNF-α、I/G比值无显著降低,I/G比值与瘦素仍然有显著的相关关系.[结论]肥胖大鼠血清瘦素、IL-6水平增高,可能参与了肥胖相关胰岛素抵抗;鱼油饮食能显著降低模型大鼠血清IL-6水平,但未能降低血清瘦素水平,高瘦素血症仍然存在可能是鱼油组大鼠胰岛素抵抗未得到显著改善的重要原因之一.     

锌对红细胞膜ATP酶活性影响的研究

从体内和体外 2方面研究锌对红细胞膜 Na+ ,K+ - ATP酶和 Ca2 + ,Mg2 + - ATP酶活性的影响。健康雄性 Wistar大鼠分别喂饲低锌、常量锌和高锌饲料 (饲料锌含量分别为 2 .2、2 8、12 8mg/kg) ,2 5天后各组随机取 8只动物腹主动脉取血后处死 ,测定血清锌含量和红细胞膜 Na+ ,K+ - ATP酶和 Ca2 + ,Mg2 + - ATP酶活性 ;各组剩余 6只动物改变其锌摄入量后继续喂饲 7天后 ,观察锌对红细胞膜 2种 ATP酶活性影响的敏感性。体外实验用新鲜制备的人红细胞膜 ,在不同浓度锌 (0、5、10、5 0、10 0和 5 0 0 μmol/L)溶液中温浴 ,观察 2种 ATP酶活性的变化趋势。结果表明 ,锌对红细胞膜的 2种 ATP酶活性均有影响 ,锌浓度过低或过高可抑制酶活性。与 Na+ ,K+ - ATP酶相比 ,Ca2 + ,Mg2 + - ATP酶对缺锌更敏感且补锌后不易恢复 ,但其对高锌有较强的耐受性。本次研究结果提示锌对于维持红细胞膜 ATP酶的正常活性有重要意义。     

Kinetic modifications of the acetylcholinesterase and (Ca2+ + Mg2+)-ATPase in rat erythrocytes by cholesterol feeding.

The influence of cholesterol on the membrane-bound acetylcholinesterase and (Ca2+ + Mg2+)-ATPase was studied in erythrocytes of five groups of male rats fed different fat-supplemented diets. Two groups of rats were fed essential fatty acid (EFA) sufficient diets with 5% lard or corn oil as the dietary fat, and two groups were fed EFA-deficient diets: a basic, fat-free diet and the same diet supplemented with 5% hydrogenated beef fat. One additional group of rats was fed a stock diet. The kinetic changes recorded were in the degree of the cooperativity of the inhibition by F- of the acetylcholinesterase and the activation by Ca2+, and by Mg2+ of the (Ca2+ + Mg2+)-ATPase. The kinetic behavior of the enzymes was only modified by cholesterol feeding when they were bound to a membrane with a high fatty acid fluidity (e.g. derived from rats fed the corn oil-supplemented diet). The enzymes from a membrane with a low fatty acid fluidity (e.g. derived from rats fed a lard-supplemented diet) were not altered by cholesterol feeding. The changes were noticeable after 24 hours of cholesterol feeding. It is suggested that the in vivo cholesterol sites are involved in a regulatory mechanism for mammalian membrane-bound enzymes.     

Interrelationship of dietary Mg intake and electrolyte homeostasis in hamsters: I. Severe Mg deficiency, electrolyte homeostasis, and myocardial necrosis

Epidemiological studies indicate a strong relationship between dietary Mg intake and the incidence of sudden cardiac death. The mechanism by which dietary Mg leads to an increased incidence of cardiovascular disease is unknown but may involve alteration of electrolyte balance. In the present study, tissue electrolyte levels and myocardial pathology were investigated in adult hamsters fed a diet containing no added Mg. Control animals were fed the same diet supplemented with Mg or standard laboratory chow. Hamsters were killed after 4, 8, 12, or 18 days on the test diet, and levels of Na, K, Ca, and Mg were measured in the serum, myocardium, bone, and kidney. The earliest change induced by the test diet was a decrease of the serum Mg and an increase in the Na concentration of the myocardium and other tissues. Following the rise in myocardial Na, the myocardial Ca rose, attaining a fourfold increase by 18 days. K fell in heart and kidney, but not significantly. Although there was no significant change in myocardial Mg, foci of myocardial necrosis, considered to be typical of acute severe Mg deficiency, were found. Myocardial necrosis and the increase in myocardial Ca occurred in parallel. Because of the pattern of observed changes in electrolyte levels, and the potential role of Ca in myocardial injury, the occurrence of myocardial necrosis in these Mg-deficient hamsters is attributable to the increased level of myocardial Ca, rather than to any change in intracellular Mg levels. It is postulated that reduced extracellular Mg levels increase [Na]i through reduction of sarcolemmal (Na+ + K+)-ATPase activity. This would lead to an increase in [Ca]i through Na-Ca exchange.     

The effect of diets adequate and deficient in calcium on blood pressures and the activities of intestinal and kidney plasma membrane enzymes in normotensive and spontaneously hypertensive rats

Basolateral and brush-border membranes were prepared from the intestines and kidneys of spontaneously hypertensive (SHR) and normotensive (WKY) rats fed on a calcium-adequate diet and assayed for their enzyme activities. In intestinal basolateral membranes the activities of Na+ K(+)-ATPase (EC 3.6.1.37) Ca2(+)-ATPase (EC 3.6.1.38) and alkaline phosphatase (EC 3.1.3.1) were lower in SHR rats when compared with WKY rats, whilst 5'-nucleotidase (EC 3.1.3.5) (a marker for basolateral membranes) was unaffected. In kidney basolateral membranes all enzymes were similar in activity in SHR and WKY rats. In intestinal brush-border membranes the activities of Ca2(+)-ATPase and alkaline phosphatase were lower in SHR rats when compared with WKY rats, whilst microvillus aminopeptidase (EC 3.4.11.2) (a marker for brush-border membranes) was unaffected. In kidney brush-border membranes all enzymes were similar in activity in SHR and WKY rats. The blood pressures of the SHR rats were considerably higher than those of the WKY rats. When SHR rats were fed on a Ca-deficient diet the activities of Na+K(+)-ATPase, Ca2(+)-ATPase and alkaline phosphatase in basolateral membranes and Ca2(+)-ATPase and alkaline phosphatase in brush-border membranes were all increased in the intestine when compared with SHR rats fed on a Ca-adequate diet. The equivalent enzymes in the kidneys of SHR rats, and the intestines and kidneys of WKY rats, were not affected by altering the Ca in the diet. The blood pressures of SHR rats fed on a Ca-deficient diet were higher than in those fed on a Ca-adequate diet. Blood pressures of WKY rats were not affected by altering the diet in this way. The results indicate that the absorption of Ca by active mechanisms may be reduced in SHR rats compared with WKY rats. Changing the level of Ca in the diet modified both blood pressure and the activities of enzymes which catalyse active Ca transport. The implications of these results to the aetiology, and possible nutritional treatment, of essential hypertension are discussed.     

姜黄素对大鼠调节血脂及抗氧化作用的研究

为研究姜黄素的降脂作用抗氧化作用,将高脂血症模型大鼠根据血总胆固醇水平随机分为４组：基础饲料对照组喂基础饲料＋姜黄素组喂加入姜黄素５ｇ／ｋｇ的基础饲料;高脂饲料对照组喂高脂饲料;高脂饲料＋姜黄素组喂加入姜黄素ｇ／ｋｇ的高脂饲料。再喂养４周,测定血脂及抗氧化指标。结果显示姜黄素能降低高脂模型大鼠血中总胆固醇、甘油三酯水平,提高载脂蛋白Ａ水平,并降低血及肝中过氧化脂质,直匀浆总抗氧化能力和ＳＯＤ活性、     

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。     

牛磺酸对应激大鼠第二信使及心肌离子含量变化的影响

目的：探索牛磺酸对应激性心肌损伤的保护机制。方法：以异丙肾上腺素诱导的大鼠应激为模型，测定心肌及血浆中第二信使ｃＡＭＰ、ｃＧＭＰ、Ｃａ２＋及心肌细胞中Ｎａ、Ｋ、Ｍｎ、Ｚｎ、Ｍｇ、Ｆｅ、Ｃｕ、Ｃｏ、Ｃｒ离子和心肌线粒体中Ｎａ、Ｋ、Ｍｎ、Ｚｎ、Ｍｇ、Ｆｅ、Ｃｕ离子含量的变化。结果：ＩＳＯ组心肌及血浆中ｃＡＭＰ、ｃＧＭＰ含量，心肌细胞中Ｃａ、Ｎａ、Ｋ离子及心肌线粒体中的Ｃａ离子含量显著高于对照组及牛磺酸组；而牛磺酸组心肌细胞中Ｍｎ、Ｚｎ、Ｍｇ、Ｆｅ、Ｃｕ及线粒体中Ｆｅ、Ｚｎ离子含量显著高于ＩＳＯ组及对照组。三组心肌组织中Ｃｏ、Ｃｒ含量未见显著差异。结论：牛磺酸可显著抑制应激大鼠第二信使水平的升高及心肌细胞和线粒体中的钙超载现象，并使心肌细胞中的Ｍｎ、Ｚｎ、Ｍｇ、Ｆｅ、Ｃｕ及线粒体中Ｆｅ、Ｚｎ离子维持在较高水平，依此来减轻大鼠的应激性心肌损伤。     

Fat Quality Influences the Obesogenic Effect of High Fat Diets

High fat and/or carbohydrate intake are associated with an elevated risk for obesity and chronic diseases such as diabetes and cardiovascular diseases. The harmful effects of a high fat diet could be different, depending on dietary fat quality. In fact, high fat diets rich in unsaturated fatty acids are considered less deleterious for human health than those rich in saturated fat. In our previous studies, we have shown that rats fed a high fat diet developed obesity and exhibited a decrease in oxidative capacity and an increase in oxidative stress in liver mitochondria. To investigate whether polyunsaturated fats could attenuate the above deleterious effects of high fat diets, energy balance and body composition were assessed after two weeks in rats fed isocaloric amounts of a high-fat diet (58.2% by energy) rich either in lard or safflower/linseed oil. Hepatic functionality, plasma parameters, and oxidative status were also measured. The results show that feeding on safflower/linseed oil diet attenuates the obesogenic effect of high fat diets and ameliorates the blood lipid profile. Conversely, hepatic steatosis and mitochondrial oxidative stress appear to be negatively affected by a diet rich in unsaturated fatty acids.     

Rutin attenuates metabolic changes, nonalcoholic steatohepatitis, and cardiovascular remodeling in high-carbohydrate, high-fat diet-fed rats

Metabolic syndrome (obesity, diabetes, and hypertension) increases hepatic and cardiovascular damage. This study investigated preventive or reversal responses to rutin in high-carbohydrate, high-fat diet-fed rats as a model of metabolic syndrome. Rats were divided into 6 groups: 2 groups were fed a corn starch-rich diet for 8 or 16 wk, 2 groups were fed a high-carbohydrate, high-fat diet for 8 or 16 wk, and 2 groups received rutin (1.6 g/kg diet) in either diet for the last 8 wk only of the 16-wk protocol. Metabolic changes and hepatic and cardiovascular structure and function were then evaluated in these rats. The corn starch-rich diet contained 68% carbohydrate (mainly cornstarch) and 0.7% fat, whereas the high-carbohydrate, high-fat diet contained 50% carbohydrate (mainly fructose) and 24% fat (mainly beef tallow) along with 25% fructose in drinking water (total 68% carbohydrate using mean food and water intakes). The high-carbohydrate, high-fat diet produced obesity, dyslipidemia, hypertension, impaired glucose tolerance, hepatic steatosis, infiltration of inflammatory cells in the liver and the heart, higher cardiac stiffness, endothelial dysfunction, and higher plasma markers of oxidative stress with lower expression of markers for oxidative stress and apoptosis in the liver. Rutin reversed or prevented metabolic changes such as abdominal fat pads and glucose tolerance, reversed or prevented changes in hepatic and cardiovascular structure and function, reversed oxidative stress and inflammation in the liver and heart, and normalized expression of liver markers. These results suggest a non-nutritive role for rutin to attenuate chronic changes in metabolic syndrome.     

断乳后低钙膳食对高脂膳食大鼠肥胖影响

目的探讨断乳后低钙膳食对高脂膳食大鼠肥胖的影响。方法80只刚断乳雄性Wistar大鼠按体重随机分为2组,分别给予低钙或正常钙膳食3周,然后以正常饲料喂养3周。第6周末各组动物又随机分成2组,分别喂饲高脂饲料和基础饲料,观察肥胖发生情况。结果断乳后低钙膳食大鼠食用高脂饲料后体脂含量、血脂、瘦素水平显著升高,高密度脂蛋白（HDL）、游离三碘甲状腺原氨酸（FT3）水平显著降低。结论断乳后给予低钙膳食可能促进高脂膳食大鼠肥胖的发生。