不同膳食脂肪酸对大鼠乳腺癌组织脂肪酸组成和脂代谢基因表达的影响

目的探讨不同膳食脂肪酸组成影响大鼠乳腺癌发生、发展的可能分子机制。方法用8种不同膳食脂肪酸组成(SFA、MUFA、n-6PUFA、n-3PUFA、1∶1n-6/n-3、5∶1n-6/n-3、10∶1n-6/n-3、1∶2∶1S/M/P其中n-6/n-31∶1)喂养SD雌性大鼠,并在大鼠乳腺癌模型的基础上,用气相色谱内标法观察大鼠乳腺组织脂肪酸组成改变,RT-PCR分析组织脂代谢调控基因(FAS、COX-2和5-LOX)的表达。结果在不同膳食脂肪酸构成中,只有1∶1n-6/n-3能有效抑制大鼠乳腺癌的发生。不同膳食脂肪酸构成可导致大鼠乳腺组织脂肪酸组成发生相应变化,且各组间的脂肪酸含量有显著差异。高乳腺癌诱发的SFA、MUFA、n-6PUFA、5∶1n-6/n-3、10∶1n-6/n-3和1∶2∶1S/M/P喂养组乳腺组织含有较多的C18∶1、C18∶2和C20∶4,而EPA和DHA含量极少。无或低乳腺癌诱发的n-3PUFA和1∶1n-6/n-3喂养组乳腺组织EPA和DHA明显增多,C20∶4含量显著减少。RT-PCR结果显示1∶1n-6/n-3低诱癌组较相应对喂组上调FAS、COX-2和5-LOXmRNA表达力度明显弱于其它高乳腺癌诱发组。结论不同膳食脂肪酸组成能明显改变大鼠乳腺组织脂肪酸组成,进而影响脂代谢基因FAS、COX-2和5-LOX表达,可能是大鼠乳腺癌发生的分子机制之一。     

n-6/n-3 PUFA对乳腺癌大鼠ER及p53表达影响

目的 探讨不同比例的n-6/n-3多不饱和脂肪酸(PUFA)对N-甲基亚硝基脲(MNU)诱导的乳腺癌大鼠乳腺组织中雌激素受体(ER)和p53表达的影响。方法 雌性SD大鼠随机分为n-6 PUFA、10:1 n-6/n-3、5:1n-6/n-3、1:1 n-6/n-3和正常对照5组,前4组以50mg/(kg·bw)MNU单次腹腔注射诱导乳腺肿瘤发生,正常对照组注射等体积无菌生理盐水。给药后立即分组喂养不同饲料,在8和18周时处死动物,RT-PCR和蛋白印迹(Western blot)技术检测各组大鼠乳腺组织ER和p53表达。结果 4组乳腺癌大鼠乳腺组织中ER和p53的表达均较正常对照组((0.73±0.11),(0.08±0.01))有所升高,其中n-6组最高((1.32±0.18),(1.43±0.56)),其余各组随n-6/n-3比值减小而下降,1:1 n-6/n-3组((0.95±0.12),(0.12±0.06))显著低于n-6组(P<0.05)。结论 不同比例n-6/n-3多不饱和脂肪酸对MNU诱导的乳腺癌大鼠乳腺组织ER和p53的表达具有不同影响,1:1 n-6/n-3膳食脂肪酸构成能有效抑制乳腺癌大鼠乳腺组织ER和p53表达的升高。     

中国成人膳食脂肪酸摄入和食物来源状况分析

目的分析我国成人膳食脂肪酸摄入量及主要脂肪酸的食物来源。方法利用2002年中国居民营养与健康状况调查中3d24h回顾膳食调查结果,结合食物成分表中脂肪酸数据及补充测定的34种食物脂肪酸数据,对44905名成人(不包括孕妇和乳母)的膳食脂肪酸摄入量及食物来源进行分析。结果城市居民饱和脂肪酸(SFA)、单不饱和脂肪酸(MUFA)和多不饱和脂肪酸(PUFA)摄入量中位数分别为15.9、23.6和20.2,农村居民分别为13.8、23.4和13.7g/d;城市居民α亚麻酸(ALA)、二十碳五烯酸(EPA)、二十二碳六烯酸(DHA)、亚油酸(LA)和花生四烯酸(AA)摄入量中位数分别为2.3g/d、1.8mg/d、22.1mg/d、17.6g/d、45.4mg/d,农村居民分别为1.3g/d、0.0mg/d、6.0mg/d、11.3g/d、43.1mg/d。城市、农村居民膳食中S/M/P比值分别为1:1.4:1.3和1:1.5:1.1;n-6/n-3系列多不饱和脂肪酸比例分别为7.6和8.0。全国居民SFA、MUFA和PUFA供能百分比中位数分别为6.1、9.8和6.3。城市居民51.4%的膳食SFA来自动物性食物,农村为38.5%。城市和农村居民膳食中MUFA的主要来源是食用油和动物性食物。城市居民膳食脂肪中约50%的PUFA、n-6PUFA和n-3PUFA来自于豆油和色拉油;农村PUFA和n-6系列PUFA来源广泛。农村居民膳食n-3PUFA近一半来自于菜籽油。结论城乡居民SFA、MUFA、PUFA的摄入比例合理;与参考摄入量相比,城乡居民n-6/n-3PUFA比例偏高,应增加膳食中n-3系列PUFA摄入量所占比例。     

膳食脂肪酸对正常和携瘤小鼠血浆脂肪酸谱的影响

目的研究膳食中的脂肪酸对正常和携瘤小鼠血浆脂肪酸谱的影响并研究肿瘤代谢是否影响血浆脂肪酸谱。方法正常(无瘤)鼠和携瘤鼠在两个独立的实验中分别进行。每个实验均包含普通餐和4种高脂餐。这些高脂餐均含20%(质量比w/w)的脂肪,因脂肪来源的不同而分别富含饱和脂肪酸(SFA,月桂酸C12:0和肉豆蔻酸C14:0),单不饱和脂肪酸(MUFA,油酸C18:1),n-6多不饱和脂肪酸(n-6PUFA,亚油酸C18:2)和n-3多不饱和脂肪酸(n-3PUFA,亚麻酸C18:3)。在正常鼠实验中,20只雄性Balb/C小鼠被随机分成普通饲料对照(NC)组和4个高脂餐组(即SFA组、MUFA组、n-6PUFA组、n-3PUFA组),用相应的饲料喂养6w。在另一实验中,48只雄性Balb/C裸鼠被随机分成2个正常饲料组和4个高脂餐组。将Mia Pa Ca2人胰腺癌细胞移植到除一个普通饲料组外的5组裸鼠皮下。将6组动物用相应的饲料喂养7w。每一实验结束后,用气相色谱的方法分析血浆脂肪酸谱的变化。结果以普通餐组为对照组,血浆脂肪酸变化如下:(1)在无瘤和携瘤两种状态下,属于SFA的C12:0和C14:0含量在SFA组增高(P0.01)而属于MUFA的C18:1在MUFA组增高(P0.01)。(2)在无瘤状态下,属于n-6PUFA的C18:2在n-6PUFA组没有显著变化(P0.05),且与n-3PUFA组相比还有降低。而在携瘤状态下,C18:2的含量在n-6PUFA组却有增高趋势。(3)在无瘤和携瘤两种状态下,属于n-3PUFA的C18:3的含量在n-3PUFA组增高(P0.01)。结论 1.当无瘤鼠进食4种高脂餐时,餐中富含的SFA,MUFA和n-3PUFA可在血浆中增高,而餐中富含的n-6PUFA则不高。2.携瘤鼠对实验餐的反应与无瘤鼠大体相同,但n-6PUFA高脂餐也可增进携瘤鼠血浆中的n-6PUFA。3.癌细胞对n-6PUFA代谢的影响导致了血浆n-6PUFA在无瘤和携瘤鼠间的差异,该差异可能对癌症的诊断和治疗有所帮助。     

膳食脂肪酸对胰腺癌小鼠骨骼肌和肝脏细胞中脂肪酸构成的影响（英文）

目的探讨含不同类型脂肪酸的高脂膳食对荷胰腺癌小鼠骨骼肌和肝脏细胞中脂肪酸构成的影响。方法将60只健康5w龄雄性C57BL/6裸鼠随机分为6组:饱和脂肪酸(SFA)组、单不饱和脂肪酸(MUFA)组、n-6多不饱和脂肪酸(n-6 PUFA)组、n-3多不饱和脂肪酸(n-3 PUFA)组、等能量对照(ISO-C)组和正常对照(NC)组。四个高脂膳食组用四种高脂(15%g/100g)饲料分别喂养,其油脂来源分别为椰子油(富含SFA),橄榄油(富含MUFA),大豆油(富含n-6 PUFA)和亚麻籽油(富含n-3 PUFA)。ISO-C组和NC组的饲料含4%⁵%的大豆油。各组裸鼠在用各自的试验饲料喂养1w后,将HPAF-Ⅱ胰腺癌细胞接种到胰腺内,继续该饲料喂养至第14w末。处死小鼠,取股四头肌和肝组织,用气相色谱-质谱联用仪分析脂肪酸构成。结果骨骼肌和肝脏的脂肪酸构成在ISO-C组和NC组之间大致相同,以ISO-C组为对照组,我们发现小鼠骨骼肌脂肪酸的变化如下:(1)属于饱和脂肪酸的棕榈酸(C16:0)、十七烷酸(C17:0)、硬脂酸(C18:0)和花生酸(C20:0)的含量在SFA组增高(P<0.05);(2)属于单不饱和脂肪酸的油酸(C18:1)的含量在MUFA组增高(P<0.05);(3)属于n-6多不饱和脂肪酸的γ-亚麻酸(γC18:3)的含量在n-6 PUFA组增高(P<0.05);(4)属于n-3多不饱和脂肪酸的亚麻酸(C18:3)、二十碳五烯酸(C20:5)和二十二碳五烯酸(C22:5)的含量在n-3 PUFA组增高(P<0.05)。小鼠肝脏脂肪酸的构成结果显示:(1)饱和脂肪酸的含量在SFA组没有增高;(2)单不饱和脂肪酸中仅二十烯酸(C20:1)的含量在MUFA组增高(P<0.05);(3)n-6多不饱和脂肪酸二十碳二烯酸(C20:2)和花生四烯酸(C20:4)的含量在n-6 PUFA组增高(P<0.05);(4)亚麻酸(C18:3)、二十碳五烯酸(C20:5)、二十二碳五烯酸(C22:5)和二十二碳六烯酸(C22:6)的含量在n-3 PUFA组均增高(P<0.05)。结论荷瘤小鼠进食由不同类型脂肪酸组成的高脂膳食后,骨骼肌脂肪酸的构成反映了饲料脂肪酸的构成,而肝脏脂肪酸的构成与饲料脂肪酸的构成仅部分相同。     

不同水产品消费地区孕妇脂肪酸摄入量调查

目的分析我国不同水产品消费地区孕妇脂肪酸摄入状况。方法应用食物频率法分别在淡水产品消费量较高的江苏省句容市、海产品消费量较高的山东省即墨市以及水产品消费量很低的河南省辉县市,对180名22~35岁孕妇进行妊娠中、晚期膳食调查,分析脂肪酸摄入状况。结果句容、即墨、辉县孕妇膳食中饱和脂肪酸(SFA),单不饱和脂肪酸(MUFA),多不饱和脂肪酸(PUFA)的比例分别为1:2.50:1.05、1:1.44:1.31、1:1.48:1.24。n-6PUFA/n-3PUFA分别为5.51、17.62、13.85。辉县孕妇膳食中SFA和n-6PUFA摄入量最高;句容孕妇膳食中MUFA和n-3PUFA摄入量最高;即墨孕妇膳食中二十碳五烯酸(EPA,20:5n-3)和二十二碳六烯酸(DHA,22:6n-3)摄入量最高。句容和辉县孕妇膳食中的花生四烯酸(AA,20:4n-6)摄入量均高于即墨。三地孕妇膳食中EPA和DHA均主要来自水产品;AA主要来自畜禽肉类和蛋类;亚麻酸(ALA,18:3n-3)和亚油酸(LA,18:2n-6)主要来自食用油、畜禽肉类、坚果和主食及糕点类。结论三地区SFA、MUFA、PUFA的摄入比例合理。即墨、辉县孕妇膳食中n-6/n-3PUFA比例偏高;即墨市孕妇膳食中DHA和EPA摄入量高于其它两地,但仍明显低于推荐量。建议增加孕妇膳食n-3PUFA,特别是DHA和EPA的摄入量。     

限食与不饱和脂肪酸对大鼠实验性结肠炎的影响

目的探讨限食(CR)和n-6、n-3多不饱和脂肪酸(PUFA)对大鼠溃疡性结肠炎模型的影响,以制备溃疡性结肠炎。方法 40只SD雌性大鼠按体重随机分为5组,即对照组、模型组、限食组、5∶1 PUFA自由进食组、5∶1 PUFA限食组。限食组喂食量是自由进食组的60%。喂养14周后,除对照组外,其余组给予5%葡聚糖硫酸钠(DSS)水溶液,自由饮用7 d造模。结果与自由进食组相比,限食组体重增长缓慢,尤其是5∶1PUFA限食组大鼠体重最轻(P0.05)。与模型组比,5∶1 PUFA限食组大鼠的血清MPO活性、疾病活动指数、结肠大体和组织病理学评分降低(P0.05)。与限食组比较,5∶1 PUFA限食组大鼠血清IL-6和TNF-α含量均降低,而IL-10含量升高(P0.05)。结论膳食中添加n-6与n-3比例为5∶1的PUFA和限食联合作用对DSS诱导的大鼠结肠炎有明显保护作用。     

中国18～59岁居民膳食脂肪酸的摄入状况及食物来源分析

目的 分析我国18～59岁居民膳食脂肪酸的摄入状况及食物来源。方法 利用中国成人慢性病与营养监测(2015)中3d 24h膳食调查数据,对36 118名年龄在18～59岁人群的膳食脂肪酸摄入状况及食物来源进行分析。结果我国18～59岁居民膳食总脂肪(TFA)、饱和脂肪酸(SFA)、单不饱和脂肪酸(MUFA)及多不饱和脂肪酸(PUFA)摄入量的中位数分别为62.8、15.9、27.4、16.2g/d。农村TFA和MUFA的摄入量高于城市、而SFA和PUFA的摄入量低于城市(P<0.001)。城乡居民的SFA、MUFA、PUFA之比均为1:1.5:1.1。城市和农村n-6/n-3PUFA比例分别为8.6和7.9,城市高于农村(P<0.001)。膳食SFA、MUFA和PUFA的供能百分比分别为7.8%、13.5%和8.0%。城市SFA和PUFA的供能比高于农村(P<0.001),MUFA供能比在城乡间无差异(P=0.051)。植物油和动物性食物分别提供了膳食中49.4%和30.9%的TFA、29.1%和44.6%的SFA、49.7%和33.3%的MUFA、64.6%和14....     

不同膳食脂肪酸对结肠炎大鼠作用的实验研究

目的比较三种不同膳食脂肪酸对葡聚糖硫酸钠(Dextran Sulfate Sodium,DSS)诱导大鼠溃疡性结肠炎作用,并初步探讨其可能的作用机制。方法健康雄性SD大鼠随机分为正常对照组、DSS模型组、n-6PUFA组、n-3PUFA组和反式脂肪酸组。实验开始后,正常对照组和DSS模型组均喂饲基础饲料,各干预组给予配制的干预饲料。观察大鼠体重变化和粪便性状等一般情况;生化法检测血清髓过氧化物酶(myeloperoxidase,MPO)、ELISA法测定血清白介素(Interleukin)(IL-1β、IL-6、IL-10)含量以及前列腺素E2、白三烯B4、肿瘤坏死因子α。结果与DSS模型组比较,n-3PUFA组血清IL-1β降低,IL-10升高,反式脂肪酸组与n-6PUFA组使IL-1β和IL-6升高,IL-10水平明显降低。结论 n-6PUFA组和反式脂肪酸组会加剧DSS诱导大鼠溃疡性结肠炎的作用,n-3PUFA组对结肠炎大鼠有保护作用。     

乙型肝炎病毒感染与磷脂代谢和胰岛素抵抗的相关性

目的探究乙型肝炎病毒(HBV)表面抗原水平与磷脂代谢和胰岛素抵抗的相关性。方法选取暨南大学附属第一医院2017年1月-2019年6月门诊423例代谢综合征患者为研究对象,以乙型肝炎表面抗原(HBsAg)和(或)HBV DNA结果分为HBV感染阳性组(n=95)和HBV感染阴性组(n=328),分析患者血清磷脂脂肪酸构成谱[饱和脂肪酸(SFA)、单不饱和脂肪酸(MUFA)、多不饱和脂肪酸(PUFA)]以及胰岛素抵抗相关指标[空腹血糖(FBG)、空腹胰岛素(FINS),胰岛素敏感指数(ISI)和胰岛素抵抗指数(HOMA-IR)],并采用Spearman分析乙型肝炎表面抗原水平与磷脂脂肪酸构成谱、胰岛素抵抗相关指标的相关性。结果 HBV感染阳性组患者血清中SFA、n-6/n-3PUFA水平高于HBV感染阴性组,n-6PUFA、n-3PUFA、PUFA、PUFA/SFA水平均低于HBV感染阴性组,比较差异有统计学意义(P0.05); HBV感染阳性组患者FBG、HOMA-IR水平高于HBV感染阴性组,FINS、ISI低于HBV感染阴性组,比较差异有统计学意义(P0.05); Spearman相关性分析显示,HBsAg水平与SFA、n-6/n-3PUFA呈正相关,与n-3PUFA、n-6PUFA、PUFA、PUFA/SFA呈负相关,与MUFA无相关;HBsAg水平与FBG、HOMA-IR呈正相关,与FINS、ISI呈负相关。结论 HBV感染可能会引起代谢综合征患者血清磷脂脂肪酸构成改变以及胰岛素抵抗。     

Effects of Different Dietary Fatty Acids on the Fatty Acid Compositions and the Expression of Lipid Metabolic-Related Genes in Mammary Tumor Tissues of Rats

In this study, the effects of dietary fatty acids on the fatty acid compositions and lipid metabolic-related genes expression in N-methyl-N-nitrosourea (MNU)-induced rat mammary carcinogenesis were evaluated. The 50-day-old female Sprague-Dawley rats were intervened by different dietary fats (15% wt/wt), including saturated fatty acid (SFA), monounsaturated fatty acid (MUFA), n-6 polyunsaturated fatty acid (PUFA), n-3 PUFA, 1:1 n-6/n-3, 5:1 n-6/n-3, 10:1 n-6/n-3, and 1:2:1 S/M/P (1:1 n-6/n-3), alone or in combination with MNU. There was no mammary tumor occurrence in the control and MNU-treated n-3 PUFA groups after 18 wk. n-3 PUFA diet retarded the weight growth of rats. 1:1 n-6/n-3 diet significantly reduced the MNU-induced tumor incidence and tumor multiplicity compared with SFA, MUFA, n-6 PUFA, 5:1 n-6/n-3, 10:1 n-6/n-3 and 1:2:1 S/M/P diets (42.86% vs. 83.33%–92.31%, 0.79 vs. 2.62–2.85, P < 0.01). Additionally, 1:1 n-6/n-3 diet substantially increased cis-5,8,11,14,17-eicosapentaenoic acid and cis-4,7,10,13,16,19-docosahexaenoic acid levels, whereas it decreased C20:4 level and the mRNA expressions of fatty acid synthase, Cyclooxygenase-2 (COX-2), and 5-lipoxygenase (5-LOX) in mammary tissues (P < 0.05). These results suggest that 1:1 n-6/n-3 in the diet is effective in the prevention of mammary tumor development by increasing the n-3 PUFA content and reducing the expression of lipid metabolic-related genes.     

不同膳食脂肪酸对大鼠乳腺癌细胞核受体基因表达的影响

目的 探讨核受体基因表达在不同膳食脂肪酸影响大鼠乳腺癌发生中的作用。方法用8种不同膳食脂肪酸（饱和脂肪酸、单不饱和脂肪酸、n-6多不饱和脂肪酸、n-3多不饱和脂肪酸、1：1n-6／n-3多不饱和脂肪酸、5：1n-6／n-3多不饱和脂肪酸、10：1n-6／n-3多不饱和脂肪酸、1：2：1饱和脂肪酸／单不饱和脂肪酸／多不饱和脂肪酸其中n-6／n-3多不饱和脂肪酸1：1）喂养SD雌性幼年大鼠,采用50mg／kg的甲基亚硝基脲单次腹腔注射诱导大鼠乳腺癌发生,电镜观察大鼠乳腺细胞结构变化,BrdU体内标记法检测大鼠乳腺细胞增殖活性,RT—PCR分析乳腺组织过氧化物酶增殖活化受体（PPARβ和PPARγ）mRNA表达。结果 无乳腺癌诱发的各对照和n-3多不饱和脂肪酸诱癌组大鼠乳腺细胞超微结构正常,细胞增殖活性低。而有大鼠乳腺癌诱发的组织细胞内可见明显的腺癌标志,且高乳腺癌诱发的饱和脂肪酸、单不饱和脂肪酸、n-6多不饱和脂肪酸、5：1n-6／n-3多不饱和脂肪酸、10：1n-6／n-3多不饱和脂肪酸和1：2：1饱和脂肪酸／单不饱和脂肪酸／多不饱和脂肪酸喂养组大鼠乳腺细胞增殖活性升高（BrdU阳性率为21％～22％）,但1：1n-6／n-3多不饱和脂肪酸低诱癌组乳腺细胞增殖活性明显降低上述高乳腺癌诱发组（BrdU阳性率为13％,P〈0．05）。此外,过氧化物酶增殖活化受体作为与脂代谢密切相关的细胞核受体基因,1：1n-6／n-3多不饱和脂肪酸低诱癌组较相应对照组上调PPARβ和PPARγ mRNA表达力度明显弱于高乳腺癌诱发组。结论 不同膳食脂肪酸对PPAR基因表达的调节截然不同,这可能是差异性调节大鼠乳腺癌发生的分子机制之一。     

不同脂肪酸构成比对小鼠血脂影响的实验研究

目的:以小鼠饲料正常脂肪摄入量7.84%为基础,比较不同脂肪酸构成比对小鼠血脂水平的影响。方法:以小鼠正常饲料脂肪及脂肪酸构成为对照,分别设S/M/P比值为1∶1.7∶1.2和1∶1∶1的饲料,其中n-6/n-3比值在1～10∶1各设计4组,共10组, 喂小鼠10 w,测定血脂水平。结果: S/M/P为1∶1.7∶1.2, n-6/n-3在1～5∶1时TC和TC/HDL-C水平显著低于8∶1和10∶1组(P<0.05); S/M/P为1∶1∶1,n-6/n-3为1∶1时的TC和LDL-C水平显著低于其余各比值组(P<0.05);当n-6/n-3为10∶1时,S/M/P为1∶1.7∶1.2的TC、LDL-C、HDL-C以及TC/HDL-C和LDL-C/HDL-C水平均显著低于1∶1∶2组(P<0.05),S/M/P为1∶1∶2的LDL-C和TC/HDL-C水平显著低于1∶1∶1组(P<0.05)。结论: S/M/P现状1∶1.7∶1.2时,n-6/n-3在1～5∶1可维持血脂在较低水平;如脂肪酸构成比为1∶1∶1时,维持较低血脂所需的n-6/n-3为1∶1;在现状膳食n-6/n-3为10∶1时,S/M/P在1∶1.7∶1.2有利于维持低血脂。     

Effects of different quantities of fat on serum and liver lipids, phospholipid class distribution and fatty acid composition in alcohol-treated rats

The present study investigated the quantitative effect of dietary fats and ingestion of alcohol on serum and liver lipids, fatty acid bound to phospholipids and their class distribution of male Wistar rats. The rats in C (control) and A (alcohol) groups were fed a standard laboratory diet, HFC (high fat-control) and HFA (high fat-alcohol) groups were fed a high fat diet (standard diet supplemented with 20 g%w/w, sunflower oil: lard mixture 1: 1) for 6 wk. Alcohol-treated rats consumed alcohol at the rate of 9 g/kgbw/d (15-20% energy). Liver phospholipid (PL) content was decreased, and phospholipid/cholesterol liver molar ratio increased in the alcohol treated rats. The proportion of serum sphingophospholipid (Sph) was significantly lower and proportion of phosphatidylcholin (PC) significantly higher in serum PL in alcohol-treated rats. Phospholipid class distribution was unaffected by alcohol feeding in liver. Significantly lower levels of 16:1n-7 and higher levels of 20:5n-3 and 22:4n-6 in the serum PL were observed in the alcohol-treated rats. The groups on the HF diet increased levels of 20:4n-6, 22:4n-6 and total n-6, polyunsaturated fatty acid (PUFA) and decreased levels of 18:1n-9 and total monounsaturated fatty acids (MUFA)in both liver and serum PL, but n-3 fatty acid increased in serum PL and decreased in liver PL compared to groups on the standard diet. Alcohol fat interaction was evident in MUFA and PUFA/SFA in serum PL and n-6, MUFA, PUFA and polyunsaturated/saturated fatty acid ratios (PUFA/SFA) in liver PL. This study showed that the high fat intake in alcohol-treated rats increased levels of 20:4n-6, 22:4n-6 and 20:4/18:2 ratio, and decreased level of 18:1n-9 in liver and serum phospholipids.     

The cholesterolaemic effects of dietary fats in cholesteryl ester transfer protein transgenic mice.

In order to investigate the role of cholesteryl ester transfer protein (CETP) in the cholesterolaemic response to dietary fats, we analysed plasma lipid profiles of CETP-transgenic and control C57BL/6 mice fed standard chow (AIN-93G; AIN), a low-fat diet, and diets high in butter (saturated fatty acids; SFA), high-oleic acid safflower oil (monounsaturated fatty acids; MUFA), and safflower oil (polyunsaturated fatty acids; PUFA) for 5 weeks. Each group contained four or five mice. There were significant diet and dietxgenotype effects on plasma total cholesterol (TC; and respectively), liver TC ( and respectively), and esterified cholesterol (EC; and respectively); diet effects on plasma triacylglycerol liver free cholesterol and body weight a genotype effect on body-weight gain and a dietxgenotype effect on energy intake In transgenic mice the SFA diet caused significantly higher plasma TC than the PUFA diet In control mice MUFA and PUFA diets, but not the SFA diet, caused significantly higher plasma TC than the low-fat and AIN diets Transgenic mice fed PUFA had lower plasma TC while transgenic mice fed MUFA had lower LDL+VLDL-cholesterol than controls in the same dietary groups. Transgenic mice fed MUFA and PUFA diets also had significantly higher liver TC and respectively) and EC and respectively) than controls fed the same diets. In the present study we showed that: (1) CETP transgenic mice had a cholesterolaemic response to dietary fats similar to that in human subjects; (2) CETP transgenic mice fed PUFA showed significantly lower plasma TC, while those fed MUFA had lower LDL+VLDL-cholesterol than controls; (3) hepatic accumulation of cholesterol, possibly resulting from the combination of the enhanced cholesteryl ester transfer to apolipoprotein B-containing lipoproteins and increased hepatic uptake of cholesterol, may contribute to the cholesterol-lowering effect of MUFA and PUFA in CETP-transgenic mice; (4) CETP may play a role in appetite and/or energy regulation.     

Influence of high-fat diet from differential dietary sources on bone mineral density, bone strength, and bone fatty acid composition in rats

Previous studies have suggested that high-fat diets adversely affect bone development. However, these studies included other dietary manipulations, including low calcium, folic acid, and fibre, and (or) high sucrose or cholesterol, and did not directly compare several common sources of dietary fat. Thus, the overall objective of this study was to investigate the effect of high-fat diets that differ in fat quality, representing diets high in saturated fatty acids (SFA), n-3 polyunsaturated fatty acids (PUFA), or n-6 PUFA, on femur bone mineral density (BMD), strength, and fatty acid composition. Forty-day-old male Sprague-Dawley rats were maintained for 65?days on high-fat diets (20% by weight), containing coconut oil (SFA; n = 10), flaxseed oil (n-3 PUFA; n = 10), or safflower oil (n-6 PUFA; n = 11). Chow-fed rats (n = 10), at 105?days of age, were included to represent animals on a control diet. Rats fed high-fat diets had higher body weights than the chow-fed rats (p?< 0.001). Among all high-fat groups, there were no differences in femur BMD (p?> 0.05) or biomechanical strength properties (p?> 0.05). Femurs of groups fed either the high n-3 or high n-6 PUFA diets were stronger (as measured by peak load) than those of the chow-fed group, after adjustment for significant differences in body weight (p = 0.001). As expected, the femur fatty acid profile reflected the fatty acid composition of the diet consumed. These results suggest that high-fat diets, containing high levels of PUFA in the form of flaxseed or safflower oil, have a positive effect on bone strength when fed to male rats 6 to 15?weeks of age.     

Dietary docosahexaenoic acid suppresses N-methyl-N-nitrosourea-induced mammary carcinogenesis in rats more effectively than eicosapentaenoic acid

We compared the effects of identical amounts but different proportions of dietary n-3 polyunsaturated fatty acids (PUFAs) on N-methyl-N-nitrosourea (MNU)-induced mammary cancer in a rat model. The ability of dietary docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) to suppress mammary cancer was evaluated. Female Sprague-Dawley rats were randomly assigned to three groups and maintained on diets containing 10% fatty acid consisting of EPA, a 1:1 mixture of EPA-plus-DHA, or DHA. The experimental diet was started after administration of MNU at 49 days of age, and the rats were maintained on the respective diets until the largest mammary tumor reached >1 cm in diameter or until the end of the study period (20 wk after MNU). All histologically detected mammary carcinomas were evaluated, irrespective of size. The DHA diet was associated with significant suppression of the carcinogenic effect of MNU compared with the EPA and EPA-plus-DHA diets: tumor incidence decreased to 23% (3/13) compared with 73% (11/15) and 65% (12/17) (P < 0.01 and P < 0.05, respectively); tumor multiplicity decreased to 0.23 compared with 1.67 and 1.59 (P < 0.01 and P < 0.05, respectively). There was no significant difference in tumor latency among the DHA, EPA, and EPA-plus-DHA groups (119, 105, and 117 days, respectively). Over 20 wk, the fatty acid composition of serum and mammary fat tissue reflected differences in the dietary n-3 PUFAs. Although DHA suppressed MNU-induced mammary carcinogenesis more effectively than EPA, generalized steatosis including mammary fat tissue appeared in all three groups.     

不同n-3/n-6多不饱和脂肪酸构成比对大鼠脂代谢和食欲的影响

目的研究不同n-3/n-6配比脂肪酸对大鼠食欲影响及其与腺苷酸活化蛋白激酶(AMPK)基因表达的关系。方法58只SD大鼠适应性喂养7天后,尾静脉取血。根据血清总胆固醇(TC)水平随机分为6组:空白组(基础饲料),高脂组(高脂饲料),高脂1∶1组(高脂饲料+n-3/n-6=1∶1油),高脂1∶5组(高脂饲料+n-3/n-6=1∶5油),低脂1∶1组(脱脂基础饲料+n-3/n-6=1∶1油),低脂1∶5组(脱脂基础饲料+n-3/n-6=1∶5油),喂养45天,观察大鼠摄食与体重增长,并于实验第0、15、30和45天测定血清总胆固醇(TC)和甘油三酯(TG)含量。于45天处死动物,取下丘脑,用RT-PCR分别测下丘脑组织中NPY、AMPK-α2 mRNA表达。结果添加PUFA的四个组血清TC、TG、摄食量、体重及NPY、AMPK-α2mRNA表达均比高脂组大鼠明显降低(P<0.05)。结论PUFA改善血脂可能是通过影响AMPK表达,从而抑制下丘脑食欲相关基因表达,进而影响血脂代谢。     

饲料脂肪酸组成对大鼠胃肠等肿瘤生成的影响

目的：　研究脂肪酸组成对甲基亚硝基脲（ Ｍ Ｎ Ｕ） 诱导的大鼠结肠等肿瘤生成的影响。方法：　雄性 Ｓ Ｄ 大鼠喂以用牛油、豆油、紫草油、玉米油和鱼油按不同比例调配，含脂肪量为１５ ％ 的半合成饲料，分５ 组。各组脂肪酸组成为：１ 组以牛油为主富含饱和脂肪酸；２ 组以豆油为主富含亚油酸，１ 组和２ 组基本不含有ｎ ３ 系列多不饱和脂肪酸；３ 组以紫草油为主富含亚油酸，α和γ亚麻酸，ｎ ６／ｎ ３ 脂肪酸之比为４ ．５３ ；４ 组以鱼油为主富含ｎ ３ 系列多不饱和脂肪酸，ｎ ６／ｎ ３ 脂肪酸之比为０ ．７３ ；５ 组为混合油组，ｎ ６／ｎ ３ 脂肪酸之比为１ ．９５ 。对照组和实验组分别经腹腔注射磷酸盐生理盐水缓冲液和３０ ｍｇ／ｋｇ ．ｂｗ 的 Ｍ Ｎ Ｕ，每周一次，共６ 次，喂养１８０ 天。实验期控制了影响肿瘤产生的因素。结果：１ 、２ 和３ 组产生的结肠肿瘤均显著高于４组（ Ｐ＜ ０ ．０５） ，也相对高于５ 组（ Ｐ＞ ０ ．０５） ；１ 、２ 、３ 和５ 组产生的胃肿瘤也相对地高于４ 组，但是，各组之间无显著的统计学差异。除了４ 组和１ 组外，其它各组在其它部位也产生了肿瘤。结论：　 Ｍ Ｎ Ｕ 能诱导喂以不同脂肪酸组成的大鼠产生以结肠癌为主的癌症；饲?