高脂血症大鼠血液流变学及肝脏微循环的改变

目的 探讨高脂血症大鼠血液流变学及肝脏微循环的改变。方法 Wistar大鼠随机分为（1）正常组：喂普通饲料；（2）高脂血症组：喂高脂饲料4周，每组6只。于造模4周后测定血清血脂水平、体质量及肝质量与体质量之比、血液流变学和肝脏活体微循环的改变。结果 喂高脂饲料4周后肝脏体积增大，体质量及肝质量明显高于正常对照组（P〈0．01）。肝组织标本显示肝细胞肿胀、脂肪性变，肝细胞的胞浆内充满大小不等的脂滴。血清胆固醇、低密度脂蛋白较正常对照组明显增高（P〈0．01），高密度脂蛋白减少，甘油三脂变化不大；血压及血浆黏度较正常组增高明显（P〈0．05）；肝脏活体微循环观察显示肝脏微血管数明显减少，肝细胞索增大，泡沫状突起压迫周围血管，血流速度减慢，血管内有红细胞聚集和白细胞黏附。结论 短期内高脂食物的摄入可造成脂质代谢紊乱，继而发生血液流变学及肝脏微循环障碍。     

不同脂肪含量的高脂纯化配方饲料对大、小鼠代谢综合征发生的影响

 摘要： 目的 探讨不同脂肪含量的高脂纯化配方饲料对大、小鼠体重、血糖、血胰岛素、血脂、脂肪肝及白蛋白尿的影响。 方法 雄性SD大鼠及C57BL/6小鼠随机分为MS10%、MS45%和MS60%脂肪含量饲料组,喂养3个月,检测动物体重、血糖、血胰岛素水平、血脂和蛋白尿水平,以及主要脏器重量及肝脏脂质含量。 结果 与正常组（MS10%脂肪含量）相比,高脂组（MS45%和MS60%脂肪含量）动物体重显著增加,出现明显的糖耐量异常、胰岛素抵抗和血脂水平升高,同时伴有肝脏脂质含量和蛋白尿水平的增加,并且以MS45%高脂组体重增加及胰岛素抵抗更加显著。 结论 MS45%和MS60%高脂配方饲料均可在大、小鼠较好地诱导代谢综合征的发生,而且前者优于后者。 关键词： 高脂饲料;胰岛素抵抗;肥胖;代谢综合征     

活血降脂方对小鼠脂肪肝的防治作用

目的:探讨活血降脂方对小鼠脂肪肝的防治作用及机制。方法:高脂饲料喂养小鼠,分别用不同剂量的活血降脂方(由人参、三七、天麻组成,命名为GST)给小鼠灌胃2周,检测血脂、肝组织甘油三酯(TG)含量,并观察肝指数和肝脏病理变化,筛选出药物的最佳用药剂量。此外,小鼠分为正常对照(NC)组,喂基础饲料;模型组喂高脂饲料。12周后将模型小鼠随机分为高脂(HF)组,正常饮食(ND)组和GST组。除HF组饲高脂饲料外,其余各组饲基础饲料;GST组给予GST灌胃2周,其余各组以同等容积蒸馏水灌胃。检测血清总胆固醇(TC)、TG、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)及肝组织TC、TG含量,观察肝指数、肝组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,肝组织病理变化及过氧化物酶体增殖物激活受体α(PPARα)、细胞色素P450 2E1(CYP2E1)的mRNA表达。结果:GST可显著降低血脂、肝脂和MDA水平,增加SOD活性,明显降低肝指数并改善肝组织脂肪变性,增加肝组织PPARαmRNA表达、抑制CYP2E1 mRNA的表达。结论:GST具有有效防治脂肪肝的作用,其机制可能与上调肝组织PPARαmRNA的表达、降低血清和肝组织TG含量、下调CYP2E1 mRNA的表达以及抗脂质过氧化反应有关。     

Time course of liver lipid infiltration in ovariectomized rats: impact of a high-fat diet

OBJECTIVES: The present study was undertaken to determine the time course of liver lipid infiltration in ovariectomized (Ovx) rats and the impact of high-fat (HF; 42% kJ) feeding on this response. METHODS: In a first step, Ovx rats were compared to Sham-operated (Sham) and Ovx rats supplemented with 17beta-estradiol (OvxE2) to evaluate the effect of estrogen removal. In a second time, Ovx rats fed a HF diet (OvxHf) were compared with normally fed Ovx rats. Animals were killed after 3, 8, and 13 weeks of their respective treatment (n=8 rats/group). We measured liver triacylglycerol (TAG) content, fat pad mass, and several other plasma parameters. RESULTS: Ovariectomy resulted in the typical increase in energy intake and body weight. Liver TAG accumulation was 35, 43, and 99% higher in Ovx than in Sham rats after 3, 8, and 13 weeks, respectively. The ovariectomy-induced liver lipid infiltration was completely prevented by estrogen replacement. On the opposite, plasma TAG concentrations were lower in Ovx than in Sham and OvxE2 rats. HF feeding in Ovx rats resulted in a significant (P<0.05; 38 versus 22 mg/g at 13-week) accumulation of fat in liver as compared to normally fed Ovx rats. CONCLUSIONS: Ovariectomy results in a progressive accumulation of fat in liver over a 13-week period. In addition, HF feeding in Ovx rats lead to an even more severe liver lipid infiltration. These data indicate that the absence of estrogens in rat favours fat accretion in liver, which is highly amplified by a HF diet.     

Hepatic lipids of dogs fed on arteriosclerosis-inducing diet

Lipid composition of liver in dogs was investigated after feeding them either an arteriosclerosis-inducing diet which contained 16% hydrogenated coconut oil and 5% cholesterol, the same diet but without cholesterol supplement, or meat-chow. Animals fed the last diet did not develop vascular lesions and were regarded as controls. The composition and concentration of free fatty acid and phospholipid fractions of hepatic lipids from dogs fed either experimental diet for 4 months were similar but differed from controls. However, cholesteryl oleate, total cholesteryl ester and triglyceride concentrations were significantly higher in liver of the group with cholesterol supplement than in the group without cholesterol added to their diet. In addition, the cholesterol supplemented diet fed for 12–16 months caused greater hepatic lipid changes than those induced by the same diet in 4 months.Unlike adipose tissue, kidney, or myocardial and skeletal muscle, hepatic cholesterol esters showed a profound difference between the four month feedings of cholesterol supplemented and cholesterol free diets. These findings suggest that the liver may play a predominant regulatory role in the onset of diet-induced hyperlipemia and that exogenous cholesterol enhances the effects seen by feeding saturated medium chain fatty acids without cholesterol.Lipid changes observed in mitochondrial and microsomal fractions generally were similar, and also like those observed in lipid extracts of whole liver.     

Smooth endoplasmic reticulum proliferation and increased cell multiplication in cultured hepatocytes of the newborn rat in the presence of phenobarbital

Twenty-eight-day old male Sprague-Dawley rats were fed diets containing 2, 5, 10, 15, 25, or 50% protein and varying levels of fat and energy for 8 weeks and were then killed. The livers of rats fed the 2% lactalbumin protein diet ad libitum but not the others showed visible fat. This difference was confirmed histologically. Chemical analyses of the livers indicated that the rats fed the 2% protein diets ad libitum had experienced a substantial reduction in liver cell size but only a very slight reduction in the lipid content of each cell. As a consequence, their livers showed a net increase in the amount of lipid per g of tissue and this gave them a fatty appearance. The lipids formed large fat globules suspended in a greatly reduced amount of protoplasm; there were no fat globules outside the cells. Therefore, the fatty liver of protein deficiency was a physical phenomenon rather than a metabolic defect. Rats fed the 2% protein diets in restricted amounts also had shrunken cells but they did not manifest fatty liver because there was a relatively greater reduction in liver cell lipid than in liver cell size. There was a reduced amount of protein in the livers of rats fed 2 and 5% protein diets which can be explained by a reduction in liver RNA and in Protein/RNA ratio. Protein/RNA ratio was enhanced by starvation. Liver protein content showed a biphasic response to variation in dietary fat level with its lowest value in rats fed diets containing 11.9% fat.     

An experimental study of microscopic and submicroscopic lipid inclusions in hepatic cells of the mouse

Lipid spherules of microscopic (1-μ) and submicroscopic (300–1000 A) dimensions were studied by electron microscopy in livers of mice that were normally fed, fasted, fasted and refed, or fed fat-free or high-fat diets. Tissues were fixed by perfusion with osmium and post-osmicated at 37°C. Submicroscopic inclusions were present in Golgi complex, endoplasmic reticulum, cytoplasmic vesicles near space of Disse, and in the space itself. The lipid of these inclusions was sufficiently unsaturated to be fixed and rendered insoluble by postosmication in all animals save those that were fed a diet rich in saturated fat or a fat-free high-carbohydrate diet (which induces synthesis of saturated fatty acids); in animals fed the two latter diets, the central mass of the inclusions escaped fixation and was dissolved during dehydration and imbedding. The inclusions were thus shown to reflect the character of the fatty acids most freely available in the cytoplasm of the hepatic cell in a given physiological state. On the basis of morphological and biochemical considerations, the submicroscopic inclusions were identified as secretion antecedents, elaborated by the liver for export to the blood. The larger lipid inclusions, which did not dramatically reflect changes in the degree of saturation of fatty acids available in the liver cell, were concluded to represent a more stable storage pool of hepatic-cell neutral lipid.     

高脂血症大鼠心脏、主动脉和肝脏组织中HSPA12B的表达

目的观察高脂饲料喂养的大鼠心脏、主动脉和肝脏组织中热休克蛋白A12B(HSPA12B)的表达。方法模型组和对照组SD大鼠分别经高脂饲料和普通饲料喂养16周后,测定血清总胆固醇(TC)及三酰甘油(TG);病理学观察心脏、主动脉和肝脏;用RT-PCR检测心脏、主动脉和肝脏中HSPA12BmRNA水平,用免疫组织化学法检测其蛋白表达。结果模型组总胆固醇和三酰甘油分别达(15.46±4.66)mmol/L、(0.69±0.20)mmol/L,较对照组明显升高(P<0.05);病理学观察发现模型组形成高脂性心脏病变及肝脏脂肪变性;模型组心脏、主动脉和肝脏组织中HSPA12BmRNA的表达显著高于对照组(P<0.01);模型组HSPA12B呈较强阳性表达(P<0.05)。结论高脂饲料喂养能使大鼠形成高脂血症,并引起心脏、主动脉和肝脏中HSPA12B的表达升高。     

小檗碱对NAFLD大鼠肝组织氧化损伤及SIRT1/p53通路的影响

目的:研究小檗碱对非酒精性脂肪性肝病(NAFLD)大鼠肝组织氧化损伤及沉默信息调节因子2同源蛋白1(SIRT1)/p53通路的影响,探讨小檗碱抗NAFLD的作用机制。方法:选用SPF级雄性SD大鼠24只,按随机数字表均分为正常组、模型组与小檗碱组,正常组给予基础饲料喂养,模型组及小檗碱组给予高脂饲料喂养,造模同时小檗碱组给予小檗碱(100 mg·kg~(-1)·d~(-1))灌服。16周后处死大鼠并采集肝脏,检测肝组织中总胆固醇(TC)和甘油三酯(TG)含量,超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量及总抗氧化能力(T-AOC);HE、油红O染色与透射电镜观察肝脏组织学的改变;Western blot检测大鼠肝组织SIRT1、p53及乙酰化p53(Ac-p53)蛋白水平。结果:与模型组相比,小檗碱组大鼠肝组织TC、TG和MDA含量水平显著降低(P0.05或P0.01),而SOD活力和T-AOC显著升高(P0.01);组织学结果也观察到小檗碱组大鼠肝脏脂质蓄积状态明显减轻;小檗碱组肝组织SIRT1蛋白表达水平较模型组显著上调(P0.05),Ac-p53蛋白表达水平下调(P0.05)。结论:小檗碱能减轻高脂饮食诱导的NAFLD大鼠肝脏脂肪变性和氧化应激损伤,其作用机制可能是通过上调SIRT1蛋白的表达,从而抑制p53的乙酰化。     

高脂血症大鼠心肌中脂滴分布和H-FABP表达变化

目的　观察高脂血症大鼠心肌细胞脂滴含量和心功能,以及心型脂肪酸结合蛋白（heart type fatty acid binding protein,H-FABP）的表达。 方法　高脂饲料喂养SD雄性大鼠,建立高脂血症模型。饲养后4周、8周、12周,分别进行心功能检测后取出心,制作冰冻切片,光学显微镜观察脂滴在心肌的分布（油红O染色）,透射电镜观察心肌组织脂滴;采用免疫组织化学、免疫荧光、免疫印迹检测心肌细胞和心肌组织中H-FABP的表达。 结果　与普通饮食大鼠相比,高脂饮食大鼠血清甘油三酯和总胆固醇明显升高,在第12周升高最为明显,并伴有射血分数的明显下降;心肌细胞内脂滴含量增多,第4周增多最为显著,第8周、第12周逐渐减少;心肌细胞和心肌组织中H-FABP在第8周、第12周表达明显增加。 结论　高脂血症大鼠心肌发生脂肪变性,随着血脂浓度升高脂肪变性减轻,心功能降低,这一变化可能与H-FABP表达增多,增加心肌细胞内脂肪酸氧化有关。     

Food restriction and refeeding induces changes in lipid pathways and fat deposition in the adipose and hepatic tissues in rats with diet-induced obesity

The aim of this study was to determine the effects of successive cycles of a moderately restrictive diet and refeeding with a high-fat diet on the metabolism of the adipose and hepatic tissues of obese rats. Rats were assigned to the following groups: a chow diet; a high-fat diet; a moderate caloric restriction; or a moderate caloric restriction plus refeeding. Some animals in each group were given [1-(14)C]triolein intragastrically, while others received an intraperitoneal injection of 3 mCi (3)H(2)O. All animals were killed by decapitation. The retroperitoneal, visceral epididymal and omental white adipose tissues, brown adipose tissue, liver and blood were immediately removed. The lipid uptake from the diet, in vivo rate of lipogenesis, percentage of fat, lipid profile and leptin concentration were analysed. The high-fat diet promoted an increase in fatty liver (P ≤ 0.05), adiposity mass (P ≤ 0.05) and the plasma concentration of leptin (P ≤ 0.05) and a decreased lipid uptake in white adipose tissue depots (P ≤ 0.05) in relation to the chow diet. The moderate caloric restriction did not reverse the changes promoted by the high-fat diet but induced a small decrease in adiposity, which was reversed after refeeding, and the animals maintained a dyslipidaemic profile and high fat deposition in the liver. We can conclude that the high-fat diet and subsequent moderate caloric restriction plus refeeding increased the risks of developing visceral obesity, dyslipidaemia and non-alcoholic fatty liver disease, which suggests that this type of experimental protocol can be used to study mechanisms related to the metabolic syndrome.     

糖尿病非酒精性脂肪肝病大鼠肝组织胰岛素受体、瘦素受体 mRNA的表达

目的：观察2型糖尿病大鼠肝脏的病理变化,探讨肝组织胰岛素受体（insulin R）、瘦素受体（leptin R）mRNA表达在糖尿病性非酒精性脂肪肝病（NAFLD）发病机制中的作用。方法：SD大鼠随机分成2组：正常组与2型糖尿病组。2型糖尿病组在以高脂饮食4周后,加小剂量(30 mg/kg)链脲佐菌素（STZ）诱导2型糖尿病性非酒精性脂肪性肝病大鼠模型,继续给予高脂饮食12周。分别采用HE染色、苏丹Ⅲ染色、Masson染色光镜下观察肝脏组织的病理改变;透射电镜观察肝脏超微结构改变;生化法检测血糖、血甘油三酯（TG）、血总胆固醇（TC）、丙氨酸转氨酶（ALT）和天门冬氨酸转氨酶（AST）水平;放免法检测血清胰岛素水平;ELISA法检测血清瘦素水平;RT-PCR法检测肝组织磷酸烯醇式丙酮酸羧激酶（PEPCK）、葡萄糖-6-磷酸酶（G6Pase）、insulin R、leptin R mRNA表达水平。结果：糖尿病大鼠肝细胞明显脂肪变性、碎片状坏死伴炎细胞浸润及肝纤维化病变,电镜下主要表现为肝细胞核固缩,胞浆内含大量脂滴,狄氏间隙胶原纤维增生;血糖、血胰岛素、TG、ALT、AST水平明显升高（P<0.01）,TC水平升高(P<0.05）,血清瘦素水平明显下降（P<0.01）;肝组织insulin R、leptin R mRNA表达显著升高（P<0.01）,PEPCK、G6Pase mRNA表达无显著变化。结论：2型糖尿病时的胰岛素抵抗是NAFLD发生的根源,由于胰岛素抵抗而致的低血清瘦素水平、肝组织insulin R、leptin R 表达上调参与了NAFLD的发生。     

Physical activity and liver cholesterol

Summary The effects of various types and intensities of exercise on hepatic cholesterol and fecal sterol levels of rats fed a high fat diet was investigated. The results demonstrate that liver cholesterol of such animals trained either by running or swimming are lower than non-trained controls.The concentration of cholesterol in the livers of rats 4 weeks after the termination of training had increased significantly and approached the level of the control animals. Detrained animals also had higher liver cholesterol levels than trained animals. These results suggest that high fat diets produce a progressive accumulation of cholesterol in the livers of rats which can be retarded by exercise. The excretion of sterol in the fecals was significantly higher in the trained animals. The elevated excretion of cholesterol may be one of the methods by which exercise retards the accumulation of cholesterol in the livers of rats fed high fat diets.This investigation supported by Research Grant HE 08262 from the National Heart Institute, National Institutes of Health, U.S. Public Health Service.     

奥美沙坦对ob/ob小鼠血浆脂联素水平影响的研究

目的 观察ob/ob小鼠不同组间血浆脂联素浓度的变化以及奥美沙坦干预后脂联素浓度的变化.方法 以ob/ob小鼠为对象,分为三组:①ob/ob小鼠空白组;②ob/ob小鼠高脂组;③ob/ob小鼠奥美沙坦组,①喂以普通饲料;②③喂以高脂饮食,10周后,早期动脉粥样硬化成模后,给与①②组安慰剂及③组奥美沙坦分别进行干预,10...     

高脂饲养致小鼠胰岛素抵抗对脂肪肝形成的影响

目的:探讨高脂饲养致小鼠脂肪肝形成的机制。方法:随机将8周雄性C57BL/6J小鼠分成高脂饲养组(给予含60%卡路里的高饱和脂肪酸饲养)和正常对照组,饲养12周。监测体重、肝重、血甘油三酯、血总胆固醇、血糖和血胰岛素水平,通过高胰岛素正葡萄糖钳夹实验反映胰岛素敏感性,HE染色、苏丹IV染色及肝脂含量反映肝组织脂质沉积情况,确定高脂饲养致小鼠脂肪肝的形成。通过Western blot法检测磷酸化胰岛素受体底物1(IRS1)和蛋白激酶B(Akt)水平反映胰岛素信号通路激活情况,检测固醇调节元件结合蛋白1(SREBP-1)和脂肪酸合成酶(FAS)蛋白水平反映肝内脂质合成的情况。结果:高脂饲养组小鼠体重及肝重较正常对照组小鼠明显增加。与正常对照组相比,高脂组血和肝组织内甘油三酯和总胆固醇含量显著升高,血清胰岛素水平升高,葡萄糖输注率减少,磷酸化IRS1和Akt水平降低。肝组织HE染色可见高脂组肝细胞胞浆内充满大量脂肪空泡,苏丹IV染色可见肝细胞内存在大量大小不一的红色脂滴;SREBP-1和FAS蛋白水平明显升高。给予外源性油酸干预原代正常肝细胞48 h,磷酸化IRS1和Akt水平呈浓度依赖性减低,而SREBP-1和FAS蛋白表达明显升高。结论:高脂饲养导致小鼠肝脏发生胰岛素抵抗,并通过激活SREBP-FAS脂肪合成途径,促进肝脏脂质沉积,从而诱发脂肪肝。     

Effects of alternations (10 days) of high-fat with normal diet on liver lipid infiltration, fat gain, and plasma metabolic profile in rats

The purpose of the present study was to test the hypothesis that short-term alternations of high-fat with normal chow feeding result in higher fat accumulation in liver than continuous intake of the same high-fat diet. Male Sprague-Dawley rats (7 weeks of age) were divided into 3 groups according to diet composition: standard chow (SD; 12,5% kcal as fat), high-fat (HF; 42% kcal as fat), and food cycles (FC) consisting of 10-day alternations between HF and SD diets beginning with the high-fat diet. Rats in each of these 3 groups were sacrificed after 10, 30, and 50 days (n = 10 rats/sub-groups). Energy intake, body weight, liver and muscle relative weights were not significantly (P > 0.05) different between FC- and HF-fed rats. Using the total energy intake for the 50-day period, it was calculated that approximately 30% less calories as fat was ingested in the FC- compared to the HF-fed rats. In spite of this, liver lipid infiltration as well as fat accretion in abdominal adipose tissues were increased (P < 0.01) similarly in FC- and HF-fed rats. Plasma FFA and insulin levels depicted strong tendencies (P < 0.07) to be higher in FC- than in continuous HF-fed rats at the end of the 50-day period. These results indicate that, despite a 30% reduction in ingested lipids, alternations of HF with normal chow diet compared to the continuous hyperlipidic diet caused the same level of infiltration of lipids in the liver and in the abdominal adipose tissues and, to a certain extent, may even result in a larger deterioration of the metabolic profile.     

Effect of exercise on Hepatic cholesterof of rats fed diets high in saturated or unsaturated fats

Summary Rats have been fed diets containing 24.2% coconut or corn oil or an equal mixture of each for 14–18 weeks. Half of the animals in each dietary group were exercised by running in motor-driven work wheels throughout the entire experimental period. During the final 10–14 weeks, these exercised animals ran continuously for 60 min at 1.0 mph or faster each day. Comparisons between sedentary groups revealed that hepatic cholesterol and excretion of digitonin precipitated sterols in the feces increased (P < 0.01) as the per cent of unsaturated fat (corn oil) in the ingested food increased. In contrast, total liver lipid decreased (P < 0.01) as the consumption of corn oil increased. No change in plasma cholesterol occurred in the sedentary rats in response to the three diets. Hepatic cholesterol of the exercised groups was significantly less (P < 0.05–P < 0.01) than that of their respective control groups (same diet). However, the group fed the corn oil diet had a significantly higher (P < 0.01) liver cholesterol after exercise than did the exercised group fed the coconut oil diet. Liver lipid was reduced (P < 0.01) by exercise in the corn oil and mixed corn-coconut oil fed groups. Plasma cholesterol and sterol excretion were unchanged by the exercise program.This investigation supported by Research Grant HE 08262 from the National Heart Institute, National Institutes of Health, U.S. Public Health Service.     

Dietary hyperphagia in rats: role of fat, carbohydrate, and energy content

Dietary energy, fat and carbohydrate content were varied to determine the nutritional factors responsible for hyperphagia induced by feeding rats high-fat diets. In the first experiment, rats were fed isoenergetic high-fat or high-carbohydrate diets for 2 weeks. Weight gain and energy intake were lower in rats given the high-fat diet. When some of the rats were switched to a diet that was high in fat, carbohydrate and energy, gram food intake was initially unchanged, resulting in a substantial increase in energy intake and weight gain. Energy intake gradually declined over the 4 weeks following the switch to the high-energy diet. In the second experiment, rats were fed high-fat diets that were either high or low in carbohydrate content and either high or low in energy content (kcal/g). Rats fed a high-fat diet that was high in energy and carbohydrate ate the most energy and gained the most body weight and carcass fat. In the third experiment, rats were fed high-carbohydrate diets varying in fat and cellulose content. Energy intake and body weight gain varied directly as a function of caloric density regardless of the fat or cellulose content of the diets. It is concluded that hyperphagia induced by feeding high-fat diets is not due to the high dietary fat content alone. Rather, high levels of fat, carbohydrate, and energy interact to produce overeating and obesity in rats fed high-fat diets.     

A “Western Diet” promotes symptoms of hepatic steatosis in spontaneously hypertensive rats

Systemic hypertension, characterized by elevated blood pressure ≥140/90 mm Hg, is a major modifiable risk factor for cardiovascular disease. Hypertension also associates with non‐alcoholic fatty liver disease (NAFLD), which is becoming common due to a modern diet and lifestyle. The aim of the present study was to examine whether a high‐fat "Western" diet had effects on hypertension and associated NAFLD. Normotensive Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were placed on a normal chow or high‐fat diet for 8 weeks; blood pressure was measured fortnightly and body weight recorded weekly. As expected, SHR had elevated blood pressure compared to WKY. Diet did not influence blood pressure. Compared to SHR, WKY rats gained more weight, associating with increased white adipose tissue weight. Normotensive rats also had higher plasma cholesterol and triglycerides in response to a “Western” diet, with no changes in plasma glucose levels. Neither strain developed atherosclerosis. Interestingly, high‐fat diet‐fed SHR had increased liver weight, associating with a significant level of hepatic lipid accumulation not observed in WKY. Further, they exhibited hepatocellular ballooning and increased hepatic inflammation, indicative of steatohepatitis. These findings suggest that a high‐fat “Western” diet promotes features of NAFLD in SHR, but not WKY rats. Importantly, the high‐fat diet had no effect on blood pressure.     

山药决明子挂面对血脂异常大鼠模型血脂及抗氧化的影响

目的探讨山药决明子挂面对血脂异常大鼠模型血脂及抗氧化的影响。方法48只SD大鼠分为正常对照组(8只)和模型组(40只),模型组大鼠经4周高脂饮食喂养后建立血脂异常大鼠模型,采用随机数字法分为模型组、阿托伐他汀阳性对照组(10 mg/kg/d)、山药决明子挂面低、中、高剂量组,每组8只。干预5周后测定血清总甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、肝体比、肝脏胆固醇(TC)、甘油三酯(TG)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)和总抗氧化能力(T-AOC)。结果与模型组相比,中剂量山药决明子挂面组大鼠血清TC、肝脏TC、TG水平分别下降14.76%、23.75%、39.69%(P<0.05),低、中、高剂量组血清TG、LDL-C水平均有所下降(P<0.05),低剂量组肝脏SOD、GSH-Px、T-AOC分别升高24.09%、26.90%、290.24%(P<0.05)。结论山药决明子挂面能降低血脂异常大鼠血脂水平,提高抗氧化水平,对辅助治疗血脂异常及抗氧化有一定的应用价值。