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1.
Herbal dietary supplements have attracted more and more attention owing to their relative effectiveness in obesity ‐related metabolic disorders and diseases. This study investigated the therapeutic effects and underlying mechanisms of Capsosiphon fulvescens (CF) extracts on obesity, their associated metabolic disorders and hepatic steatosis in high‐fat diet (HFD)‐induced obese mice. Male C57BL/6 mice were fed with normal, HFD/Vehicle and HFD/CF (orally 300 mg/kg/day for CF). After 12 weeks, CF blocked HFD‐induced body weight, food intake, liver weight, hepatic triglyceride (TG), fat mass (weight of abdominal subcutaneous fat and epididymal adipose tissue) and biochemical parameters (total cohlesterol, glucose, TG, creatinine, high‐density lipoproteins cholesterol and low‐density lipoprotein cholesterol) of serum. CF also had improved serum levels of adiponectin, leptin and insulin‐like growth factor‐1 in HFD/CF mice. Moreover, CF ameliorated the hepatic steatosis‐reducing size of white adipose tissue. These results indicate that CF have anti‐obesity effects and are effective for reducing metabolic risk and hepatic steatosis.  相似文献   

2.
The onset and progression of type II diabetes is closely related to environmental factors, in particular dietary habit. Moreover, the environmental exposures very early in life can influence the risk for development of type II diabetes later in life. In this study, we investigated pathophysiological changes in the pups of maternal Spontaneously Diabetic Torii (SDT) rats that were fed a high‐fat diet (HFD) throughout gestation and lactation. Maternal SDT rats were continued on HFD for 5 weeks, from day 8 of gestation to day 21 after birth, and biological analyses of the pups were performed from 2 to 22 weeks of age. Results of serum lipid levels in pups from dams fed HFD were higher than pups from dams fed a standard diet, and the onset of diabetes was significantly accelerated in pups from dams fed HFD. In pathological analyses, pups from dams fed HFD showed increases in liver weight and vacuolation of hepatic cells at 2 weeks of age. In conclusion, the metabolic disorder of lipids and glucose in SDT rats is closely related to the nutritional condition of dams during the periods of gestation and lactation.  相似文献   

3.
To assess modification of thioacetamide-induced hepatotoxicity in mice fed a high-fat diet, male C57BL/6J mice were fed a normal rodent diet or a high-fat diet for 8 weeks and then treated once intraperitoneally with thioacetamide at 50 mg/kg body weight. At 24 and 48 hours after administration, massive centrilobular hepatocellular necrosis was observed in mice fed the normal rodent diet, while the necrosis was less severe in mice fed the high-fat diet. In contrast, severe swelling of hepatocytes was observed in mice fed the high-fat diet. In addition, mice fed the high-fat diet displayed more than a 4-fold higher number of BrdU-positive hepatocytes compared with mice fed the normal rodent diet at 48 hours after thioacetamide treatment. To clarify the mechanisms by which the hepatic necrosis was attenuated, we investigated exposure to thioacetamide and one of its metabolites, the expression of CYP2E1, which converts thioacetamide to reactive metabolites, and the content of glutathione S-transferases in the liver. However, the reduced hepatocellular necrosis noted in mice fed the high-fat diet could not be explained by the differences in exposure to thioacetamide or thioacetamide sulfoxide or by differences in the expression of drug-metabolizing enzymes. On the other hand, at 8 hours after thioacetamide administration, hepatic total glutathione in mice fed the high-fat diet was significantly lower than that in mice fed the normal diet. Hence, decreased hepatic glutathione amount is a candidate for the mechanism of the attenuated necrosis. In conclusion, this study revealed that thioacetamide-induced hepatic necrosis was attenuated in mice fed the high-fat diet.  相似文献   

4.
本研究旨在探讨鱼油对高脂日粮饲喂小鼠发情周期和机体代谢产热的影响。试验选用36只4周龄C57BL/6 J雌性小鼠,随机分成3组（n=12）：对照组、高脂组和高脂+鱼油组。对照组饲喂标准啮齿动物饲料（AIN-93G）,高脂组和高脂+鱼油组分别饲喂高脂日粮（脂肪提供60%能量）和添加5%鱼油（等能替代猪油）的高脂日粮。试验期间,对小鼠体组成（12周龄）、整体代谢（16周龄）、褐色脂肪温度（18周龄）、体核温度（直肠温度,18周龄）和发情周期（20周龄）等进行检测。试验结束后,眼球采血分离血清,检测促卵泡激素（follicle-stimulating hormone,FSH）和雌二醇（estradiol,E2）的水平。此外,采集皮下脂肪、腹部脂肪和肩胛间褐色脂肪,称重并使用Western blot检测脂肪组织中产热相关基因的蛋白表达（UCP1、Cyto C）,使用实时荧光定量PCR检测褐色脂肪组织中产热基因的mRNA表达（UCP1, PRDM16,PGC1α,Cidea,Elovl3）。结果显示,与对照组相比,高脂日粮显著增加了小鼠的体脂含量（12周龄）及皮下和腹部脂肪的沉积量（21周龄）（P<0.05）,而添加鱼油显著降低了高脂饮食引起的体脂含量增加（P<0.05）。另外,高脂日粮导致小鼠的发情周期紊乱,伴随着周期延长、发情期缩短,以及血清中FSH和E2的水平降低（P<0.05）,而添加鱼油可缓解高脂日粮导致的小鼠发情周期紊乱,提高血清中FSH和E2的水平（P<0.05）。同时,添加鱼油可增加高脂饲喂小鼠肩胛间褐色脂肪（interscapular brown adipose tissue,iBAT）和腹股沟白色脂肪（inguinal white adipose tissue,iWAT）中产热相关基因的表达（P<0.05）,进而促进iBAT激活/产热和iWAT褐色化。结果提示,日粮鱼油可缓解高脂日粮导致的发情周期紊乱,可能与BAT激活和WAT褐色化造成的机体代谢产热增强有关。  相似文献   

5.
旨在探究风柜斗草提取物(Sarcopyramis napalensis Wall extract,SNE)对蛋氨酸胆碱缺乏(MCD)饮食诱导的肝脏脂质沉积的作用与机制。本研究将60只雄性C57BL/6小鼠随机分为6组,每组10只,设置MCS组(MCD饲料的对照饲料组)、MCS+风柜斗草提取物组(400 mg·(kg·bw)-1)、MCD组、MCD+风柜斗草提取物低、中、高剂量组(100、200、400 mg·(kg·bw)-1),造模及药物干预6周。进行肝组织切片HE染色、天狼猩红染色,检测血清碱性磷酸酶(AKP)、谷草转氨酶(AST)、谷丙转氨酶(ALT),肝组织谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活力水平及丙二醛(MDA)含量以评估肝脂质沉积、肝纤维化以及肝抗氧化情况。使用Western blot技术检测腺苷酸激活蛋白激酶(AMPK)蛋白的激活情况,使用qRT-PCR技术检测固醇调节元件结合蛋白-1C (SREBP-1c)、肝型脂肪酸结合蛋白(L-FABP)、脂肪酸转运蛋白-3(FATP-3)、脂肪酸转运蛋白-4(FATP-4)、细胞间黏附分子-l (ICAM-1)、血管细胞黏附分子-l (VCAM-1)、基质金属蛋白酶-2(MMP-2)、组织金属蛋白酶抑制剂-2(TIMP-2) mRNA表达水平,同时采用LC-MS/MS技术进行肝组织非靶向脂质组学分析。结果表明,给予200、400 mg·(kg·bw)-1剂量的风柜斗草提取物时均可显著改善MCD饲料饲喂的小鼠肝脂肪变性,减少炎症簇以及肝纤维化程度。给予风柜斗草提取物100、200、400 mg·(kg·bw)-1时均可显著降低MCD饲料饲喂的小鼠血清中ALT和AKP的活力以及肝组织中MDA的含量,显著提高小鼠肝中GSH-Px的活力。Western blot及qRT-PCR检测结果显示,风柜斗草提取物显著激活MCD饲料饲喂的小鼠肝组织AMPK;显著抑制MCD饲料饲喂的小鼠肝组织SREBP-1c、L-FABP、FATP-3、FATP-4、ICAM-1、VCAM-1、MMP-2、TIMP-2的mRNA表达水平。肝脂质组学检测结果显示,风柜斗草提取物显著降低MCD饲料饲喂的小鼠肝中甘油三酯(TG)、磷脂酰甘油(PG)以及神经酰胺(Cer)的相对含量;显著提高鞘磷脂(SM)以及辅酶Q9相对含量。结果提示,风柜斗草提取物可通过AMPK/SREBP-1c途径抑制TG合成,以及通过抑制FATP与L-FABP表达来减少肝对脂肪酸的摄取,从而改善MCD饲料饲喂的小鼠肝脂肪变性;通过提高MCD饲料饲喂的小鼠肝组织中SM和辅酶Q9相对含量以及降低Cer相对含量,改善肝细胞氧化应激损伤情况,进而改善MCD饮食诱导的小鼠肝炎症和纤维化,最终达到改善肝脂质沉积症的作用。  相似文献   

6.
Increased levels of plasma free amino acids (pFAAs) can disturb the blood glucose levels in patients with obesity, diabetes mellitus and metabolic syndrome (MS) and are associated with enhanced protein oxidation. Oxidation of proteins, especially in the muscles, can promote protein degradation and elevate the levels of pFAAs. Gamma‐aminobutyric acid (GABA), a food additive, can reduce high‐fat diet (HFD)‐induced hyperglycaemia; however, the mechanisms remain unclear. The aim of this study was to evaluate the effects of GABA on protein oxidation and pFAAs changes. One hundred male C57BL/6 mice were randomly divided into five groups that were fed with control diet, HFD and HFD supplied with 0.2%, 0.12% and 0.06% GABA in drinking water for 20 weeks respectively. HFD feeding led to muscular oxidative stress, protein oxidation, pFAA disorders, hyperglycaemia and augmented plasma GABA levels. Treatment with GABA restored normally fasting blood glucose level and dose‐dependently inhibited body weight gains, muscular oxidation and protein degradation. While medium and low doses of GABA mitigated HFD‐induced pFAA disorders, the high dose of GABA deteriorated the pFAA disorders. Medium dose of GABA increased the levels of GABA, but high dose of GABA reduced the levels of plasma GABA and increased the activity of succinic semialdehyde dehydrogenase in the liver. Therefore, treatment with GABA mitigated HFD‐induced hyperglycaemia probably by repairing HFD‐induced muscular oxidative stress and pFAA disorders in mice. Our data also suggest that an optimal dose of GABA is crucial for the prevention of excess GABA‐related decrease in the levels of pFAA and GABA as well as obesity.  相似文献   

7.
In this study, we determined how rosiglitazone (RSG) differentially affected hippocampal neurogenesis in mice fed a low-fat diet (LFD) or high-fat diet (HFD; 60% fat). LFD and HFD were given to the mice for 8 weeks. Four weeks after initiating the LFD and HFD feeding, vehicle or RSG was administered orally once a day to both groups of mice. We measured cell proliferation and neuroblast differentiation in the subgranular zone of the dentate gyrus using Ki67 and doublecortin (DCX), respectively, as markers. In addition, we monitored the effects of RSG on the levels of DCX and brain-derived neurotrophic factor (BDNF) in hippocampal homogenates. At 8 weeks after the LFD feeding, the numbers of Ki67- and DCX-positive cells as well as hippocampal levels of DCX and BDNF were significantly decreased in the RSG-treated group compared to the vehicle-treated animals. In contrast, the numbers of Ki67- and DCX-positive cells along with hippocampal levels of DCX and BDNF in the HFD fed mice were significantly increased in the RSG-treated mice compared to the vehicle-treated group. Our data demonstrate that RSG can modulate the levels of BDNF, which could play a pivotal role in cell proliferation and neuroblast differentiation in the hippocampal dentate gyrus.  相似文献   

8.
Young male white Swiss mice were fed control diet or diet supplemented with 20 or 10 parts per million (ppm) of T-2 toxin for two or three weeks. These mice then were inoculated with herpes simplex virus type 1 (HSV-1) (9.6 x 10(6) plaque forming units) intraperitoneally. To compare the effects of T-2 toxin against a known immunosuppressive drug, cyclophosphamide was injected intraperitoneally at 150 mg/kg, 24 hours after treatment with HSV-1, into mice fed the control diet. Mice were necropsied and tissues were collected for microscopic and virologic examination. White Swiss mice which consumed a daily diet containing 20 ppm of T-2 toxin for two or three weeks were highly susceptible to HSV-1 infection and 27 of 36 (75%) died as a result of extensive hepatic and adrenal necrosis. Although HSV-1 was isolated from livers and brains of mice fed 20 ppm of T-2 toxin for two or three weeks, there was little or no inflammatory response found in the adrenals, livers, spinal cords, brains, or ganglia. The necrotizing encephalomyelitis observed in control mice was absent. High levels of dietary T-2 toxin appeared to be more immunosuppressive than cyclophosphamide because only one mouse died after treatment with HSV-1 and cyclophosphamide. Mice treated with cyclophosphamide had changes in brain, spinal cord, spleens, thymus, and bone marrow which were similar to those fed 20 ppm of T-2 toxin and infected with HSV-1, however, liver lesions were much less severe. HSV-1-infected mice on a diet with 10 ppm T-2 toxin had lesions of intermediate severity when compared with HSV-1-infected mice fed a diet with 20 ppm T-2 toxin and HSV-1-infected mice on control diets. Necrosis was less extensive in the livers and adrenals. The infrequent isolation of virus from liver and brain was consistent with the lack of intranuclear inclusion bodies and a more marked inflammatory response. Ten ppm of dietary T-2 toxin only depressed bone marrow and splenic red pulp to a mild or moderate degree. This may have enhanced the necrotizing encephalomyelitis observed in mice killed on days 6 and 8 after HSV-1 infection. Liver lesions were mild and those of the adrenals were moderate in mice fed control diet. The rare isolation of HSV-1 from the liver and brain and the findings of a moderate to severe necrotizing encephalomyelitis in these mice was consistent with an essentially functional immune system.  相似文献   

9.
To examine the tumor modification activity of kojic acid (KA) by sodium ascorbic acid (AA), 5-week-old male ICR mice were administered intraperitoneally with N-diethylnitrosamine (DEN) as an initiation treatment. Two weeks after the initiation treatment, animals were fed basal diet containing 0 (Group 1: DEN alone) or 3% KA (Group 3: DEN+KA), drinking water containing 5,000 ppm AA (Group 2: DEN+AA) or 3% KA and 5,000 ppm AA (Group 4: DEN+KA+AA) for 6 weeks. One week after the administration of KA and/or AA, all mice were subjected to two-thirds partial hepatectomy. At the end of the experimental period, all surviving mice were sacrificed and removed the liver. The liver weights of the Groups 3 and 4 were significantly increased, and the number of proliferating cell nuclear antigen positive hepatocytes and the gene expressions of Ccnc, Ccnd1, Ercc and Cyp7a1 were significantly increased in the Group 4, as compared to the Group 1. These results of the present study suggest that AA enhances the hepatocellular proliferative activity of KA in mice.  相似文献   

10.
探讨苜蓿皂甙对高脂血症大鼠胆固醇代谢及肝脏胆固醇酰基转移酶2(ACAT-2),羟甲基戊二酸单酰辅酶A还原酶(HMG-CoAr)基因表达的影响。取雄性健康Sprague Dawley大鼠(SD)40只,随机分为4组,分别为:正常对照组A、高脂模型组B、苜蓿皂甙预防组C和苜蓿皂甙治疗组D。除正常对照组外,其余各组均饲喂高脂饲料,其中预防组从第1周开始灌胃苜蓿皂甙,治疗组从第5周开始灌胃苜蓿皂甙,试验期8周。观察试验大鼠体重、肝脏系数、血脂水平和肝脏病理变化情况,并用酶联免疫法(ELISA)和Real-time PCR技术分别检测大鼠肝脏HMG-CoAr和ACAT-2的蛋白和mRNA表达结果。结果表明,1)苜蓿皂甙可以显著降低高脂模型大鼠体重、肝脏系数、血清TC和低密度脂蛋白(LDL-C)水平及改善肝脏脂化程度(P<0.05)。2)苜蓿皂甙预防组和治疗组ACAT-2的蛋白和mRNA表达量极显著低于模型组(P<0.01),而HMG-CoAr 的蛋白及mRNA表达水平与模型组比较则差异不显著。苜蓿皂甙通过降低肝脏ACAT-2的表达,抑制机体对外源胆固醇的吸收,发挥对高脂血症的预防和治疗作用。  相似文献   

11.
Mild hepatic fibrosis in cholesterol and sodium cholate diet-fed rats   总被引：4，自引：0，他引：4  
To date, the majority of research on hypercholesterolemia has focused on the effects of a high cholesterol diet on atherosclerosis and coronary heart disease. The toxic effects of cholesterol on the liver and the relationship between the intake of a high cholesterol diet and hepatic fibrosis, however, have not been investigated clearly or histopathologically. Male Wistar rats were fed a diet supplemented with 1.0% cholesterol and 0.3% sodium cholate for 12 weeks. Rats were sacrificed and analyzed via blood biochemistry, traditional microscopy and immunohistochemistry. Following the feeding of this diet, the rates of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and total cholesterol in the rats were elevated consistently from week 3 and throughout the remainder of the experiment. From microscopic observation, hepatic necrosis, macrophage infiltration and steatosis increased markedly throughout the experiment. Hepatic fibrosis and myofibroblast proliferation were detected at weeks 9 and 12. Mast cell appearance was proportional to the degree of hepatic damage. These findings suggest that hepatic fibrosis is inducible by a high cholesterol diet and is likely the result of the interaction between several different cell types (i.e., macrophages, myofibroblasts, and mast cells) in an inflammatory milieu. Hypercholesterolemia should be considered as a risk factor for hepatic fibrosis as well as atherosclerosis and coronary artery disease.  相似文献   

12.
The objective of this study was to examine the effects of diet energy density (high versus low) and increased milk yield, induced by increased milking frequency (two versus three times daily), on the hepatic status of triacylglycerol (TAG) and glycogen content and hepatic long chain fatty acid (LCFA) oxidation capacity in early lactation in a 2 x 2 factorial design. Forty multiparous Danish-Holstein dairy cows were used from 8 weeks before to 8 weeks after calving. Liver biopsies and blood samples were taken in weeks -2, 2, and 7 from calving. The cows fed the high energy density diet, compared with the cows fed the low energy density diet, had an 18 and 28% higher milk production and net energy intake, respectively. Milk yield was increased by 10% when the cows were milked three times compared with twice daily. Complete (CO2 production) and incomplete (ketone body production) LCFA oxidation capacity in the liver were 35 and 32% higher, respectively, and liver TAG content was 48% lower for the cows fed the high energy density diet compared with the low energy density diet. Overall there was no effect of milking frequency on liver parameters. However, a significant interaction between diet and milking frequency showed that the cows milked three times daily and fed the low energy density diet had the lowest liver LCFA oxidation (CO2 and ketone body) capacity. Furthermore, these cows had the numerically highest liver TAG content. The results for liver LCFA metabolism are discussed in relation to the plasma concentration of metabolites and insulin. In conclusion, cows in early lactation given a high energy density diet will, in general, have a lower risk of high TAG infiltration in the liver.  相似文献   

13.
A lean phenotype has been detected in vitamin D receptor (VDR) knockout mice; however, the gender differences in fat metabolism between male and female mice both with age and in response to a high‐fat diet have not been studied before. The objective of our study was to assess changes in body and fat tissue weight, food intake and serum cholesterol and triglyceride in VDR knockout mice from weaning to adulthood and after a challenge of adult animals with a high‐fat diet. Although VDR knockout mice of both sexes consumed more food than wild‐type and heterozygous littermates, their body weight and the weight of fat depots was lower after 6 months on a diet with 5% crude fat content. When adult animals were challenged with a high‐fat diet containing 21% crude fat content for 8 weeks, VDR knockout mice of both sexes had a significantly higher food intake but gained less weight than their wild‐type littermates. Cholesterol levels were higher after 2 days on the high‐fat diet in both sexes, but in the VDR knockout mice, less cholesterol was detected in the serum after 8 weeks. Wild‐type male mice showed signs of fatty liver disease at the end of the experiment, which was not detected in the other groups. In conclusion, lack of the VDR receptor results in reduced fat accumulation with age and when adult mice are fed a high‐fat diet, despite a higher food intake of VDR knockout mice relative to their wild‐type littermates. These effects can be detected in both sexes. Wild‐type male mice react with the highest weight gain and cholesterol levels of all groups and develop fatty liver disease after 8 weeks on a high‐fat diet, while male VDR knockout mice appear to be protected.  相似文献   

14.
试验旨在研究镰刀菌毒素污染日粮对断奶仔猪血清酶、肝脏抗氧化功能及组织病理学的影响。选择35日龄体重为(8.45±0.94) kg的健康三元杂交(杜×长×大)断奶雌性仔猪40头,随机分为2组,每组20个重复,每个重复1头猪。对照组饲喂基础日粮,试验组饲喂用霉变玉米和霉变玉米蛋白粉替代基础日粮中50%的玉米和玉米蛋白粉配制而成的镰刀菌毒素污染日粮(玉米赤霉烯酮(ZEN) 0.90 mg/kg,呕吐毒素(DON) 1.43 mg/kg,烟曲霉毒素(FUM) 5.85 mg/kg)。仔猪单栏饲喂,预试期7 d,正试期35 d。结果表明:①与对照组相比,试验组断奶仔猪血清中谷草转氨酶(AST)、谷丙转氨酶(ALT)和碱性磷酸酶(ALP)活性均显著升高(P<0.05),肝脏相对重显著降低(P<0.05);②与对照组相比,试验组断奶仔猪血清和肝脏中谷胱甘肽过氧化物酶(GSH-Px)和总超氧化物歧化酶(T-SOD)活性均显著降低(P<0.05),而丙二醛(MDA)含量显著升高(P<0.05);③病理组织学观察发现,试验组断奶仔猪肝脏出现一定程度的组织损伤,部分肝小叶边缘发生明显的炎性细胞浸润,肝细胞发生局部空泡变性。由此可知,镰刀菌毒素污染日粮(0.90 mg/kg ZEN,1.43 mg/kg DON,5.85 mg/kg FUM)饲喂断奶仔猪可引起仔猪血清酶活性改变,肝脏抗氧化功能降低,肝脏组织出现一定程度的病理损伤,从而影响肝脏功能的发挥。  相似文献   

15.
A previous study demonstrated that a dietary treatment of young geese with cholesterol and cholic acid raises lipid concentrations in the liver. The present study was carried out to investigate whether such a lipid accumulation caused by those hyperlipidemic compounds can be intensified by low dietary choline concentrations. Therefore, 38 eight-week old geese were divided into four groups of 9 or 10 animals each and received a basal diet poor in choline which consisted predominately of maize and soy protein isolate over a period of 8 weeks. Treatment factors were supplementation of diets with cholesterol and cholic acid (0 vs. 5 g of cholesterol and cholic acid each per kg) and supplementation of choline chloride (0 vs. 1.5 g/kg). Final body weights as well as carcass weights were neither influenced significantly by dietary treatment with cholesterol and cholic acid nor by low dietary choline concentrations. However, feeding diets supplemented with cholesterol and cholic acid markedly increased liver weights (two-fold), hepatic triglyceride (3.7-fold) and cholesterol (12-fold) concentrations and percentages of monounsaturated fatty acids at the expense of saturated and polyunsaturated fatty acids in the liver. In geese fed diets with cholesterol and cholic acid, insufficient choline supply did not intensify, but even slightly reduced hepatic lipid accumulation. Geese fed diets with cholesterol and cholic acid exhibited markedly increased levels of cholesterol, triglycerides and phospholipids in plasma and very low-density lipoproteins, regardless of the choline supply. Muscle tissue of geese fed diets supplemented with cholesterol and cholic acid exhibited also increased concentrations of triglycerides and cholesterol whereas the fatty acid composition of muscle lipids remained unchanged. Among geese without hyperlipidemic treatment, concentrations of triglycerides in plasma and very low-density lipoproteins as well as the concentrations of phosphatidylcholine in liver and muscle tissue were not reduced by low dietary choline concentrations. Therefore, it is suggested that those animals were able to synthesize endogenous sufficient choline.  相似文献   

16.
The assay was aimed to establish high fat diet induced metabolic syndrome (MS) model in male SD rat of nutrition.Four weeks old male SD rats were randomly divided into experimental group (n=24) and control group (n=6).The control group was fed with normal diet and the experimental group was fed with high fat diet which was composed of normal diet, egg yolk and peanuts.Two weeks later, the obesity resistant rats were excluded from the experimental group.Weight, systolic blood pressure and Lee's index were observed after thirty-two weeks.After twelve hours fasted, made the OGTT.Then all rats were sacrificed and tested for total cholesterol (TC) and serum triglyceride (TG).The experimental group weighted (794.0±63.5)g and the control group weighted (571.8±61.9)g, and the weights of rats of experimental group were 38.9% higher than that of control group.Lee's index of the experimental group was 343.0±8.7, while the control group was 319.2±7.1 (P<0.01).The levels of serum TC and TG of experimental group were extremely significantly higher than that of control group (P<0.01).Systolic blood pressure of the experimental group was 140.0±15.4, while the control group was 117.9±11.4, differences comparison of systolic blood pressure between experimental group and control group were significant (P<0.05).Insulin resistance of the experimental group was significantly (P<0.05).This study showed that four weeks old male SD rats were fed with high fat diet which was composed of normal diet, egg yolk and peanuts for thirty-two weeks could successfully and stably established metabolic syndrome model.  相似文献   

17.
本试验旨在通过对雄性SD大鼠长期饲喂高脂饲料建立大鼠代谢综合征模型。将30只4周龄SD雄性大鼠随机分为两组,其中试验组24只,对照组6只。试验组饲喂正常饲料并添加鸡蛋黄、花生,两周后将体重排在后1/3的肥胖抵抗大鼠剔除,对照组饲喂正常饲料,饲喂32周后称量大鼠体重并计算Lee's指数,采用小动物无创血压计测量大鼠收缩压。禁食12 h,做口服糖耐量试验后腹主动脉采血测定血清中总胆固醇(TC)、甘油三酯(TG)含量。结果显示,饲喂32周后,试验组大鼠体重达到(794.0±63.5)g,对照组大鼠体重(571.8±61.9)g,试验组大鼠体重超过对照大鼠体重的38.9%;试验组大鼠的Lee's指数为343.0±8.7,对照组大鼠的Lee's指数为319.2±7.1,试验组与对照组相比差异极显著(P<0.01);试验组大鼠TC、TG含量均极显著高于对照组(P<0.01);试验组大鼠收缩压为140.0±15.4,对照组大鼠收缩压为117.9±11.4,试验组大鼠血压显著高于对照组(P<0.05);口服糖耐量试验结果显示试验组大鼠有显著的胰岛素抵抗作用(P<0.05)。结果表明通过高脂饲料饲养32周诱导SD雄性大鼠能成功的建立大鼠代谢综合征模型。  相似文献   

18.
The objective of the present study was to investigate the effects of Fusarium toxins contaminated diet on serum enzymes, liver antioxidant function and histopathology of weaned gilts.Forty healthy weaned gilts (Duroc×Landrace×Yorkshire) aged 35 d with body weight of (8.45±0.94) kg were randomly allocated into 2 groups with 20 replicates per group and 1 pigs per replicate.Gilts in the control group were fed with basal diet, and those in the experiment group were fed with Fusarium toxins contaminated diet made by replacing 50% of corn and corn gluten meal in the basal diet with the naturally contaminated corn and corn gluten meal (0.90 mg/kg ZEN, 1.43 mg/kg DON, 5.85 mg/kg FUM).Gilts were fed individually in a metabolic cage for 35 d after 7 d adaptation.The results showed as follows:① Compared with control group, the serum activities of AST, ALT and ALP in experimental group were significantly increased (P<0.05), and the liver index of experiment group was significantly decreased (P<0.05).②Compared with control group, the activities of GSH-Px and T-SOD in serum and liver of experimental group were significantly decreased (P<0.05), and the MDA content in serum and liver were significantly increased (P<0.05).③ Histological examination of liver in experiment group revealed a certain degree of damage, with obvious inflammatory cell infiltration partly at the margin of hepatic lobule and vacuoles degeneration of local hepatic cells.The results indicated that Fusarium toxins contaminated diets (0.90 mg/kg ZEN, 1.43 mg/kg DON, 5.85 mg/kg FUM) could change serum enzymes activity and impair liver antioxidant function, with a certain degree of pathological injury of liver in the present study, which had a negative impact on the normal liver function in weaned gilts.  相似文献   

19.
[目的] 探索二十二碳六烯酸（DHA）对高脂饲粮诱导肝脏脂肪积累的预防机制。[方法] 将32只雄性SPF级C57BL/6小鼠均分为4组,对照组（Con）饲喂普通饲粮,模型组（Model）饲喂高脂饲粮,DHA组分别在高脂饲粮中添加0.2 g DHA（DHAL）和1.0 g DHA（DHAH）,饲喂周期为20周。饲喂期间每天称量体重及食物重量,计算摄食量;饲喂结束,采集肝脏和血液,ELISA法检测肝脏脂联素和血清甘油三酯（TG）的含量,实时荧光定量PCR检测新生脂肪合成关键酶（SREBP-1c、FAS）、脂肪酸氧化关键基因（PPARα、PPARγ、CPT-1A和ACOX）、线粒体基因（PGC-1α）、褐色脂肪化基因（Prdm16、UCP1）的表达,Western blotting法检测肝脏磷酸化ACC、AMPK和AKT蛋白的表达。[结果] 与Con组相比,Model组终体重、体脂重量和TG含量均显著增加（P<0.05）,肝脏脂联素浓度显著降低（P<0.05）。与Model组相比,DHAL和DHAH组终体重、体脂重量和TG含量均显著降低（P<0.05）,肝脏脂联素水平显著增加（P<0.05）。实时荧光定量PCR结果表明,与Con组相比,Model组SREBP-1c和FAS mRNA表达量均显著增加（P<0.05）,PPARα、CPT-1A、ACOX、PGC-1α和UCP1 mRNA表达均显著降低（P<0.05）;与Model组相比,DHAL和DHAH组SREBP-1c和FAS mRNA表达量均显著降低（P<0.05）,且DHAH组表达量均显著低于DHAL组（P<0.05）,DHAL和DHAH组PPARα、CPT-1A、ACOX、PGC-1α、Prdm16和UCP1 mRNA表达量均显著增加（P<0.05）,DHAH组CPT-1A和ACOX mRNA表达量显著低于DHAL组（P<0.05）,PPARγ的mRNA表达量在4组中没有显著差异（P>0.05）。Western blotting结果表明,Model组p-ACC显著高于Con和DHAH组,但显著低于DHAL组;Model组p-AMPK/AMPK和pAKT/AKT比值均显著低于Con组（P<0.05）,DHAH组p-AMPK/AMPK和pAKT/AKT比值均显著高于Model和DHAL组（P<0.05）。[结论] DHA可降低高脂饲粮导致的C57BL/6小鼠终体重、体脂和TG含量的升高,增加肝脏脂联素的水平,促进脂肪酸氧化和白色脂肪细胞褐色化,从而预防肝脏的脂肪积累。  相似文献   

20.
The ameliorating effects of Cu++ and SO4--ions on concurrent selenite toxicity were compared in two factorial experiments using 60 weanling rats each. In the first experiment, 0, 500 and 1,000 mg Cu (as CuCl2)/kg diet were fed in conjunction with 0, 5, 10 and 20 mg Se (as Na2SeO3)/kg diet. In the second experiment, the treatments were 0, 500 and 1,000 mg SO4 (as Na2SO4)/kg fed in conjunction with 0, 5, 10 and 20 mg Se/kg diet. A paired-feeding experiment using 10, 15 and 20 mg Se/kg diet was also conducted with 28 rats to compare the influence of inanition in control and selenite-fed rats. Cupric++ ion, but not SO4--ion, prevented mortality among selenite-intoxicated rats. There were significant Cu X Se interaction effects on feed intake, daily gain, packed cell volume (PCV), serum Cu and Fe, sperm counts, and weights of liver, kidney and testis. There were main effects of Cu and Se on serum Se and liver Cu. In Exp. 2 there were significant SO4 X Se interaction effects on feed intake, daily gain, serum Cu and testis weight. There were main effects of Se on PCV, sperm count, serum testosterone, liver Se, liver Cu and the absolute weights of liver and kidney. The only main effect of SO4 was that of increased liver Cu concentrations. Among the pair-fed rats, the selenite-fed rats, with one exception, died before their paired rats.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

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