运动对高脂饮食诱导非酒精性脂肪肝的治疗作用

目的 观察运动对高脂饮食诱导非酒精性脂肪肝的治疗作用,并初步探讨其相关机制.方法 将30只Wistar大鼠分为对照组及高脂组,分别给予基础饲料和高脂饲料喂养;高脂组大鼠经喂养18周后制成胰岛素抵抗(IR)模型,并进一步细分为静息组和运动组,继续给予高脂饲料喂养,运动组同时进行游泳训练,共持续6周.于实验进行24周后处死各组大鼠,计算肝指数,观察肝脏病理学改变,检测各组大鼠肝脏甘油三酯(TG)含量,同时应用蛋白免疫印迹法检测肝脏组织一磷酸腺苷活化蛋白激酶(AMPK)磷酸化水平.结果 实验进行24周后,与对照组比较,静息组大鼠胰岛素敏感性显著降低,肝脏TG含量、肝指数明显增高,光镜下肝脏出现明显脂肪变性,肝脏内AMPK磷酸化水平降至对照组水平的50.8%;与静息组比较,运动组大鼠胰岛素敏感性明显提高,肝指数及肝脏TG含量均显著降低,光镜下可见肝脏脂肪变性程度明显改善,肝组织内AMPK磷酸化水平亦显著提高.结论 运动干预对高脂饮食诱导的非酒精性脂肪肝具有治疗作用,其机制可能与运动上调肝脏组织中AMPK磷酸化水平,从而改善IR及减少肝脏内TG含量有关.     

运动对高脂饮食诱导非酒精性脂肪肝的治疗作用

目的 观察运动对高脂饮食诱导非酒精性脂肪肝的治疗作用,并初步探讨其相关机制.方法 将30只Wistar大鼠分为对照组及高脂组,分别给予基础饲料和高脂饲料喂养;高脂组大鼠经喂养18周后制成胰岛素抵抗(IR)模型,并进一步细分为静息组和运动组,继续给予高脂饲料喂养,运动组同时进行游泳训练,共持续6周.于实验进行24周后处死各组大鼠,计算肝指数,观察肝脏病理学改变,检测各组大鼠肝脏甘油三酯(TG)含量,同时应用蛋白免疫印迹法检测肝脏组织一磷酸腺苷活化蛋白激酶(AMPK)磷酸化水平.结果 实验进行24周后,与对照组比较,静息组大鼠胰岛素敏感性显著降低,肝脏TG含量、肝指数明显增高,光镜下肝脏出现明显脂肪变性,肝脏内AMPK磷酸化水平降至对照组水平的50.8%;与静息组比较,运动组大鼠胰岛素敏感性明显提高,肝指数及肝脏TG含量均显著降低,光镜下可见肝脏脂肪变性程度明显改善,肝组织内AMPK磷酸化水平亦显著提高.结论 运动干预对高脂饮食诱导的非酒精性脂肪肝具有治疗作用,其机制可能与运动上调肝脏组织中AMPK磷酸化水平,从而改善IR及减少肝脏内TG含量有关.

Abstract：

Objective To observe the effect of exercise on nonalcoholic fatty liver disease (NAFLD) induced by high-fat diet and explore the mechanism.Methods Thirty healthy male rats were randomly divided into a normal control group( NC group) and a high-fat group( HF group), fed with normal chow and high-fat diet, respectively.Eighteen weeks later, the high-fat established as insulin resistance model and group was randomly divided into high-fat diet control group (HC group) and high-fat diet exercise group (HE group).HC group was continually given high-fat diet; HE group accepted swimming training for 6 weeks.After 24 weeks, the insulin sensitivity index (ISI) was calculated.After rats were sacrificed, weight of liver and body were measured to calculate liver mass index.Liver histology was detected by hematoxylin and eosin staining.Hepatic triglyceride content was detected.Phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) level was detected by Western blot technique.Results At the 18th week, compared to NC group, ISI of HF group decreased obviously.It suggested that insulin resistance appeared in HF group.At the 24th week, compared to NC group, ISI of HC group decreased significantly.But hepatic triglycefide content and liver mass index both increased.Pathology observation under light microscope showed obvious liver steatosis in HC group.Phosphorylation of AMPK level in HC group decreased to 50.8% of NC group.Exercise greatly improved the liver mass index, hepatic triglyceride content and ISI as well as liver steatosis compared to HC group.Phosphorylation of AMPK was also elevated to 78.1% of NC group in HE group.However,compared to NC group, liver mass index and hepatic triglyceride content increased simultaneously, while ISI and phosphorylation of AMPK level obviously decreased in HE group.Conclusion Elevated level of phosphorylation of AMPK contributed to improve insulin resistance and decrease the hepatic triglyceride content.Exercise could markedly improve NAFLD induced by high-fat diet through elevating phosphorylation of AMPK in liver.     

白藜芦醇对高脂喂养诱导的脂肪肝大鼠血清TNF-α含量的影响

目的：观察白藜芦醇对非酒精性脂肪肝的治疗效果及其对血清肿瘤坏死因子（TNF-α）含量的影响。方法：30只雄性Wistar大鼠随机分为3组各10只，对照组（NC组）给予基础饲料喂养，模型组（IR组）和干预组（HR组）均给予高脂饲料喂养，其中HR组从第7周开始给予100mg／（kg·d）白藜芦醇灌胃。喂养16周后，以高胰岛素一正糖钳夹技术评价3组大鼠胰岛素敏感性；肝脏石蜡切片HE染色观察病理学改变；酶联免疫吸附试验（ELISA）检测血清TNFha的含量。结果：与NC组比较，IR组大鼠葡萄糖输注率下降，光镜下肝脏出现明显脂肪变性，血清TNF—α含量升高69．3％（P〈0．01）。与IR组比较，HR组葡萄糖输注率明显升高，光镜下肝脏脂肪变性变化不显著；血清TNF-α含量降低31．5％（P％0．01）；与对照组比较，HR组除葡萄糖输注率有所降低（P〈0．01）外，其余检测指标水平均接近。结论：白藜芦醇可能通过降低高脂喂养大鼠的血清TNF-α含量而改善胰岛素抵抗，从而减轻脂肪肝。     

运动对高脂喂养大鼠胰岛素抵抗的治疗作用

目的 观察运动对高脂饮食喂养大鼠胰岛素抵抗(IR)的影响,并初步探讨其机制.方法 将30只雄性Wistar大鼠分为对照组及高脂组,分别给予基础饲料和高脂饲料喂养;高脂组大鼠经喂养18周后制成IR模型,并进一步细分为静息组和运动组,继续给予高脂饲料喂养,运动组同时进行游泳训练,共持续6周.于实验进行24周后处死各组大鼠,检测各组大鼠血液中游离脂肪酸(FFA)水平及骨骼肌中甘油三酯(TG)含量,同时应用蛋白免疫印迹法检测各组大鼠骨骼肌中一磷酸腺苷活化蛋白激酶α(AMPKα)的磷酸化水平.结果 实验进行24周后,与对照组比较,发现静息组大鼠胰岛素敏感性显著降低,FFA水平及骨骼肌中TG含量明显增高,骨骼肌中AMPKα磷酸化水平降至对照组水平的48.7%;与静息组比较,运动组大鼠胰岛素敏感性及骨骼肌中AMPKα磷酸化水平均明显提高,FFA水平及骨骼肌中TG含量则显著降低;但与对照组比较,运动组大鼠FFA水平及骨骼肌中TG含量依然偏高,胰岛素敏感性及骨骼肌中AMPKα磷酸化水平仍然偏低.结论 运动干预可改善由高脂饮食诱导的IR,其治疗机制可能与降低血液中FFA水平及减轻骨骼肌中脂质异位沉积有关.

Abstract：

Objective To observe the effect of exercise on insulin resistance induced by a high fat diet and to explore the underlying mechanism.Methods Thirty healthy male Wistar rats were randomly divided into a normal control group (NC group) and a high-fat group (HF group),fed with normal chow and a high fat diet respectively.Eighteen weeks later,insulin resistance had appeared in the HF group.The HF group was then randomly subdivided into a high-fat diet control group (HC group,fed a high fat diet) and an exercise group (HE group,fed a high fat diet and subjected to swimming training for 6 weeks).After 24 weeks,an insulin sensitivity index was calculated.Serum free fatty acid (FFA) and skeletal muscle triglyceride (TG) were detected.Phosphorylation of adenosine monophosphate kinase-α (AMPKα) in skeletal muscle was detected by Western blotting.Results At twenty-four weeks the insulin sensitivity of the HC group had decreased significantly compared to the NC group.Serum FFA level and skeletal muscle TG content had both increased.Average phosphorylation of AMPKα in the HC group decreased to 48.7% of the NC group average.Compared to the HC group,insulin sensitivity and phosporylation of AMPK-α were elevated significantly in the HE group.Serum FFA level and skeletal muscle TG content were both lower.However,compared to the NC group,both serum FFA level and skeletal muscle TG content had increased in the HE group,while insulin sensitivity and phosphorylation of AMPKα had significantly decreased.Conclusions Exercise can significantly improve insulin resistance induced by a high-fat diet through decreasing serum FFA level and ectopic li-pid accumulation in skeletal muscle.     

运动对胰岛素抵抗大鼠脂肪组织肿瘤坏死因子-α表达的影响

目的研究运动对高脂饮食诱导的胰岛素抵抗(IR)大鼠脂肪组织中肿瘤坏死因子-α（TNF-α）表达的影响。 方法将30只Wistar大鼠随机分为对照组和高脂组，分别给予基础饲料与高脂饲料喂养18周；将造模成功的高脂组IR大鼠随机分为静息组和运动组，均继续给予高脂饲料喂养，同时对运动组大鼠实施游泳训练，共持续6周。于实验进行24周时检测各组大鼠体重、血清空腹血糖（FBG）、空腹胰岛素(FINS)和游离脂肪酸(FFA)水平，并同时计算胰岛素敏感指数（ISI）；采用实时荧光定量聚合酶链反应、免疫印迹技术分别检测各组大鼠脂肪组织中TNF-α mRNA及蛋白表达水平。 结果喂养18周时发现高脂组ISI较对照组明显降低，提示高脂组IR模型制作成功；运动组大鼠经游泳训练6周后，其ISI较静息组明显升高（P<0.05），但仍显著低于对照组水平（P<0.01）；静息组大鼠脂肪组织中TNF-α mRNA及蛋白表达水平均较对照组明显升高（P<0.05）；运动组大鼠脂肪组织中TNF-α mRNA和蛋白表达较静息组进一步升高(P<0.05)。 结论高脂喂养可诱导大鼠产生IR，规律运动可减轻大鼠IR状态，其机制可能与上调脂肪组织中TNF-α表达有关。     

罗格列酮对2型糖尿病合并非酒精性脂肪肝病大鼠肝脏保护作用的研究

目的：探讨罗格列酮对2型糖尿病（T2DM）合并非酒精性脂肪肝病（NAFLD）大鼠的肝脏保护作用及可能机制。方法：将48只8周龄雄性健康远交系大鼠随机分为3组,每组16只。对照组大鼠以普通饲料喂养,模型组及治疗组大鼠均以高脂饲料喂养,于第8周末腹腔内注射链脲佐菌素制作糖尿病大鼠模型,成功后2组继续以高脂饲料喂养,在此基础上治疗组予罗格列酮3mg／（kg·d）灌胃。于第17周、21周末分批处死动物,检测其血糖、肝功能、血脂和胰岛素等指标,光镜下观察大鼠肝脏组织学形态,RT—PCR法检测肝组织解偶联蛋白（UCP）2mRNA的表达情况。结果：与对照组比较,17周及21周模型组大鼠的血糖、胰岛素、ALT、AST、三酰甘油、总胆固醇、LDL—C、游离脂肪酸均明显升高（P均〈0．01）,光镜下肝组织呈重度脂肪变性,且肝组织UCP2mRNA表达水平明显升高（P〈0．01）。与模型组比较,17周及21周治疗组大鼠血糖、ALT、AST、三酰甘油、总胆固醇及游离脂肪酸均有改善（P〈0．05或0．01）,光镜下肝组织呈轻度脂肪变性,肝组织UCP2mRNA表达水平明显下降（P〈0．01）。结论：罗格列酮作用于T2DM合并NAFLD大鼠,不仅可降低血糖、血脂水平,还可改善肝功能、减轻肝脏的脂肪变性,而罗格列酮降低T2DM合并NAFLD大鼠肝脏UCP2的表达,可能是作用机制之一。     

己酮可可碱对非酒精性脂肪肝大鼠能量储备的影响

目的:探讨己酮可可碱(PTX)对非酒精性脂肪肝(NAFLD)大鼠能量储备的影响.方法:SD大鼠72只,正常喂养1周后,随机分为3组.对照组24只以普通饲料喂养.模型组和干预组各24只,以2%胆固醇+10%猪油+88%普通饲料构成高脂饲料喂养.实验动物自由进食和饮水.干预组高脂饮食4周后,在饮水中加用PTX100 mg/(kg·d),即干预组高脂饮食的同时合并喂养PTX.实验动物于第24周处死,由肝右叶固定部位切取2块肝组织.荧光测定法检测肝脏三磷酸腺苷(ATP)含量.结果:模型组肝脏ATP含量较对照组明显减低,干预组肝脏ATP含量较对照组低,但较模型组明显升高.结论:持续24周高脂饮食可成功复制大鼠NAFLD模型,模型大鼠肝脏ATP含量减少,己酮可可碱可提高NAFLD大鼠肝脏ATP含量.     

运动对胰岛素抵抗大鼠骨骼肌脂联素受体的影响

目的观察运动对高脂饮食诱导胰岛素抵抗大鼠血清脂联素（APN）及骨骼肌APN受体（AdipoR）的影响。 方法将30只Wistar大鼠分为对照组及高脂组,分别给予基础饲料和高脂饲料喂养;经喂养18周后再将高脂组大鼠随机分为静息组和运动组,继续给予高脂饲料喂养,运动组同时进行游泳训练,共持续6周。于实验进行24周后测量各组大鼠体重,检测空腹胰岛素(FINS)及空腹血糖(FBG)水平,计算胰岛素敏感指数（ISI）;采用酶联免疫吸附法检测血清APN含量;选用实时荧光定量聚合酶链反应检测骨骼肌APN受体1（AdipoR1）及APN受体2（AdipoR2）mRNA的表达。 结果高脂组大鼠经高脂饲料喂养18周后,其ISI较对照组明显降低,提示胰岛素抵抗模型制作成功。实验进行24周后,与对照组比较,静息组大鼠ISI显著降低,血清APN含量及骨骼肌AdipoR1、AdipoR2 mRNA表达分别降低至对照组71.9%、59.9%及69.2%水平（均P<0.05）;与静息组比较,运动组大鼠ISI明显提高（P<0.05）;骨骼肌中AdipoR1 mRNA表达亦显示提高,约是静息组的1.33倍（P<0.01）,但血清APN含量及骨骼肌AdipoR2 mRNA表达组间差异均无统计学意义（P&rt;0.05）。 结论运动干预可提高大鼠胰岛素敏感性,其机制可能与上调大鼠骨骼肌AdipoR1表达有关。     

运动对胰岛素抵抗大鼠血清肿瘤坏死因子α水平的影响

目的：观察运动对高脂诱导胰岛素抵抗（IR）大鼠胰岛素敏感性的影响及血清肿瘤坏死因子α（TNF-α）水平的变化。方法：30只雄性大鼠分为对照组8只和高脂组22只，分别给予基础饲料与高脂饲料喂养18周，诱导IR大鼠模型，将IR成功大鼠分为高脂组A10只，高脂组B12只，均继续高脂饮食，高脂组B配合游泳训练6周。结果：高脂组大鼠与对照组比较，胰岛素敏感指数（ISI）显著降低，体重、血脂、血糖及血清TNF-α水平均升高，高脂组A更明显（均P〈0．01）；高脂组B训练后各项指标均与对照组接近。结论：运动可改善IR，其作用可能与降低血清TNF-α水平有关。     

有氧运动与饮食控制对高脂喂养大鼠脂质代谢的影响

目的 :在用高脂饮食诱导大鼠出现肥胖、高胰岛素血症等胰岛素抵抗综合征表现的基础上 ,观察有氧运动及饮食控制对该动物模型脂质代谢的影响。方法 :选取离乳雄性SD大鼠 5 5只 ,随机分为正常对照组 13只 ,给予基础饲料 ;实验组 4 2只 ,给予高脂饮食 (含脂量 38.9% )。实验组大鼠经高脂喂养 12周后 ,随机分为 4组 ,干预 8周。H组 :继续高脂饮食 ;HL组 :低脂饮食 ;HE组 :继续高脂饮食 游泳 ;LE组 :低脂饮食 游泳。于实验的第 12周和2 0周 ,分别检测大鼠的胰岛素敏感性及血脂谱。结果 :12周后 ,高脂喂养鼠的Lee指数、空腹胰岛素水平及胰岛素敏感性指数明显升高。游泳干预和饮食控制组大鼠的Lee指数、甘油三酯 /高密度脂蛋白水平比值皆明显的下降 ,饮食控制组大鼠的HDL显著升高 ,而游泳干预组大鼠的TG显著降低。结论 :本实验的运动和饮食控制方案均可使大鼠的TG/HDL比值下降 ,饮食控制明显升高了大鼠的HDL水平而运动降低TG水平的作用更显著     

The lipogenic transcription factor ChREBP dissociates hepatic steatosis from insulin resistance in mice and humans

Nonalcoholic fatty liver disease (NAFLD) is associated with all features of the metabolic syndrome. Although deposition of excess triglycerides within liver cells, a hallmark of NAFLD, is associated with a loss of insulin sensitivity, it is not clear which cellular abnormality arises first. We have explored this in mice overexpressing carbohydrate responsive element-binding protein (ChREBP). On a standard diet, mice overexpressing ChREBP remained insulin sensitive, despite increased expression of genes involved in lipogenesis/fatty acid esterification and resultant hepatic steatosis (simple fatty liver). Lipidomic analysis revealed that the steatosis was associated with increased accumulation of monounsaturated fatty acids (MUFAs). In primary cultures of mouse hepatocytes, ChREBP overexpression induced expression of stearoyl-CoA desaturase 1 (Scd1), the enzyme responsible for the conversion of saturated fatty acids (SFAs) into MUFAs. SFA impairment of insulin-responsive Akt phosphorylation was therefore rescued by the elevation of Scd1 levels upon ChREBP overexpression, whereas pharmacological or shRNA-mediated reduction of Scd1 activity decreased the beneficial effect of ChREBP on Akt phosphorylation. Importantly, ChREBP-overexpressing mice fed a high-fat diet showed normal insulin levels and improved insulin signaling and glucose tolerance compared with controls, despite having greater hepatic steatosis. Finally, ChREBP expression in liver biopsies from patients with nonalcoholic steatohepatitis was increased when steatosis was greater than 50% and decreased in the presence of severe insulin resistance. Together, these results demonstrate that increased ChREBP can dissociate hepatic steatosis from insulin resistance, with beneficial effects on both glucose and lipid metabolism.     

Beneficial effects of rosuvastatin on insulin resistance, adiposity, inflammatory markers and non-alcoholic fatty liver disease in mice fed on a high-fat diet

The aim of the present study was to evaluate the effects of ST (rosuvastatin) and GZ (rosiglitazone) on IR (insulin resistance) and on liver as well as adipose tissue in mice fed on an HF (high-fat) diet. Our data show that treatment with ST resulted in a marked improvement in insulin sensitivity characterized by enhanced glucose clearance during the insulin tolerance test and a 70% decrease in the HOMA-IR (homoeostasis model assessment of insulin resistance) index level (P=0.0008). The ST-treated mice exhibited lower gains in BM (body mass; -8%; P<0.01) and visceral fat pad thickness (-60%; P<0.01) compared with the untreated HF group. In comparison with HF-diet-fed mice, HF+ST-treated mice showed a significant reduction in hepatomegaly and liver steatosis (-6%, P<0.05; and -21%, P<0.01 respectively). In HF+ST-treated mice, the hepatic TAG (triacylglycerol) levels were reduced by 58% compared with the HF group (P<0.01). In addition, the expression of SREBP-1c (sterol-regulatory-element-binding protein-1c) was decreased by 50% in the livers of HF+ST-treated mice (P<0.01) relative to the HF-diet-fed mice. The levels of resistin were lower in the HF+ST-treated group compared with the HF group (44% less, P< 0.01). In conclusion, we demonstrated that ST treatment improved insulin sensitivity and decreased liver steatosis in mice fed on an HF diet. Furthermore, ST reduced BM gains, improved the circulating levels of plasma cholesterol and TAG, and reduced hepatic TAG, which was concomitant with lower resistin levels.     

吡格列酮对大鼠非酒精性脂肪肝病的治疗作用及其机制

【目的】探讨吡格列酮对SD大鼠非酒精性脂肪肝病（NAFLD ）的治疗作用及其机制。【方法】36只雄性SD大鼠随机分为正常对照组（NG组）、吡格列酮治疗组（PIOG组）及高脂饮食组（FG组）,均饲养12周;NG组喂饲普通饲料,剩余两组喂饲高脂饲料;PIOG组于实验第8～12周予吡格列酮灌胃,其余两组同期予蒸馏水灌胃;比较三组空腹血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、三酰甘油（TG）、总胆固醇（TC）、空腹血糖（FPG）、空腹胰岛素（FINS）、空腹胰岛素抵抗指数（FIRI）、肿瘤坏死因子-α（TNF-α）及一氧化氮（NO）的水平;HE染色分析肝组织切片病理学改变;观察Kupffer细胞（KCs）形态变化。【结果】FG组大鼠FIRI、TG、TC均高于NG组,其差异均有统计学意义（ P ＜0．05）,肝组织呈大泡性脂肪变性并出现炎症细胞浸润及点状坏死,肝脏KCs发生形态改变,其产生的TNF、NO水平与肝组织病理学改变呈正相关（ P ＜0．05）;PIOG组大鼠 FIRI、TG、TC均低于FG组,其差异均有统计学意义（ P ＜0．05）,肝组织脂肪变性程度减轻,仍可见炎症细胞浸润和肝细胞气球样变性,肝脏KCs形态及功能仍存在异常。【结论】吡格列酮可部分延缓高脂饮食诱导的NAFLD的进展;其机制可能与改善胰岛素抵抗、降低血脂有关,与调节KCs功能无关。     

MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity

Adipocytes secrete a variety of bioactive molecules that affect the insulin sensitivity of other tissues. We now show that the abundance of monocyte chemoattractant protein-1 (MCP-1) mRNA in adipose tissue and the plasma concentration of MCP-1 were increased both in genetically obese diabetic (db/db) mice and in WT mice with obesity induced by a high-fat diet. Mice engineered to express an MCP-1 transgene in adipose tissue under the control of the aP2 gene promoter exhibited insulin resistance, macrophage infiltration into adipose tissue, and increased hepatic triglyceride content. Furthermore, insulin resistance, hepatic steatosis, and macrophage accumulation in adipose tissue induced by a high-fat diet were reduced extensively in MCP-1 homozygous KO mice compared with WT animals. Finally, acute expression of a dominant-negative mutant of MCP-1 ameliorated insulin resistance in db/db mice and in WT mice fed a high-fat diet. These findings suggest that an increase in MCP-1 expression in adipose tissue contributes to the macrophage infiltration into this tissue, insulin resistance, and hepatic steatosis associated with obesity in mice.     

新生大鼠低血糖与非酒精性脂肪性肝病的关系研究

目的本研究通过建立新生大鼠低血糖模型,然后再以此为基础,诱发非酒精性脂肪性肝病（NAFLD）,通过比较不同组间病变程度、胰岛素抵抗强弱、肝功能等指标的差异,了解新生大鼠低血糖和NAFLD易感性之间的关系,为了解NAFLD的发生机制和寻找有效的防治措施提供实验依据。方法购SPF级成熟Wistar雌性大鼠20只和雄性大鼠10只,合笼交配,从所生仔鼠中每窝随机抽取0—1只,总共12只作为正常血糖＋正常饮食组;然后将相同母鼠所生3只新生大鼠,随机分入正常血糖＋高脂饮食组、低血糖＋正常饮食组、低血糖＋高脂饮食组各12只,在第20周末处死,测血清空腹血糖（FBG）、血清空腹胰岛素（FINS）、脂肪酸、总胆固醇（TCH）、三酰甘油（TG）、丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）等指标。肝组织石蜡切片染色判断肝脂变和炎症活动情况。结果20周末大鼠胰岛素抵抗指数（IRI）、脂肪酸、TG、ALT、AST在正常血糖＋高脂饮食组、低血糖＋正常饮食组中明显高于正常血糖＋正常饮食组,低血糖＋高脂饮食组中明显高于正常血糖＋高脂饮食组、低血糖＋正常饮食组;TCH在正常血糖＋高脂饮食组、低血糖＋高脂饮食组中明显高于正常血糖＋正常饮食组、低血糖＋正常饮食组。病理学指标检测中,肝脂变指数及炎症指数在正常血糖＋高脂饮食组、低血糖＋正常饮食组中明显高于正常血糖＋正常饮食组,低血糖＋高脂饮食组中明显高于正常血糖＋高脂饮食组、低血糖＋正常饮食组。结论新生大鼠低血糖所导致的代谢紊乱会导致NAFLD的发生。     

15d-PGJ2对非酒精性脂肪肝大鼠的保护作用

目的 探讨15-脱氧前列腺素J2(15 d-PGJ2)对非酒精性脂肪性肝病(NAFLD)大鼠的保护作用.方法 将50只雄性Wistar大鼠随机分为正常对照组(NC组)和模型组,分别给予普通饲料和高脂饲料喂养,12周末制成NAFLD大鼠模型;再将模型组随机分为4组:15 d-PGJ2低剂量治疗组(LT组),15 d-PGJ2高剂量治疗组(HT组),模型对照组(MC组),饮食疗法组(DT组).治疗2周后处死大鼠,观察各组大鼠的肝组织病理变化,检测血清丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)、空腹血糖(GLU)、甘油三酯(TG)、总胆固醇(TC)的水平.结果 与MC组大鼠相比,LT组、HT组及DT组大鼠血清ALT、AST、ALP、GLU、TG、TC的水平降低,肝细胞脂肪变性及炎症浸润均有减轻,其中以LT组改变最明显(P<0.05).结论 适量的15d-PGJ2对NAFLD大鼠有明显的保护作用,可以改善大鼠的NAFLD.     

血清脂联素水平与老年人脂肪肝的相关性

目的探讨老年人血清脂联素水平的变化,以及老年人脂肪肝与血清脂联素水平和代谢综合征的相关性。方法根据B超检查结果,将264例老年人分为脂肪肝组87例和对照组177例,测定两组老年人的身高、体重、腰围、血脂、血糖、胰岛素和血清脂联素水平,分析上述变量与脂肪肝的相关性,并应用Logistic回归分析评估血清脂联素水平与代谢综合征对老年人脂肪肝的预测性。结果脂肪肝组的脂联素水平明显低于对照组(P<0.01),代谢综合征患病率显著高于对照组(P<0.001),且脂肪肝组的体质量指数、腰围、空腹血糖、餐后2h血糖、胰岛素抵抗指数、总胆固醇、三酰甘油和低密度脂蛋白增高,高密度脂蛋白降低。Lo-gistic回归分析显示,高水平脂联素对脂肪肝有预防作用,而代谢综合征则增加患脂肪肝的危险。结论血清脂联素水平和代谢综合征是预测脂肪肝的有效参数。     

抑制血清TNF-α对大鼠脂肪肝的影响的实验研究

目的观察肿瘤坏死因子-α抑制剂己酮可可碱，对乙醇及高脂饮食诱导造模的大鼠脂肪肝形成的影响。方法将24只大鼠分成对照组、造模组和己酮可可碱组（PTX组）三组，造模组、PTX组采用乙醇及高脂饮食诱导进行脂肪肝造模，同时分别给予蒸馏水、己酮可可碱预防治疗12周。治疗后测定各参数及肝脏病理检查。结果PTX组大鼠血清TNF—α、ALT、AST浓度及肝脂的含量、肝病理脂肪化程度均低于造模组（P〈0．05）。结论肿瘤坏死因子-α抑制剂己酮可可碱能有效防治大鼠脂肪肝形成。     

健脾祛湿法改善高脂饮食诱导胰岛素抵抗的实验研究

目的观察健脾祛湿中药复方对高脂饮食诱导的大鼠胰岛素抵抗的效果,探讨其作用机制。方法高脂饮食诱导大鼠胰岛素抵抗模型,分别给予健脾祛湿中药及罗格列酮干预,观察大鼠胰岛素敏感性、血浆游离脂肪酸、白细胞介素-1、肿瘤坏死因子-α、肝脏脂肪沉积、肝组织甘油三酯、丙二醛变化。结果健脾祛湿复方可明显改善高脂饮食诱导的大鼠胰岛素抵抗,降低血浆游离脂肪酸和白细胞介素-1,减轻肝脏脂肪沉积,改善肝组织甘油三酯和丙二醛升高情况,其效果与罗格列酮无显著差异。结论健脾祛湿法对于高脂饮食诱导的大鼠胰岛素抵抗具有明显的治疗效果,其作用机制与降低炎症细胞因子IL-6、减轻肝脏脂质沉积、缓解氧化应激损伤有关。