牙周炎对非酒精性脂肪肝病影响的研究进展

非酒精性脂肪肝病(non-alcoholic fatty liver disease,NAFLD)是一种常见的不是由过量饮酒或其他病因引起的肝病,其特征是肝脂肪沉积.NAFLD与肥胖、高血压、糖尿病等代谢性疾病有双向关系,肠道微生物组的改变也可能在NAFLD的发病机制中发挥作用.牙周炎是一种由口腔中的致病菌侵犯牙周组织...     

化脂复肝颗粒对糖尿病非酒精性脂肪性肝病小鼠胃肠功能及肠道菌群的影响

目的 探讨化脂复肝颗粒对糖尿病非酒精性脂肪性肝病小鼠胃肠功能及肠道菌群的影响。方法 制备自发性2型糖尿病db/db小鼠非酒精性脂肪性肝病模型,将其随机分为对照组、模型组、化脂复肝颗粒组、非诺贝特组、西沙必利组,行血清学指标检测及肠道粪便基因测序,观察肠道组织病理形态。结果 与对照组相比,模型组总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、谷丙转氨酶（ALT）、谷草转氨酶（AST）水平有所升高,高密度脂蛋白胆固醇（HDL-C）、胰岛素水平有所降低;化脂复肝颗粒在降低TG、LDL-C,升高HDL-C方面的效果较西沙必利更好;化脂复肝颗粒组、非诺贝特组、西沙必利组的ALT、AST水平低于模型组（P<0.01）;化脂复肝颗粒组、非诺贝特组的胰岛素水平高于模型组（P<0.0001）。高通量测序结果显示,在门分类学水平上有拟杆菌门、厚壁菌门、放线菌门、疣微菌门等8类主要细菌。与对照组相比,化脂复肝颗粒组、非诺贝特组、西沙必利组拟杆菌门的丰度偏高,厚壁菌门丰度偏低（P<0.001）。模型组小鼠肠道组织结构紊乱,黏膜及黏膜下层糜烂,严重部位可见溃疡、出血及肉芽...     

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.     

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.     

黄连素对高脂饮食诱导非酒精性脂肪性肝病小鼠肝脂毒性的保护作用及相关机制研究

目的研究黄连素对高脂饮食诱导非酒精性脂肪性肝病(NAFLD)小鼠肝脂毒性的保护作用及其可能作用机制。方法将24只C57BL/6J雄性小鼠随机分为对照组(给予基础饲料进行常规饲养)、高脂组(给予高脂饮食)及干预组(在高脂饮食的同时应用黄连素200 mg/kg进行灌胃3个月),三组各8只。对小鼠原代肝巨噬细胞进行培养,分为A组(未进行处理)、B组(应用0. 5 mmol/L棕榈酸)、C组(应用黄连素1μmol/L)、D组(应用0. 5 mmol/L棕榈酸+黄连素1μmol/L)。检测小鼠空腹血糖(FBG)、总胆固醇(TC)、甘油三酯(TG)、天门冬氨酸氨基转移酶(AST)及丙氨酸氨基转移酶(ALT)浓度;用油红染色法观察三组小鼠肝脏脂质的沉积状况;检测小鼠肝组织白介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)、血清脂多糖水平及促炎细胞因子表达水平。结果高脂组血清FBG、TC、TG、AST及ALT浓度显著高于对照组(P 0. 05);干预组血清FBG、TC、TG及ALT浓度较高脂组显著下降(P 0. 05)。高脂组小鼠肝组织中IL-6和血清脂多糖水平显著高于对照组,干预组小鼠肝组织中IL-6和血清脂多糖水平显著低于高脂组(P 0. 05)。经透射电镜观察可见,B组原代肝巨噬细胞脂质沉积明显,可见胞质中诸多不规则形脂滴; C组与A组原代肝巨噬细胞形态和结构并无显著差异; D组原代肝巨噬细胞内脂滴较少。高脂组小鼠原代肝巨噬细胞中IL-6和TNF-α表达水平显著高于对照组(P 0. 05);干预组小鼠IL-6和TNF-α表达水平较高脂组显著下降(P 0. 05)。结论高脂饮食诱导的NAFLD小鼠应用黄连素进行干预可有效改善其肝脏脂质沉积,减轻肝脏炎症损伤程度,且作用可能与抑制脂多糖生成,进一步阻滞肝内巨噬细胞中炎症因子IL-6和TNF-α等的释放密切相关。     

丹皮酚对高脂饮食诱导大鼠非酒精性脂肪肝的保护作用

目的:研究丹皮酚(Paeonal,Pae)对高脂诱导的大鼠非酒精性脂肪肝(non-alcoholicfattyliverdisease,NAFLD)的保护作用。方法:用高脂乳剂灌胃获得大鼠NAFLD模型,继用Pae和水飞蓟宾(Silymarin)给NAFLD模型大鼠灌胃并与正常组、模型组平行对照,测定各组大鼠的肝脏相关生化指标并观察各组大鼠肝脏的病理变化。结果:Pae对高脂诱导的大鼠NAFLD的生化指标谷草转氨酶(AST)、谷丙转氨酶(ALT)、总胆固醇(TC)、甘油三脂(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)均有影响,其中对ALT、TG,LDL-C的影响有统计学意义(P0.05);肝脏病理切片HE染色也显示Pae药物组的大鼠肝脏损害明显好于模型组。结论:Pae对高脂诱导的大鼠NAFLD模型有一定的保护作用。     

低聚果糖对双歧杆菌增殖效果及肠道菌群的影响

目的　分析低聚果糖体外对双歧杆菌的增殖效果,及体内对肠道菌群的影响。方法　在厌氧菌液体 培养基中加入低聚果糖,观察双歧杆菌的增殖情况;用培养方法检测肠道菌群。结果　在厌氧菌液体培养基中 加入低聚果糖前后双歧杆菌菌数分别为1.5亿/ml和3亿/ml;服用低聚果糖后,35～50患者肠道内肠杆菌及类 杆菌显著减少,50岁以上者肠道内双歧杆菌显著增多。结论　低聚果糖对双歧杆菌有增殖效果,对人体肠道菌 群具有一定的调节作用。     

低聚果糖对双歧杆菌增殖效果及肠道菌群的影响

目的分析低聚果糖体外对双歧杆菌的增殖效果,及体内对肠道菌群的影响。方法在厌氧菌液体培养基中加入低聚果糖,观察双歧杆菌的增殖情况;用培养方法检测肠道菌群。结果在厌氧菌液体培养基中加入低聚果糖前后双歧杆菌菌数分别为1．5亿／ml和3亿／ml;服用低聚果糖后,35～50患者肠道内肠杆菌及类杆菌显著减少,50岁以上者肠道内双歧杆菌显著增多。结论低聚果糖对双歧杆菌有增殖效果,对人体肠道菌群具有一定的调节作用。     

软脉灵对非酒精性脂肪肝大鼠肝组织抗氧化能力的影响

目的观察软脉灵对非酒精性脂肪性肝病大鼠肝组织抗氧化能力的影响。方法采用高脂饲料喂养方式建立SD大鼠模型。模型A组采用高脂饲料喂养，药物A组高脂饲料喂养同时予软脉灵灌胃，两组均于8、16周处死；模型B组高脂饲料喂养16周后改基础饲料喂养，药物B组高脂饲料喂养16周后改基础饲料喂养，并予软脉灵灌胃，两组均于24、32周处死；空白对照组应用基础饲料喂养，于第16、32周处死。观察肝组织抗氧化指标。结果预防实验中，软脉灵能减小肝组织MDA升高的水平及SOD降低的程度（P〈0．05～0.01）；治疗实验中，软脉灵能降低肝组织MDA水平（P〈0．05～0．01），提高SOD活力（P〈0．01）。结论在非酒精性脂肪性肝病大鼠模型中，软脉灵有改善肝脏抗氧化能力的作用。     

非酒精性脂肪肝对急性心肌梗死患者预后的影响

目的探讨急性心肌梗死(acute myocardial infarction, AMI)并发非酒精性脂肪肝(non-alcoholic fatty liver disease, NAFLD)患者血脂、血清炎性因子水平变化,及NAFLD对AMI预后的影响。方法 AMI患者712例,其中350例有NAFLD者为观察组,362例无NAFLD者为对照组。比较2组入院时年龄,性别比例,体质量指数(body mass index, BMI),合并高血压、2型糖尿病情况,ST段抬高型心肌梗死(ST-segment elevation myocardial infarction, STEMI)及非STEMI比率,冠状动脉病变支数,行经皮冠状动脉介入术(percutaneous coronary intervention, PCI)比率,药物治疗情况以及血清肌钙蛋白I(cardiac troponin I, cTnI)、尿酸(uric acid, UA)、同型半胱氨酸(homocysteine, Hcy)、C反应蛋白(C-reactive protein, CRP)、总胆固醇(total cholesterol, TC)、三酰甘油(triacylglycerol, TG)、高密度脂蛋白胆固醇(high-density lipoprotein cholesterol, HDL-C)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol, LDL-C)、白细胞计数(white blood cell count, WBC),D-二聚体(D-dimer, D-D)、血小板/淋巴细胞比值(platelet lymphocyte ratio, PLR);随访观察主要心脑血管不良事件(major cardiovascular and cerebrovascular adverse events, MACCE)发生率及生存时间;Pearson相关分析SYNTAX积分与UA等指标的相关性。结果观察组BMI[(29.00±1.41)kg/m^2]、合并2型糖尿病比率(60.57%)、SYNTAX积分[(24.50±2.37)分]及血清TC[(5.67±0.63)mmol/L]、TG[(2.31±0.27)mmol/L]、LDL-C[(3.13±0.51)mmol/L]、UA[(502.20±31.51)μmol/L]、Hcy[(16.91±1.85)μmol/L]、CRP[(22.30±0.37)mg/L]、WBC[(13.08±2.09)×10^9/L]、D-D[(1.36±0.32)g/L]、PLR(191.34±8.15)均高于对照组[BMI:(27.00±1.69)kg/m^2,合并糖尿病比率:41.99%,SYNTAX积分:(19.60±3.95)分,TC:(5.02±0.35)mmol/L,TG:(1.91±0.40)mmol/L,LDL-C:(2.38±0.55)mmol/L,UA:(446.20±51.08)μmol/L,Hcy:(13.63±1.50)μmol/L,CRP:(13.20±0.33)mg/L,WBC:(11.16±0.98)×10^9/L,D-D:(0.95±0.26)g/L,PLR:158.85±8.35](P<0.05);2组年龄,性别比例,合并高血压比率,冠状动脉病变支数,STEMI、非STEMI、PCI比率,阿司匹林等药物应用比率,血清HDL-C、cTnI水平比较差异无统计学意义(P>0.05);观察组MACCE发生率(9.71%)高于对照组(5.52%)(P<0.05),中位生存时间(14.5个月)较对照组(15.4个月)短(P<0.05);Pearson相关分析显示,SYNTAX积分与UA(r=0.876,P<0.001)、Hcy(r=0.736,P<0.001)、CRP(r=0.278,P=0.038)、TC(r=0.644,P<0.001)、TG(r=0.641,P<0.001)、LDL-C(r=0.633,P<0.001),BMI(r=0.599,P<0.001)、PLR(r=0.456,P<0.001)均呈正相关。结论 NFALD可能加剧AMI患者炎性反应,增高血脂,加重冠状动脉血管狭窄程度,增加MACCE发生率,影响AMI患者预后。     

进展性非酒精性脂肪性肝病无创性诊断的临床研究进展

非酒精性脂肪性肝病(NAFLD)目前已是世界第一大慢性肝脏疾病,为全球终末期肝病、肝细胞癌和肝移植的主要原因。NAFLD的病理变化是从单纯性肝脂肪病变进展为非酒精性脂肪性肝炎(NASH),最终可进展至中晚期肝纤维化,因此准确诊断和鉴别NASH和纤维化对NAFLD的治疗和管理是十分必要的。近年来,肝活组织检查的局限性促使无创诊断技术迅速发展。本文就进展性NAFLD(NASH及纤维化)的无创性诊断方法展开论述,明确各种新的无创性诊断手段的特点,旨在进一步优化NAFLD的临床管理,推动本领域科学研究进展。     

小檗碱对非酒精性脂肪性肝病患者血清骨钙素的影响

目的:探讨小檗碱对伴糖代谢紊乱的非酒精性脂肪性肝病(NAFLD)患者的血清未羧化骨钙素(ucOC)水平的影响。方法:对伴有糖耐量受损或2型糖尿病的114例NAFLD患者,进行生活方式干预,其中57例(小檗碱组)加小檗碱治疗(0.5 g/次,每日3次),共干预16周,其余57例仅进行生活方式干预,作为对照组。评价干预前后患者ucOC水平变化及血糖、血脂和肝脏脂肪含量(HFC)等指标,分析ucOC变化的影响因素。结果:与对照组相比,小檗碱组患者血清ucOC水平升高更明显(P0.001)。校正年龄、性别和体质指数(BMI)后,小檗碱组血清ucOC的改善情况[4.60(3.50, 5.70)]仍明显优于对照组[0.96(-0.14, 2.05),P0.001],平均差异为3.64 (95%CI 1.74～5.55)。亚组分析显示,在非肥胖老年男性患者中,小檗碱升高ucOC的作用更加明显。偏相关分析显示,在校正年龄、性别后,治疗前后血清ucOC水平差值与BMI、体质量、腰围、HFC、糖化血红蛋白(HbA1c)、总胆固醇(TC)的差值负相关(P0.05)。结论:小檗碱能改善伴糖代谢紊乱的非酒精性脂肪性肝病患者代谢异常,可能与其升高血清ucOC水平有关。     

The association of non-alcoholic fatty liver disease and atrial fibrillation: a review

Non-alcoholic fatty liver disease (NAFLD) is highly prevalent and causes an enormous burden to human health and health-care systems all over the world. A great proportion of this burden results from increased risk of cardiovascular diseases. Atrial fibrillation (AF) is the most common chronic heart arrhythmia globally and it increases the risk of embolic stroke and heart failure. Recent studies have explored the association between NAFLD and AF with somewhat conflicting results. However, ultrasound-verified prospective studies concur that NAFLD is associated with the incidence of AF. According to epidemiological evidence, the greater the prevalence of NALFD in a population, the stronger the association with AF incidence and prevalence. Specifically, diabetic individuals with NAFLD are at the greatest risk of AF. Additionally, the risk of AF may concentrate most in individuals with advanced NAFLD, particularly those with liver fibrosis. The possible mechanistic factors between NAFLD and AF, particularly obesity and systemic inflammation, are diverse and form a complex interplaying network. However, further studies are needed to elucidate whether NAFLD has a causative role in the development of AF. The purpose of this article is to review and discuss the epidemiologic evidence and possible mechanistic links between these two conditions.

• KEY MESSAGES

• Although epidemiologic studies have provided conflicting results on the association of NAFLD and AF, prospective studies with ultrasound-verified NAFLD concur that NAFLD is associated with about 2-fold greater incidence of AF among general population and about 6-fold greater incidence among subjects with type 2 diabetes.

• The risk of AF among individuals with NAFLD is increased by other cardiovascular risk factors, especially type 2 diabetes and advanced age.

• The possible mechanistic links between NALFD and AF are diverse, with obesity and systemic inflammation having a significant role, but further studies are needed until NAFLD can be established as a causal factor in the incidence of AF.

     

化滞柔肝颗粒治疗非酒精性脂肪肝的临床研究

目的观察化滞柔肝颗粒治疗非酒精性脂肪肝(NAFLD)的临床疗效。方法将本院门诊收冶的120例NAFLD患者随机分为2组,每组60例。治疗组给予化滞柔肝颗粒,对照组给予水飞蓟宾胶囊,比较2组临床症状、血脂、肝功能及体质量指数(BMI)改善情况。结果治疗组总有效率以及肝区胀痛、疲乏、易怒、上腹闷痛、食欲减退的改善率均显著高于对照组,且治疗组血脂、肝功能及BMI的改善程度也显著优于对照组。结论与水飞蓟宾胶囊相比较,化滞柔肝颗粒对NAFLD患者临床症状、血脂、肝功能及BMI的改善作用更好,值得临床推广应用。     

4周有氧运动干预对大鼠非酒精性脂肪肝和肝内细胞色素P450 2E1的影响

目的:探讨4周有氧运动干预对大鼠非酒精性脂肪肝(NAFLD)和肝内细胞色素P4502E1(CYP2E1)的影响。方法:实验大鼠随机分为对照组、模型组和模型+运动组。模型组和模型+运动组经6周脂肪乳灌胃,制成非酒精性脂肪肝模型。随后模型+运动组进行为期4周有氧运动干预。检测各组大鼠胆固醇、甘油三酯、肝脏组织病理改变和肝组织CYP2E1表达。结果:造模组大鼠体重及血脂明显增高(P0.05),肝脏病理学检查证实非酒精性脂肪肝模型造模成功。模型组及模型+运动组肝脏CYP2E1明显较对照组增高(P0.05)。经过4周游泳训练后,模型+运动组大鼠与模型组比较胆固醇、甘油三酯和肝脏CYP2E1呈下降趋势(P0.05);肝脏病理学检查提示脂肪肝较模型组明显好转。结论:有氧运动不仅能够改善高脂血症状态,也能降低CYP2E1表达,可以预防和治疗NAFLD时肝组织所受的过氧化损伤。     

非酒精性脂肪性肝病患者抗阻运动效果的系统评价

目的系统评价抗阻运动对非酒精性脂肪性肝病患者的干预效果。方法计算机检索Cochrane、Pubmed、Embase、EBSCO、中国生物医学文献光盘数据库(CBMdisc)、CNKI和万方数据库中关于非酒精性脂肪性肝病患者抗阻运动的相关对照研究,包括随机对照试验或类随机对照试验。检索年限从建库至2015年4月。由2名研究者对文献质量进行严格评价和资料提取。结果纳入3个随机对照试验和1个类随机对照试验,共135例患者为研究对象。质量评价结果表明,4个研究的总体质量水平均不高。由于有2个随机对照试验研究无法获得干预后数据,1个研究不是随机对照试验,所以本系统评价无法进行Meta分析,仅采用描述性分析。评价结果显示,抗阻运动可降低非酒精性脂肪性肝病患者的体质量和脂肪量,并增加肌肉量,同时可改善胰岛素抵抗和肝脏脂肪变性的程度。结论抗阻运动可以作为有氧运动的一种补充形式,对非酒精性脂肪性肝病患者的治疗有帮助。     

大黄酸对小鼠非酒精性脂肪肝病的治疗效果分析

目的:探讨脂肪相关基因(fat mass and obesity associated gene,FTO)及其抑制剂大黄酸(rhein)在非酒精性脂肪肝病(non-alcoholic fatty liver disease,NAFLD)中的作用.方法:采用高脂饲料喂养的方法构建NAFLD小鼠模型,利用灌胃的方式使用rh...     

Association of homocysteine level with biopsy-proven non-alcoholic fatty liver disease: a meta-analysis

Previous studies have reported inconsistent findings regarding the association between plasmatic higher of homocysteine level and non-alcoholic fatty liver disease. We aimed to investigate this association by conducting a meta-analysis. Literature was searched on PubMed from inception to January 2015. Eight studies evaluating plasma level of homocysteine in biopsy-proven non-alcoholic fatty liver disease subjects compared to healthy controls were included. Compared with the controls, non-alcoholic fatty liver disease patients witnessed a higher level of homocysteine [standard mean difference (SMD): 0.66 µmol/L, 95% CI: 0.41, 0.92 µmol/L], and were associated with a significant increased risk for hyperhomocysteinemia [odds ratio (OR) 5.09, 95% CI: 1.69, 15.32]. In addition, patients with non-alcoholic fatty liver presented 0.45 µmol/L higher levels of homocysteine compared to healthy controls (95% CI: 0.09, 0.82 µmol/L), whereas non-alcoholic steatohepatitis patients had 1.02 µmol/L higher levels of homocysteine (95% CI: 0.28, 1.76 µmol/L). There was neither difference of folate level nor vitamin B12 level between non-alcoholic fatty liver disease subjects and healthy controls. This study revealed that non-alcoholic fatty liver disease patients presented an increased serum concentration of homocysteine, and were associated with an increased risk of hyperhomocysteinemia. Further studies are needed to demonstrate a causal role of hyperhomocysteinemia in non-alcoholic fatty liver disease.     

Sinapine-enriched rapeseed oils reduced fatty liver formation in high-fat diet-fed C57BL/6J mice

Oil enrichment with trace amounts of components has significant effects on animal nutrition and health. In this work, the potential impact of sinapine, a trace amount of polyphenol naturally present in rapeseeds, was investigated in high-fat diet (HF)-fed C57BL/6J mice. The mice were fed with different diets including chow diet (LF), HF diet, rapeseed oil-containing HF diet (RO), and rapeseed oils enriched with sinapine (500 mg kg⁻¹ oil, high-fat diet, RP) for 12 weeks. Here, it was demonstrated that sinapine supplementation significantly reduced (P < 0.05) body weight increase, fat accumulation, and fatty liver formation in mice when compared with those fed with a high-fat diet. The TG, LDL-C, ALT and AST levels in the RP group were significantly reduced (P < 0.05) by 15.67%, 73.62%, 20.67%, and 31.58%, respectively, compared with that in the HF group. Besides, the addition of sinapine prevented the degeneration of mouse adipocytes and lipid accumulation in the liver. Moreover, this change was achieved by downregulating SREBP-1c and FAS and upregulating PPAR-α and ACOX1 gene expression levels. Our results indicate that sinapine can be used as a prebiotic to enhance the nutritional function of vegetable oils to prevent obesity-related chronic diseases such as NAFLD.

Sinapine reduces lipid accumulation in cells and the liver by regulating lipid metabolism.