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1.
目的了解甲状腺功能减退症患者血脂水平变化及非酒精性脂肪性肝病的发生情况。方法检测甲状腺功能减退症患者和对照人群甲状腺功能和血脂水平,同时进行肝脏B超或CT检查比较两组脂肪肝的检出率。结果甲状腺功能减退症患者比对照组血脂水平升高,脂肪肝检出率(35.7%对10.7%,P〈0.001)明显增加;血脂水平与甲状腺激素水平呈负相关。甲状腺功能减退伴脂肪肝患者与无脂肪肝患者比,在年龄、体重指数和甲状腺激素水平方面均无显著性差异,而脂肪肝患者血脂水平显著高于非脂肪肝患者。结论与对照组比,甲状腺功能减退症患者血脂水平升高,非酒精性脂肪性肝病的发生率增加。  相似文献   

2.
非酒精性脂肪性肝病(NAFLD)目前已经成为全球流行的慢性肝脏疾病.运动能够改善NAFLD.研究证实,运动能够减轻肝脏脂肪沉积及炎性反应,但其具体机制尚不明确,有待进一步研究.  相似文献   

3.
Autophagy is a mechanism involved in cellular homeostasis under basal and stressed conditions delivering cytoplasmic content to the lysosomes for degradation to macronutrients. The potential role of autophagy in disease is increasingly recognised and investigated in the last decade. Nowadays it is commonly accepted that autophagy plays a role in the hepatic lipid metabolism. Hence, dysfunction of autophagy may be an underlying cause of non-alcoholic fatty liver disease. However, controversy of the exact role of autophagy in the lipid metabolism exists: some publications report a lipolytic function of autophagy, whereas others claim a lipogenic function. This review aims to give an update of the present knowledge on autophagy in the hepatic lipid metabolism, hepatic insulin resistance, steatohepatitis and hepatic fibrogenesis.  相似文献   

4.
Non-alcoholic fatty liver disease(NAFLD) is the hepatic manifestation of metabolic syndrome and is one of the most prevalent liver disorders worldwide. NAFLD can gradually progress to liver inflammation, fibrosis, cirrhosis and even hepatocellular carcinoma. However, the pathogenesis of NAFLD is complex, and no efficient pharmaceutic treatments have yet been established for NAFLD. Accumulating data have shown that the farnesoid X receptor(FXR) plays important roles not only in bile acid metabolism, but also in lipid and carbohydrate homeostasis, inflammatory responses, among others. In this review, we aim to highlight the role of FXR in the pathogenesis and treatment of NAFLD.  相似文献   

5.
目前,非酒精性脂肪肝病(NAFLD)的发病率逐年攀升,已成为危害人类健康的三大肝病之一。解偶联蛋白-2(UCP-2)是新发现的一种位于线粒体内膜上的载体蛋白,具有刺激产热,减少ATP生成,抑制反应性氧簇的产生,负性调节胰岛素分泌以及抗凋亡作用。在脂肪肝中,UCP-2表达增加。现就UCP-2在NAFLD中的作用进行综述。  相似文献   

6.
In recent years, there has been a steady growth of interest in non-alcoholic fatty liver disease(NAFLD), which is associated with negative epidemiological data on the prevalence of the disease and its clinical significance. NAFLD is closely related to the metabolic syndrome and these relationships are the subject of active research. A growing body of evidence shows cross-linkages between metabolic abnormalities and the innate immune system in the development and progression of NAFLD. These links...  相似文献   

7.
非酒精性脂肪性肝病(non-alcoholic fatty liver disease, NAFLD)已成为目前全球最主要的慢性肝病病因,是当前研究的热点问题,其预防和治疗也成了研究的重点和难点,目前尚无批准上市的特异性药物及明确的治疗方案,本文针对NAFLD的相关治疗及新兴靶向药物作一概述,给临床医师提供参考。  相似文献   

8.
目的 分析慢性乙型肝炎(CHB)合并非酒精性脂肪性肝病(NAFLD)患者血清反应性氧化物(ROS)和脂联素(ADPN)水平的变化。方法 2018年1月~2020年1月我院收治的CHB合并NAFLD患者97例和CHB患者97例,采用全自动生化分析仪检测血生化指标,采用ELISA法检测血清ROS、ADPN和肿瘤坏死因子-α(TNF-α)水平,应用NAFLD肝纤维化评分(NFS)系统评估NFS评分,使用瞬时弹性扫描仪行肝硬度检测(LSM)和受控衰减参数(CAP)。结果 CHB合并NAFLD患者血清GGT水平为(96.5±13.3)U/L,显著高于CHB组【(67.3±12.5)U/L,P<0.05】;CHB合并NAFLD患者血清FPG、TC、TG和LDL-C水平分别为(5.9±1.0)mmol/L、(5.2±1.1)mmol/L、(2.8±0.4)mmol/L和(2.8±0.4)mmol/L,显著高于CHB组【分别为(4.9±1.0)mmol/L、(4.1±0.8)mmol/L、(1.7±0.3)mmol/L和(2.2±0.3)mmol/L,P<0.05】,而HDL-C为(0.9±0.2)mmol/L,显著低于CHB组【(1.2±0.2)mmol/L,P<0.05】;CHB合并NAFLD患者血清ROS和TNF-α水平分别为(1.7±0.4)U/mL和(32.6±5.4)ng/L,显著高于CHB组【分别为(0.9±0.2)U/mL和(21.5±4.8)ng/L,P<0.05】,而血清ADPN水平为(8.7±1.9)ng/mL,显著低于CHB组【(10.2±2.3)ng/mL,P<0.05】;CHB合并NAFLD患者NFS、LSM和CAP分别为(0.2±0.1)分、(10.2±1.3)kPa和(287.4±44.3)dB/m,均显著高于CHB组【分别为(-1.4±0.1)分、(9.1±1.2)kPa和(242.5±38.7)dB/m,P<0.05】。结论 CHB合并NAFLD患者血清ROS明显升高,而血清ADPN水平显著下降,可能参与了其发病过程。  相似文献   

9.
非酒精性脂肪性肝病的研究进展   总被引:1,自引:0,他引:1  
非酒精性脂肪性肝病经历由非酒精性单纯性脂肪肝发展至非酒精性脂肪性肝炎和肝硬化或原发性肝癌的缓慢过程,并与心血管病的发生关系密切.本文针对非酒精性脂肪性肝病的流行病学、发病机制、诊断和治疗等的研究进展进行综述.  相似文献   

10.
脂肪因子与非酒精性脂肪肝   总被引:2,自引:0,他引:2  
非酒精性脂肪性肝病的发病机制目前尚不十分清楚,脂代谢异常(尤其是TG)与胰岛素抵抗(IR)可能是其病因的关键环节,瘦素、脂联素、抵抗素、肿瘤坏死因子等多种脂肪因子在非酒精性脂肪肝的形成、炎性改变及纤维化的过程中发挥了重要作用.  相似文献   

11.
目的通过NAFLD不同发展阶段的动物模型研究线粒体的细胞色素C氧化酶(COX)和肉毒碱棕榈酰转移酶(CPT))在NAFLD进展中的变化。方法建立单纯性脂肪肝(NAFL)和非酒精性脂肪性肝炎(NASH)的大鼠模型,通过大鼠肝脏病理切片HE染色和血清生化指标的检测验证模型的成立,使用RT-PCR和Western印迹检测大鼠肝脏的COX和CPT的mRNA和蛋白的表达量。同时在大鼠肝脏中提取线粒体,检测纯化的肝脏线粒体中两种酶的活性变化。结果 NAFL大鼠肝脏呈现轻度的脂肪变性和气球样变,NASH组大鼠肝脏则呈现弥漫的大泡性脂肪变和炎性浸润。与对照组相比,肝脏COX、CPT的基因和蛋白表达量在NAFL组和NASH组均降低(P0.05)。在纯化线粒体中的检测提示,COX在NAFL和NASH组分别降低20%和35%,且NASH组显著低于NAFL组(P0.05);CPT在NAFL和NASH组分别降低35%和50%,且NASH组显著低于NAFL组(P0.05)。结论在NAFLD进程中,线粒体的能量转化和物质代谢功能都受到了不同程度的抑制,且随着疾病进展而加重。  相似文献   

12.
肝细胞癌(HCC)发病率高,乙型肝炎病毒(HBV)和丙型肝炎病毒(HCV)感染是HCC的主要病因.近年来,肥胖、2型糖尿病等代谢疾病的流行加速了非酒精性脂肪性肝病(NAFLD)的发生,导致NAFLD相关性HCC(NAFLD-HCC)的发生也逐年递增.但NAFLD-HCC与病毒相关性HCC是否有相似的发病机制、预防、监测...  相似文献   

13.
14.
The incidence of non-alcoholic fatty liver disease (NAFLD) is rapidly increasing and lifestyle interventions to treat this disease by addressing the underlying metabolic syndrome are often limited. Many pharmacological interventions are being studied to slow or even reverse NAFLD progression. This review for hepatologists aims to provide an updated understanding of the pathogenesis of NAFLD, current recommended therapies, and the most promising treatment options that are currently under development.  相似文献   

15.
目的分析非酒精性脂肪性肝病(NAFLD)与代谢综合征(MS)的关系。方法10357例在我院体检的普通人群入选本研究,检测人体学参数、生化指标及肝脏彩超,分析该人群NAFLD和MS的患病率,探讨MS组分与NAFLD的关系。结果10357例体检者中NAFLD的患病率为31.1%,MS患病率为23.6%,NAFLD合并MS患病率为15.5%。经年龄标化后NAFLD和MS患病率男性仍明显高于女性。将全部受试者按BM1分组后,各组间NAFLD、MS及NAFLD合并MS患病率差异均有统计学意义(P〈0.01)。选择同期体检无NAFLD的个体(非NAFLD组),经性别、年龄、BMI与NAFLD组相匹配后,NAFLD组MS患病率明显高于非NAFLD组(59.8%VS5.2%,P〈0.01)。多因素Logistic回归分析表明:NAFI。D危险因素的前五位为TG、BMI、FPG、LDL-C和吸烟。结论即使排除BMI因素的影响,NAFLD患者MS的患病率仍然明显增高。NAFLD危险因素由高到低依次为TG、BMI、FPG、LDL-C、吸烟、TC、性别、血压、SUA及ALT。HDL-C为NAFLD保护性因素。  相似文献   

16.
Non-alcoholic fatty liver disease(NAFLD) is the most common form of chronic liver disease and its incidence is increasing worldwide. However, the underlying mechanisms leading to the development of NAFLD are still not fully understood. Glycosyltransferases(GTs) are a diverse class of enzymes involved in catalyzing the transfer of one or multiple sugar residues to a wide range of acceptor molecules. GTs mediate a wide range of functions from structure and storage to signaling, and play a key role in many fundamental biological processes. Therefore, it is anticipated that GTs have a role in the pathogenesis of NAFLD. In this article, we present an overview of the basic information on NAFLD, particularly GTs and glycosylation modification of certain molecules and their association with NAFLD pathogenesis. In addition, the effects and mechanisms of some GTs in the development of NAFLD are summarized.  相似文献   

17.
非酒精性脂肪性肝病(NAFLD)是一种与胰岛素抵抗、脂质代谢紊乱、慢性炎症以及遗传易感性强烈关联的获得性代谢应激性肝损伤,疾病谱包括单纯性脂肪肝、脂肪性肝炎及其相关纤维化、肝硬化。由于肥胖症和代谢综合征在全球的流行,近20年亚洲国家和地区NAFLD增长迅速,导致疾病谱变迁,NAFLD现已成为欧美发达国家(流行率17%~33%)以及我国经济较发达地区的第一大慢性肝病。近几年研究发现,自噬作为一种细胞程序,在介导脂质代谢过程中具有非常关键的作用,结合NAFLD的流行病学、发病机制,本文就自噬在肝脏脂质代谢中的作用意义及其与IR的关系研究现状作一综述。  相似文献   

18.
非酒精性脂肪性肝病(NAFLD)是代谢综合征在肝脏的病理学表现。由于饮食结构的改变,NAFLD发病率呈现上升趋势,且NAFLD与肝病进展、糖尿病和心血管疾病死亡密切相关。因此,寻求NAFLD患者综合管理方法迫在眉睫。本文综述了NAFLD分级、分期、治疗和随访评估的研究进展,以期指导临床诊断、治疗和管理。  相似文献   

19.
非酒精性脂肪性肝病是由于肝脏中脂肪过度沉积,诱发炎性反应以及氧化应激损伤的一组疾病.而尿酸是人类嘌呤代谢的终产物,在体内起到抗氧化、调节免疫功能等生理作用.越来越多的证据表明高尿酸血症与非酒精性脂肪性肝病有关.不论是横断面研究还是前瞻性研究均显示高尿酸血症是非酒精性脂肪性肝病的独立危险因素.高尿酸血症可成为机体的致炎因子,诱导胰岛素抵抗,激发炎性反应信号通路,诱导炎性因子的产生,导致肝细胞中脂肪的积聚和炎性损伤.降尿酸治疗可对肝脏起到保护作用,可能成为非酒精性脂肪性肝病的治疗手段.  相似文献   

20.
There is no single pharmacologic therapy that has been approved to treat nonalcoholic fatty liver disease in the general population. The backbone of therapy currently includes intensive lifestyle modification with established targets for diet and weight loss. The use of unsweetened, unfiltered coffee along with limiting high fructose corn syrup have emerged as beneficial dietary recommendations. The use of empiric oral hypoglycemic agents and vitamin E, however, has not been widely accepted. Developing bariatric surgical techniques are promising, but additional studies with long-term follow up are needed before it can be widely recommended. Finally, liver transplantation is an increasingly frequent consideration once complications of end-stage disease have developed. The future treatment of those with nonalcoholic fatty liver disease will likely involve a personalized approach. The importance of the gut microbiome in mediating hepatocyte inflammation and intestinal permeability is emerging and may offer avenues for novel treatment. The study of anti-fibrotic agents such as pentoxifylline and FXR agonists hold promise and new pathways, such as hepatocyte cannabinoid receptor antagonists are being studied. With the incidence of obesity and the metabolic syndrome increasing throughout the developed world, the future will continue to focus on finding novel agents and new applications of existing therapies to help prevent and to mediate the progression of nonalcoholic fatty liver disease.  相似文献   

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