非酒精性脂肪肝患者血清抵抗素与胰岛素抵抗关系的研究

目的 探讨非酒精性脂肪肝患者血清抵抗素水平及其与肥胖、胰岛素抵抗、血糖、血脂的关系.方法 选择非酒精性脂肪肝患者100例,正常对照30例,采用ELISA方法测定空腹血清抵抗素,同时检测其身高、体重、腰围、臀嗣、血糖、血脂、肝功能及胰岛素水平,并计算体重指数、腰臀比和胰岛索敏感指数.结果 非酒精性脂肪肝患者血清抵抗素水平为17.68±5.2 ng.ml,高于正常对照组的12.85±4.4 ng.ml,P<0.01.相关分析显示,血清抵抗素与体重指数、甘油三酯呈正相关关系(分别为r=0.376、0.426,P<0.05),与胰岛素敏感指数呈负相关关系,(r=-0.584,P<0.01),而与腰臀比、总胆固醇、低密度酯蛋白胆固醇、高密度脂蛋白胆固醇、血糖无相关性,(P>0.05).结论 在非酒精性脂肪肝的发病过程中,抵抗素可能参与了胰岛素抵抗.     

非酒精性脂肪肝与肥胖及胰岛素抵抗的关系

探讨非酒精性脂肪肝 (NASH)的体脂含量和分布特征 ,血脂情况及与胰岛素抵抗的关系。对 87例观察对象分为NASH组 (30例 )和对照组 (5 7例 ) ,检测身高、体重、血脂、血糖、血胰岛素 ,计算胰鸟素敏感指数和体重指数 ;做腹部CT扫描以其配备软件计算腹内脂肪面积 (VA)和腹皮下脂肪面积 (SA)。 6 8例肥胖者发生NASH2 8人(41 18% ) ,19例体重正常者发生HASH2人 (10 5 3% )。 (x2 =6 175 ,P <0 0 2 5 )差异有显著性。不伴NASH的肥胖者VA(x±s,cm2 ) (男 :10 5 8± 2 9 6　女 :117 3± 33 1)与伴有NASH的肥胖者VA(男 :138 2± 5 3 7　女 :14 2 6± 31 2 )比较差异有显著性 (t =2 72 ,2 31　P <0 0 1,0 0 5 )。无NASH肥胖者与伴有NASH肥胖者比较IAI差异有显著性 (t =1 98　P <0 0 5 )。肥胖尤其是腹内型肥胖与NASH有密切的关系 ;肥胖者发生NASH ,胰岛素抵抗在其中起重要作用。     

非酒精性脂肪肝患者血浆抵抗素水平测定及与胰岛素抵抗的相关性

目的 探讨血浆抵抗素水平变化在非酒精性脂肪肝（NAFLD）发病中的作用及与胰岛素抵抗（IR）的关系。方法选择32例单纯NAFLD患者（F组）、29例NAFLD并2型糖尿病患者（FD组）和30例体检正常者（对照组）,分别测定空腹血浆抵抗素、空腹血糖（FPG）及胰岛素（FINS）水平,计算胰岛素敏感指数（ISI）,并分析其相关性。结果F组和FD组血浆抵抗素水平、FINS及ISI均明显高于对照组,尤以FD组为著;且血浆抵抗素水平与FINS、FPG呈正相关,与ISI呈负相关。结论NAFLD患者血浆抵抗素水平升高（尤以并2型糖尿病者为著）,并与ISI呈负相关;此可能在NAFLD等IR相关性疾病的发生、发展中具有一定作用。     

非酒精性脂肪肝与胰岛素抵抗的关系

探讨非酒精性脂肪肝(NAFL)发病与胰岛素抵抗的关系。对63例受检者用放免法测定血清胰岛素,稳态模型法计算胰岛素抵抗指数。同时选择20例无脂肪肝肥胖者作为对照组。脂肪肝组与对照组比较,血清胰岛素、胰岛素抵抗指数显著性增高(P<0.001),重度脂肪肝与中度脂肪肝、轻度脂肪肝比较,血清胰岛素、胰岛素抵抗指数也存在明显增高(P<0.05)。胰岛素抵抗可能系脂肪肝发病的原发因素,而非继发性改变。     

非酒精性脂肪肝与胰岛素抵抗

鉴于在一般人群特别是肥胖人群和2型糖尿病人群中合并非酒精性脂肪肝（NAFL）者增加，NAFL的重要性已引起临床重视。本期胰岛素抵抗及其相关疾病专栏刊出了颜红梅、路影和姚定国等作者撰写的有关NAFL的文章，分别对无糖尿病、糖耐量减低（IGT）和2型糖尿病三种人群伴发NAFL和胰岛素抵抗的相关性等进行了临床观察比较。为此，特请本刊编委高鑫教授就NAFL与胰岛素抵抗的相关机制及其对2型糖尿病的防治意义发表评论，期望引起读、作者和临床同道的关注，进一步开展对NAFL的临床和相关机制的研究。[编者按]     

非酒精性脂肪肝与胰岛素抵抗

目的探讨非酒精性脂肪性肝病（NAFLD）与胰岛素抵抗（IR）的关系。方法NAFLD组52例,非NAFLD组50例,比较两组间BMI、WHR、TC、TG、CRP、HDL-C、LDL-C、ALT、Cr、FBG、FINS和HOMA-IR的差异,并进行Logistic回归分析。结果NAFLD组与非NAFLD组在BMI（26.7±2.3与22.4±2.5,P〈0.01）、WHR（0.94±0.06与0.83±0.05,P〈0.01）、TG（2.4±0.6与1.8±0.6,P〈0.01）、ALT（37.3±8.3与28.1±7.2,P〈0.05）、FBG（6.2±1.4与5.2±0.7,P〈0.01）、FINS（23.6±13.6与8.6±3.5,P〈0.01）、HOMA-IR（6.7±4.7与2.0±1.6,P〈0.01）的差异有统计学意义,Logistic回归分析显示BMI（P〈0.01）、WHR（P〈0.01）、TG（P〈0.01）、ALT（P〈0.05）、HOMA-IR（P〈0.01）是NAFLD的独立影响因素。结论BMI、WHR、TG、ALT、HOMA-IR是NAFLD的独立影响因素。     

非酒精性脂肪肝患者瘦素抵抗和胰岛素抵抗研究

为了研究非酒精性脂肪肝(NAFL)患者的瘦素(Leptin)抵抗和胰岛素抵抗的状况，对40例NAFL患者和30例正常对照组的血清瘦素、胰岛素等水平进行了分析研究，现将结果报道如下。     

抵抗素在非酒精性脂肪肝病中对胰岛素抵抗和肝纤维化的作用

目的:探讨抵抗素(resistin)在非酒精性脂肪肝病(non-alcoholic fatty liver disease,NAFLD)中对胰岛素抵抗(insulin resistin,IR)及肝纤维化的作用.方法:应用高脂饮食喂养Wistar大鼠建立NAFLD肝纤维化模型.健康♂,Wistar大鼠30只,随机分成正常对照组和模型组,各15只,分别给予普通饲料和高脂饲料喂养.分别于第15、18、21周末将对照组和模型组随机各处理5只.检测空腹血糖(FBG)、空腹胰岛素(FINS)、Ⅲ型前胶原(PCⅢ)、透明质酸(HA)、Ⅳ型胶原(CⅣ)、层粘蛋白(LN)水平,采用稳态模型评估法(HOMA)评估IR(HOMA-IR);HE、VG染色及电镜观察肝组织纤维化情况.RT-PCR法检测大鼠肝组织中resistin基因mRNA表达.结果:随着高脂喂养时间的延长,HE、VG染色及电镜观察肝组织病理学显示大鼠肝脏脂肪变性及肝纤维化程度逐渐加重,NAFLD模型组HOMA-IR、PCⅢ、LN、CⅣ、HA、resistin逐渐增加,且以21wk时升高最为明显,分别为33.74g/L±10.41g/L、2.96g/L±0.76g/L、4.14g/L±1.07g/L、19.07g/L±2.78g/L、848.87g/L±204.04g/L、0.99g/L±0.10g/L,与相应时相对照组比较差异具有统计学意义(P<0.05或P<0.01).Spearman相关性分析抵抗素与HOMA-IR、PCⅢ、LN、CⅣ、HA呈显著正相关,相关系数r分别为0.77、0.80、0.68、0.67、0.76(P<0.05或P<0.01).结论:在NAFLD纤维化形成过程中,抵抗素表达升高诱导IR并促使肝纤维化的形成与进展.     

非酒精性脂肪肝与胰岛素抵抗

非酒精性脂肪肝(NAFLD)是指无酒精摄取史的人群发生类似酒精性脂肪肝的组织学及生化改变的临床综合征。NAFLD常与肥胖、2型糖尿病、高血压、高脂血症等代谢综合征相伴随,其共同之处在于存在胰岛素抵抗(IR)。IR是导致NAFLD发生及进展的根本原因,改善胰岛素敏感性有助于缓解或治疗NAFLD。     

非酒精性脂肪肝与胰岛素抵抗和糖耐量异常的关系

目的探讨胰岛素抵抗和糖耐量异常与非酒精性脂肪肝（NAFLD）的关系,分析影响NAFLD的因素。方法比较71例糖耐量异常伴有脂肪肝患者和59例糖耐量异常不伴有脂肪肝患者的体质量指数（BMI）、腰臀比（WHR）、总胆固醇（TC）、甘油三酯（TG）、血尿酸、丙氨酸氨基转移酶、仪谷氨酰转移酶、糖化血红蛋白和HOMA-IR水平。结果Logistic回归分析表明,HOMA．IR、TC、TG、WHR是NAFLD形成的独立危险因素。结论肥胖、高TG和胰岛素抵抗是糖耐量异常合并NAFLD的重要因素。     

miRNA-103: Molecular link between insulin resistance and nonalcoholic fatty liver disease

AIM: To investigate the associations between miRNA-103(mi R-103) and insulin resistance and nonalcoholic fatty liver disease(NAFLD).METHODS: Serum samples were collected from 50 NAFLD patients who were overweight or obese(NAFLD group) and from 30 healthy subjects who served as controls(normal control group). Quantitative polymerasechain reaction was used to detect expression of mi R-103. Fasting plasma glucose, fasting insulin, and triglyceride(TG) levels were measured. Homeostasis model assessment was used to evaluate basal insulin resistance(HOMA-IR). Patient height and weight were measured to calculate body mass index(BMI).RESULTS: Compared with the normal control group, higher serum levels of mi R-103 were expressed in the NAFLD group(8.18 ± 0.73 vs 4.23 ± 0.81, P = 0.000). When P = 0.01(bilateral), mi R-103 was positively correlated with HOMA-IR(r = 0.881), TG(r = 0.774) and BMI(r = 0.878), respectively. mi R-103, TG and BMI were all independent factors for HOMAIR(β = 0.438/0.657/0.251, P = 0.000/0.007/0.001). mi R-103, TG, BMI and HOMA-IR were all risk factors for NAFLD(odds ratio = 2.411/16.196/1.574/19.11, P = 0.009/0.022/0.01/0.014).CONCLUSION: mi R-103 is involved in insulin resistance and NAFLD, and may be a molecular link between insulin resistance and NAFLD and a therapeutic target for these disorders.     

非酒精性脂肪肝血尿酸水平与胰岛素抵抗的相关性

目的:研究非酒精性脂肪肝(non-alcoholic fatty liver,NAFL)患者血尿酸水平及其与胰岛素抵抗程度的相关性.方法:选取单纯NAFL患者40例,NAFL合并2型糖尿病患者(type2diabetes mellitus,T2DM)72例,健康体检者62名为研究对象.测定体重指数(body mass index,BMI),检测空腹血糖(fasting blood glucose,FBG)、尿酸(serum uric acid,SUA)、丙氨酸氨基转移酶(alanine aminotransferase,ALT)、门冬氨酸氨基转移酶(aspartate aminotransferase,AST)、胆固醇(cholesterol,TC)、甘油三酯(triglyceride,TG)、糖化血红蛋白(glycated hemoglobin,HbA1C)、尿微量白蛋白/尿肌酐(Ualb/UCr)等生化指标并行肝脏B超检查.放射免疫法测定空腹胰岛素(fasting insulin,FINS),计算胰岛素抵抗指数(HOMA IR).结果:NAFL合并T2DM组BMI、SUA、ALT、AST、TG、FBG、FINS、HOMA IR、HbA1C、Ualb/UCr、SF均高于对照组;与单纯NAFL比较,NAFL合并T2DM组胰岛素抵抗及SUA水平更重;相关性研究表明FBG、HOMA IR、HbA1C与SUA呈正相关.结论:NAFL患者存在明显的胰岛素抵抗及高血尿酸血症,且两者具有一定的相关性.降低胰岛素抵抗联合纠正尿酸代谢紊乱对防止NAFL的发生发展具有重要的临床意义.     

胰岛素抵抗与非酒精性脂肪性肝病

胰岛素抵抗(IR)在非酒精性脂肪性肝病(NAFLD)发病过程中起至关重要的作用.目前大量研究支持NAFLD“二次打击”学说,初次打击IR引起肝细胞单纯性脂肪变性,二次打击脂肪变的肝细胞发生成脂性转化,诱导炎性反应、氧化应激、内质网应激的发生,损伤肝细胞功能,加重IR,促进NAFLD发展.     

Leptin, insulin resistance, and liver fibrosis in human nonalcoholic fatty liver disease

BACKGROUND/AIMS: Data from animal models of fibrosis and fatty liver suggest that leptin may mediate the profibrogenic responses in the liver, but the association of leptin and liver fibrosis in human nonalcoholic fatty liver disease (NAFLD) remains undefined. We aimed at determining the relation between leptin and liver fibrosis in human NAFLD. METHODS: Human plasma leptin and several indicators of insulin resistance were measured in 88 NAFLD patients and matched controls. RESULTS: Leptin levels were significantly greater in patients with more advanced fibrosis (P = 0.005). By multivariate analysis, the significant association between leptin and fibrosis was abolished (adjusted P = 0.3) when controlling for confounders including age, gender, BMI, diabetes and insulin resistance. Only age (adjusted P = 0.006) and insulin sensitivity (adjusted P = 0.04) correlated significantly with fibrosis stage. A second liver biopsy was performed in 39 out of the 88 patients at 27.9 +/- 16 months. Leptin levels were not significantly different between patients who had fibrosis progression (n = 10) and those who did not (n = 29). CONCLUSIONS: In human NAFLD, no relationship between leptin levels and fibrosis stage was demonstrated. The correlation of leptin and fibrosis severity seems to be an indicator of the factors that determine leptin production.     

铁超负荷与非酒精性脂肪性肝病关系的研究进展

肝脏是储存多余铁的主要器官,因此当铁超负荷时,肝脏也是首先受到损害的靶器官。尽管铁超负荷与非酒精性脂肪性肝病之间的关系仍存在争论,但越来越多的研究表明,铁超负荷在非酒精性脂肪肝的发展过程中起到了一定作用：铁离子不但可以诱发氧化应激和脂质过氧化,还会引发胰岛素抵抗,从而加重非酒精性脂肪性肝病。     

Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease （NAFLD） is an increasingly recognized cause of liver-related morbidity and mortality. It can develop secondary to numerous causes but a great majority of NAFLD cases occur in patients who are obese or present with other components of metabolic syndrome （hypertension, dyslipidemia, diabetes）. This is called primary NAFLD and insulin resistance plays a key role in its pathogenesis. Obesity is characterized by expanded adipose tissue, which is under a state of chronic inflammation. This disturbs the normal storage and endocrine functions of adipose tissue. In obesity, the secretome （adipokines, oytokines, free fatty acids and other lipid moieties） of fatty tissue is amplified, which through its autocrine, paracrine actions in fat tissue and systemic effects especially in the liver leads to an altered metabolic state with insulin resistance （IR）. IR leads to hyperglycemia and reactive hyperinsulinemia, which stimulates lipid-accumulating processes and impairs hepatic lipid metabolism. IR enhances free fatty acid delivery to liver from the adipose tissue storage due to uninhibited lipolysis. These changes result in hepatic abnormal fat accumulation, which may initiate the hepatic IR and further aggravate the altered metabolic state of whole body. Hepatic steatosis can also be explained by the fact that there is enhanced dietary fat delivery and physical inactivity. IR and NAFLD are also seen in various lipodystrophic states in contrary to popular belief that these problems only occur due to excessive adiposity in obesity. Hence, altered physiology of adipose tissue is central to development of IR, metabolic syndrome and NAFLD.     

Metabolic aspects of adult patients with nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease(NAFLD) is a major cause of chronic liver disease and it encompasses a spectrum from simple steatosis to steatohepatitis, fibrosis, or cirrhosis. The mechanisms involved in the occurrence of NAFLD and its progression are probably due to a metabolic profile expressed within the context of a genetic predisposition and is associated with a higher energy intake. The metabolic syndrome(MS) is a cluster of metabolic alterations associated with an increased risk for the development of cardiovascular diseases and diabetes. NAFLD patients have more than one feature of the MS, and now they are considered the hepatic components of the MS. Several scientific advances in understanding the association between NAFLD and MS have identified insulin resistance(IR) as the key aspect in the pathophysiology of both diseases. In the multi parallel hits theory of NAFLD pathogenesis, IR was described to be central in the predisposition of hepatocytes to be susceptible to other multiple pathogenetic factors. The recent knowledge gained from these advances can be applied clinically in the prevention and management of NAFLD and its associated metabolic changes. The present review analyses the current literature and highlights the new evidence on the metabolic aspects in the adult patients with NAFLD.     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.