非酒精性脂肪肝患者血清肿瘤坏死因子-α、脂联素水平与胰岛素抵抗的相关性

目的:探讨非酒精性脂肪肝(NAFLD)患者肿瘤坏死因子-α、脂联素水平与胰岛素抵抗等指标的相互关系.方法:120例NAFLD患者根据空腹血糖水平分为合并2型糖尿病(T2DM)者32例(DFL组),不伴T2DM者88例(FL组),所有NAFLD患者根据B超结果分为轻度、中度、重度3组.测定NAFLD患者及42例健康对照者的体质量指数(BMI)、腰臀比(WHR)、空腹血糖(FPG)、空腹胰岛素(FINS)、肿瘤坏死因子-α(TNF-α)、脂联素(APN)水平;采用稳态模式计算胰岛素抵抗指数(HOMA-IR)、胰岛素敏感性指数(ISI)、反应胰岛β细胞分泌功能的指标(HOMA-IS)等指标.结果:NAFLD患者的FINS,HOMA-IR均显著升高,ISI显著低于NC组(P<0.01);FPG,FINS,ISI,HOMA-IS是IR抵抗的主要相关因素;DFL组的FINS,HOMA-IR较FL组为高,ISI,HOMA-IS较FL组为低,均有显著性差异(P<0.01);NAFLD患者轻、中度两组间HOMA-IR无显著差异(P>0.05),而重度脂肪肝患者的HOMA-IR明显升高(P<0.01).NAFLD患者血清TNF-α显著升高,APN显著降低(P<0.01);APN与TNF-α,IR呈显著负相关,与ISI呈显著正相关;TNF-α是影响APN水平的重要因素;TNF-α与APN,ISI呈显著负相关,与FPG,FINS,IR呈显著正相关,ISI,APN是其主要的影响因素.结论:NAFLD患者普遍存在IR,合并2型糖尿病的NAFLD患者体内胰岛素抵抗现象更为明显;TNF-α与APN呈显著负相关,且均与IR密切相关.APN作为保护性因子而TNF-α作为损害性因子在NAFLD的发生、发展中起着重要作用.     

血甘油三酯、尿酸对非酒精性脂肪性肝病患者血清肿瘤坏死因子α、白介素6及胰岛素抵抗的影响

目的观察血甘油三酯(TG)、尿酸(UA)对非酒精性脂肪性肝病(NAFLD)患者血清肿瘤坏死因子α(TNF-α)、白介素6(IL-6)及胰岛素抵抗(IR)的影响。方法从我院就诊经彩色超声诊断的脂肪肝患者中,依血TG水平分为3组,即血TG正常组(NT)、仅血TG升高组(HT组)、血TG合并UA升高组(HTU组),以血TG正常的非脂肪肝人群做对照组(Control)。测各组血清胰岛素、TNF-α、IL-6、血糖,以胰岛素抵抗指数(HOMA-IR)评价IR。结果与Control相比,NT、HT组TNF-α、IL-6、HOMA-IR均无明显增高(P>0.05);HTU组IL-6及HOMA-IR明显增高[IL-6,HTU:135.19(90.27～164.24)ng/mL vs Control:61.6(53.53～79.69)ng/mL;HOMA-IR,HTU:2.34±0.53 vs Control:1.00±0.81,P<0.01],TNF-α无明显增高(P>0.05);相关分析表明,血TG与HO-MA-IR呈明显正相关(r=0.428,P<0.01)。结论 NAFLD患者是否发生IR及IL-6、TNF-α的变化可能受不同TG水平的影响。     

TNF-α和IL-6在非酒精性脂肪性肝病患者血清中的水平及意义

目的:探讨肿瘤坏死因子-α(TNF-α)和白介素-6(IL-6)在非酒精性脂肪性肝病(NAFLD)患者血清中的水平及意义.方法:收集NAFLD组患者57例[包括单纯性脂肪肝21例、非酒精性脂肪性肝炎(NASH)29例肝硬化7例和正常对照组22例.采用ELISA法检测受试者血清TNF-α仅和IL-6水平.同时检查受试者体质量指数、血压、空腹血糖、空腹胰岛素、血脂,用以计算胰岛素抵抗指数(HOMA-IR)和了解合并代谢综合征情况.比较各组间血清TNF-α和IL-6水平的变化,并分析TNF-α、IL-6水平与胰岛素抵抗指数和代谢综合征发生的关系.结果:单纯性脂肪肝、NASH和肝硬化组患者血清TNF-α、IL-6水平均显著高于对照组(P<0.05),其中以NASH组水平最高,且显著高于单纯性脂肪肝和肝硬化组(P<0.05).受试者血清TNF-α、IL-6水平与HOMA-IR均呈显著性正相关(r=608,0.709,均P=0.000).合并代谢综合征的NAFLD患者血清TNF-α、IL-6水平均显著高于不合并代谢综合征的患者(P<0.05).患者血清TNF-α、IL-6水平与是否合并代谢综合征呈显著性相关(r=0.409,P=0.002;r=0.552,P:0.000).结论:TNF-α、IL-6通过诱导胰岛素抵抗对NAFLD疾病的发生发展起重要作用,并有助于NAFLD患者代谢综合征的形成.     

2型糖尿病合并非酒精性脂肪肝患者血清淀粉样蛋白A水平与胰岛素抵抗的相关性

目的 研究T2DM合并非酒精性脂肪肝(NAFLD)患者血清淀粉样蛋白A(SAA)水平与胰岛素抵抗(IR)的相关性.方法 测定T2DM合并NAFLD(DM+NAFLD)组32例、T2DM不合并NAFLD(DM)组34例、血糖正常的NAFLD(NAFLD)组31例及正常对照(NC)组32例SAA、肿瘤坏死因子(TNF-α)水平,计算HOMA-IR.结果 与NC组比,DM+NAFLD组、DM组及NAFLD组SAA、TNF-α水平均升高(P均<0.01);HOMA-IR(r=0.376,P<0.01)和TG(r=0.343,P<0.01)是SAA的独立影响因素.结论 SAA与IR关系密切,有可能在T2DM合并NAFLD的发生发展中起一定的作用.     

老年2型糖尿病合并非酒精性脂肪肝患者血清蛋白激酶Cε活性和胰岛素抵抗的关系研究

目的探讨老年2型糖尿病(T2DM)合并非酒精性脂肪肝(NAFLD)患者血清蛋白激酶Cε(PKCε)活性与胰岛素抵抗的相关性。方法回顾性分析2017年10月至2018年10月西安交通大学医学院第二附属医院住院的T2DM患者229例,根据病情分为T2DM组112例,T2DM+NAFLD组117例,另选同期健康对照组110例。比较3组入选者临床资料和实验室检查结果,计算稳态模型的胰岛素抵抗指数(HOMA-IR),采用酶联免疫吸附法测定血清PKCε活性,并分析其与胰岛素抵抗的相关性。结果T2DM+NAFLD组患者血清PKCε活性和HOMA-IR均高于单纯T2DM组和健康对照组[(195.5±62.1)μg/L比(188.7±61.2)μg/L和(89.1±20.2)μg/L、(12.5±7.9比14.1±5.7和5.8±4.1),F值分别为9.76、10.21,均P=0.010]。Pearson相关分析,T2DM+NAFLD组患者血清PKCε活性、HOMA-IR及三酰甘油呈正相关(r值分别为0.339、0.305、0.329,均P<0.015)。Logistic回归分析,血清PKCε活性、HOMA-IR和三酰甘油是T2DM+NAFLD组的危险因素(β值分别为0.849、0.022和0.710,均P<0.05)。血清PKCε活性升高是T2DM合并NAFLD的独立影响因素。结论老年T2DM合并NAFLD患者血清PKCε活性升高与胰岛素抵抗呈正相关,降低血清PKCε活性和改善胰岛素抵抗有助于延缓或改善T2DM及NAFLD。     

肿瘤坏死因子-α基因多态性与非酒精性脂肪性肝病的关系

目的研究肿瘤坏死因子-α(TNF-α)基因-308位点及-238位点多态性在非酒精性脂肪性肝病(NAFLD)患者中的分布,及其在胰岛素抵抗(IR)和 NAFLD 发病中的地位。方法运用聚合酶链反应-限制性片段长度多态性检测117例 NAFLD 患者 TNF-α基因—308位点及—238位点多态性,其中伴肥胖者60例,非肥胖者57例,同时测定患者空腹血清胰岛素(FINS)及空腹血糖,通过体内平衡代谢指数(HOMA)评估 IR,并与120名健康者对照。结果 NAFLD 患者与正常对照组 TNF-α基因-238位点基因多态性分布差异有统计学意义(29.9%比15.8%,P<0.05),而—308位点差异无统计学意义(P>0.05)。NAFLD 患者血清 HOMA-IR、TNF-α明显高于对照者[2.50±0.68比1.16±0.68,(10.54±3.19)ng/L 比(4.54±3.10)ng/L,P<0.01]。FINS、HOMA-IR 在 TNF-α基因-238位点基因变异组明显高于正常基因型组(P<0.05),但在—308位点变异组差异无统计学意义(P>0.05)。NAFLD 患者中无论肥胖或非肥胖患者均较正常对照人群在 TNF-α基因-238位点多态性分布及HOMA-IR、TNF-α差异有统计学意义(P<0.05)。肥胖及非肥胖的 NAFLD 患者之间 HOMA-IR、TNF-α差异无统计学意义(P>0.05)。结论 NAFLD 患者 IR 与其体重关系不显著,非肥胖 NAFLD患者同样有 IR 发生。TNFα基因-238位点 G/A 变异与 IR、NAFLD 易感性相关,TNFα基因-308位点 G/A 的突变与 IR 易感性不相关。NAFLD 发病与 IR、TNF-α密切相关。     

2型糖尿病和非酒精性脂肪肝病患者的胰岛素抵抗和胰岛β细胞功能

目的 探讨2型糖尿病(T2DM)和非酒精性脂肪肝病(NAFLD)患者胰岛β细胞功能和胰岛素抵抗的特征.方法 206例研究对象根据是否有T2DM和NAFLD分为4组,采用肝脏胰岛素抵抗指数(HIR)、HOMA胰岛素抵抗指数(HOMA-IR)及Matsuda指数(MSI)评估胰岛素抵抗性,采用HOMA-β、早相及晚相胰岛素分泌指数评估胰岛β细胞功能.结果 NAFLD组和T2DM伴NAFLD组的HIR均显著高于对照组和T2DM组(4.13±0.64,4.03±0.69比3.52±0.78,3.53±0.64,P<0.05),T2DM伴NAFLD组的HOMA-IR显著高于T2DM和NAFLD组(3.35±2.69比2.31±1.39,2.40±1.55,P<0.05);NAFLD组的早相胰岛素分泌指标显著低于对照组(2.13±0.17比2.61±0.13,P<0.05),而T2DM组和T2DM伴NAFLD组的HOMA-β、早相及晚相胰岛素分泌指标均明显低于对照组(P<0.05).结论 NAFLD患者主要表现为肝脏胰岛素抵抗,其胰岛β细胞早相胰岛素分泌受损;T2DM患者存在胰岛素抵抗,其胰岛β细胞早、晚相胰岛素分泌功能均受损.当患者既有T2DM又有NAFLD时,胰岛素抵抗将更严重.     

多烯磷脂酰胆碱对非酒精性脂肪肝患者血清 IL-6、TNF-α水平的影响

目的：观察多烯磷脂酰胆碱（ PPC）对非酒精性脂肪肝（ NAFLD）患者血清IL-6、TNF-α水平的影响。方法将60例NAFLD患者随机分为A、B组各30例。 A组口服PPC治疗,B组口服水飞蓟宾甲葡胺治疗,疗程均为3个月。检测两组治疗前、治疗3个月及停药后2周的血脂及肝功能,血清IL-6、TNF-α、空腹胰岛素（Fins）及胰岛素抵抗指数（ HOMA-IR）等指标;并与10例查体健康者（对照组）进行比较。结果与B组比较,A组治疗3个月及停药后2周的血脂、肝功能、IL-6、TNF-α均明显降低（P均＜0．05）,IL-6、TNF-α水平与对照组接近;A组治疗3个月及停药2周后Fins、HOMA-IR均较B组明显好转（P均＜0．05）。结论 PPC可明显改善NAFLD患者的肝功能,降低其血清TNF-α、IL-6水平,改善预后。     

妊娠期糖尿病血清肿瘤坏死因子-α、内脂素水平与胰岛素抵抗的相关性分析

采用稳态模型评估法评估正常糖耐量孕妇(NGT)、糖耐量减低孕妇(GIGT)和妊娠期糖尿病孕妇(GDM)的胰岛素抵抗指数,采用酶联免疫吸附法检测其血清TNF-α、内脂素及胰岛素水平。结果 GDM组和GIGT组HOMA-IR显著高于NGT组,GDM组HOMA-IR显著高于GIGT组。血清TNF-α、内脂素水平由NGT组到GIGT组和GDM组均呈显著增高,TNF-α、内脂素与空腹胰岛素、孕晚期体重指数、HOMA-IR均呈显著正相关。结论 TNF-α、内脂素水平与GDM患者IR程度密切相关,其水平可作为预测妊娠期糖尿病胰岛素敏感性的指标,将来可能是治疗妊娠期糖尿病的新靶点。     

胆宁片联合瑞舒伐他汀治疗非酒精性脂肪性肝病患者HOMA-IR和血清TNF-α水平变化

目的探讨胆宁片联合瑞舒伐他汀对非酒精性脂肪性肝病(NAFLD)患者的治疗效果及其对血清肿瘤坏死因子α(TNF-α)和胰岛素抵抗指数(HOMA-IR)的影响。方法 2015年9月~2016年9月我院就诊的NAFLD患者150例,随机将其分成观察组和对照组各75例。给予观察组患者瑞舒伐他汀联合胆宁片治疗,给予对照组患者瑞舒伐他汀治疗,两组均治疗6个月。采用酶联免疫吸附法检测TNF-α水平,常规检测空腹血糖和胰岛素水平,并计算HOMA-IR。结果治疗前,两组患者血生化指标无明显差异(P0.05);治疗后,观察组血清谷丙转氨酶(ALT)和谷草转氨酶(AST)水平分别为(46.92±10.21)U/L和(65.39±9.86)U/L,显著低于对照组的【(70.74±12.93)U/L和(99.21±10.97)U/L,P0.05】;治疗前,两组血清TNF-α和HOMA-IR比较无明显差异(P0.05);治疗后,观察组患者血清TNF-α和HOMA-IR分别为(3.44±1.26)μg/L和(1.87±0.84),显著低于对照组的【(4.08±1.29)μg/L)和(2.26±0.74),P0.05】。结论胆宁片联合瑞舒伐他汀治疗NAFLD患者能明显改善肝功能,并能降低血清TNF-α和HOMA-IR水平,临床效果显著。     

Thyroid Function in Obese Children with Non-Alcoholic Fatty Liver Disease

Ob­jec­ti­ve: To investigate the relationships between thyroid function and metabolic risk factors in obese adolescents with non-alcoholic fatty liver disease (NAFLD).Methods: One hundred sixty obese adolescents and 40 control subjects were enrolled in the study. The obese subjects were divided into two groups based on presence or absence of liver steatosis (NAFLD group and non-NAFLD group). Serum samples were assayed for glucose, insulin, cholesterol, alanine aminotransferase, aspartate aminotransferase, free thyroxine (fT4), free triiodothyronine (fT3) and thyroid-stimulating hormone (TSH). The ratio of fT3 to fT4 was evaluated as an indirect index of deiodinase activity. Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR) from fasting samples.Results: NAFLD and non-NAFLD groups had slightly higher fasting blood glucose values than the control group. Fasting insulin levels in the NAFLD group were significantly higher than those in the non-NAFLD and control groups. The NAFLD group had significantly greater HOMA-IR values compared with the non-NAFLD group and also with the control group. The NAFLD group had significantly higher fT3/fT4 ratio values compared to both non-NAFLD and control groups. fT3/fT4 was positively correlated with serum insulin levels in the NAFLD group. Conclusion: This study showed that obese adolescents with hepatosteatosis had elevated values for fT3/fT4 ratio. This finding suggested a high conversion of T4 to T3 due to increased deiodinase activity as a compensatory mechanism for fat accumulation.     

Relationship Between Aspartate Aminotransferase-to-Platelet Ratio Index and Carotid Intima-Media Thickness in Obese Adolescents with Non-Alcoholic Fatty Liver Disease

Objective: There is increasing evidence for an association between non-alcoholic fatty liver disease (NAFLD) and an increased risk of cardiovascular morbidity and mortality. The aim of this study was to investigate the association between aspartate aminotransferase-to-platelet ratio index (APRI) and carotid intima-media thickness (IMT) in obese adolescents with NAFLD.Methods: Seventy-six obese adolescents and 36 lean subjects were enrolled in this cross-sectional single-centre study. The obese subjects were divided into two subgroups based on the presence or absence of fatty liver with high transaminase levels (NAFLD group and non-NAFLD group). Fasting blood samples were assayed for transaminase, glucose, and insulin levels. Insulin resistance was calculated by the homeostasis model assessment (HOMA-IR).Results: APRI values were higher in both obese groups (NAFLD and non-NAFLD) in comparison with the lean group. The NAFLD group had significantly higher APRI values than the non-NAFLD obese group and the lean group. Carotid IMT was higher in both obese groups (NAFLD and non-NAFLD) in comparison with the lean group. The NAFLD group had significantly higher measurements of carotid IMT than the non-NAFLD group and the lean group. APRI was positively correlated with most of the metabolic parameters (total cholesterol, low-density lipoprotein cholesterol, glucose, insulin, HOMA-IR) and with carotid IMT in the NAFLD obese group.Conclusions: This study demonstrated that a significant relationship exists between APRI and carotid IMT in obese adolescents with NAFLD. We suggest that an increased APRI score in obese adolescents with NAFLD can possibly serve to predict a more adverse cardiovascular risk profile. Conflict of interest:None declared.     

芪黄胶囊对2型糖尿病患者胰岛素抵抗及TNF-α影响的临床研究

目的研究芪黄胶囊对2型糖尿病患者胰岛素抵抗(IR)及肿瘤坏死因子-α(TNF-α)的影响,观察芪黄胶囊延缓2型糖尿病及其并发症的疗效和机制。方法气阴两虚型2型糖尿病患者80例,随机分为治疗组(芪黄胶囊+二甲双胍治疗组)和对照组(二甲双胍组)。两组均以2个月为1疗程,治疗前后中医证候疗效判定,观察治疗前后TNF-α、体重指数(BMI)、血脂、糖化血红蛋白(HbA1c)、空腹血糖(FBG)、餐后2h血糖(2hPBG)、空腹胰岛素(FINS),计算胰岛素敏感指数(IAI)、IR指数(HOMA-IR)。结果芪黄胶囊可显著降低气阴两虚型2型糖尿病患者TNF-α水平,改善患者的中医证候,同时具有良好的降糖、降脂作用,增加胰岛素敏感性,改善IR的作用,与对照组比较有统计学意义。结论芪黄胶囊治疗可明显降低气阴两虚型2型糖尿病患者TNF-α水平,增加胰岛素敏感性,改善IR。     

The role of pro/anti-inflammatory adipokines on bone metabolism in NAFLD obese adolescents: effects of long-term interdisciplinary therapy

To investigate the role of pro- and anti-inflammatory adipokines in the bone metabolism of non-alcoholic fatty liver disease (NAFLD) obese adolescents as well as the effects of long-term interdisciplinary therapy on metabolic-related risk factors. Forty post-puberty obese adolescents were randomly assigned into two groups: (1) NAFLD group and (2) non-NAFLD group (diagnosis by ultrasonography) and submitted to a weight loss therapy. Body composition was analyzed by air displacement plethysmography, bone mineral density (BMD) and content by dual-energy X-ray absorptiometry, blood samples were collected to measure lipid profile, hepatic enzymes, and adipokines. Leptin and adiponectin concentrations were measured by ELISA. A decrease in total body mass, BMI, body fat, visceral and subcutaneous fat, insulin concentration, HOMA-IR, total cholesterol and an increase in lean body mass were observed in both groups after therapy. It was found positive correlation between the Δ BMD and the Δ fat mass (%) (r = 0.31, P = 0.01) and negative correlations between Δ BMC with Δ HOMA-IR (r = -0.34, P = 0.02) and Δ HOMA-IR with Δ leptin (r = -0.34, P = 0.02). In addition, increased levels of adiponectin and reduction in leptin concentrations were observed in NAFLD group. In the simple regression analysis, the HOMA-IR was an independent predictor changes in BMC in total obese adolescents and in the non-NAFLD group. One year of interdisciplinary weight loss therapy for obese adolescents with or without NAFLD, could regulate bone mineral metabolism as result of an increased BMC and improved inflammatory state.     

Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway

BACKGROUND Nonalcoholic fatty liver disease(NAFLD), the most common chronic liver disease, can progress into nonalcoholic steatohepatitis(NASH), cirrhosis, and even hepatocellular carcinoma. Bile acids such as ursodeoxycholic acid(UDCA)play an essential role in the pathogenesis of NAFLD by regulating the level of sterol regulatory element-binding protein(SREBP) 1 c, but the underlying regulatory mechanism remains elusive. Increased evidence indicates that the AKT/mTOR/SREBP-1 signaling pathway is a key pathway to regulate hepatic cellular lipid metabolism. UDCA may regulate the AKT/mTOR/SREBP-1 signaling pathway to ameliorate hepatic lipid metabolism.AIM To investigate the functional mechanism of UDCA in an oleic acid(OA)-induced cellular model of NAFLD.METHODS The cellular model of NAFLD was established using OA and treated with UDCA.First, the best concentration of UDCA was selected. For the best time-dependent assay, cells were stimulated with OA only or co-treated with OA and 2 mmol/L UDCA for 24 h, 48 h, and 72 h. Oil red O staining was used to observe the accumulation of intracellular lipids, while the intracellular contents of triglyceride, alanine aminotransferase(ALT), gamma-glutamyl transpeptidase(GGT), and aspartate aminotransferase(AST) were detected by enzymatic methods. Meanwhile, the expression levels of AKT/mTOR/SREBP-1 signaling pathway-related proteins were detected by real-time PCR and Western blot.RESULTS In the NAFLD cell model established with LO2 cells induced using OA, lipid accumulation was obvious. UDCA significantly inhibited lipid accumulation at different concentrations(especially 2 mmol/L) and decreased cell growth ability at different time points. The biochemical parameters like ALT, AST, and GGT were significant improved by UDCA. UDCA treatment vividly repressed the activation of AKT, mTOR, and CRTC2 and the expression of nSREBP-1 in LO2 cells induced with OA.CONCLUSION Our findings demonstrate the effect of UDCA in improving NAFLD. UDCA attenuates OA-induced hepatic steatosis mainly by regulation of AKT/mTOR/SREBP-1 signal transduction.     

支链氨基酸促进高脂诱导的小鼠肝脏胰岛素抵抗

目的 探讨支链氨基酸（Branched chain amino acids,BCAA）对高脂诱导胰岛素抵抗的影响。方法 将60只野生C57BL/6J小鼠随机分成4组,分别给予正常饮食+普通饮水（ND）组,正常饮食+含50 g/L BCAA饮水（ND/BCAA）组,高脂饮食（HD）组,高脂饮食+含50 g/L BCAA饮水（HD/BCAA）组,喂养18周,仔细观察小鼠生活状态并每周记录小鼠体质量,18周后进行葡萄糖耐量（IPGTT）和胰岛素耐量（ITT）实验,检测小鼠血清BCAA和胰岛素水平,Western blot检测小鼠肝脏胰岛素信号通路关键分子IRS1及其磷酸化水平〔p-IRS1(ser307)〕、AKT及其磷酸化水平〔p-AKT(ser473)〕。结果 ①BCAA抑制高脂诱导的小鼠体质量增加,表现为HD/BCAA组小鼠体质量增长比HD组缓慢（P<0.05,P<0.01）;ND/BCAA组和ND组体质量增长无明显差异;②与ND组相比,ND/BCAA组小鼠血清BCAA浓度无明显升高,HD组血清BCAA水平升高（P<0.05）;与HD组相比,HD/BCAA组血清BCAA浓度进一步升高（P<0.05）;③与ND组相比,ND/BCAA组小鼠血清胰岛素、IPGTT和ITT均无明显改变;与HD组相比,HD/BCAA组血清胰岛素水平更高,IPGTT和ITT均明显受损（P<0.05）;④Western blot检测显示:ND组和ND/BCAA组小鼠肝脏p-IRS1(ser307)和p-AKT(ser473)水平无明显改变;与ND组相比,HD组小鼠p-IRS1(ser307)上调（P<0.05）,IRS1、p-AKT(ser473)均下调（P<0.05,P<0.01）;与HD组相比,HD/BCAA组小鼠肝脏p-IRS1(ser307)进一步上调（P<0.05）,p-AKT(ser473)水平进一步下调（P<0.01）。结论 正常饮食单纯补充BCAA不影响小鼠肝脏胰岛素敏感性, BCAA能够促进高脂诱导的小鼠肝脏胰岛素抵抗。