游离脂肪酸诱导3T3-L1细胞胰岛素抵抗模型的建立

目的观察不同种类和浓度游离脂肪酸(FFA)对3T3-L1细胞葡萄糖摄取及胰岛素敏感性的影响,建立FFA诱导的胰岛素抵抗细胞模型。方法3T3-L1细胞体外诱导分化为脂肪细胞,油红O染色鉴定,不同浓度软脂酸(PA)和油酸(OA)诱导,测定基础状态和胰岛素刺激下葡萄糖特异性转运情况。结果3T3-L1脂肪细胞诱导率为98%±1.3%,PA和OA各组胰岛素刺激后的葡萄糖特异性转运呈时间和浓度依赖性下降趋势,均显著低于对照组(p<0.01);0.5mM PA作用24h后基础葡萄糖特异性转运明显低于对照组和PA 0.25mM作用24h组(p<0.05)。结论3T3-L1细胞在体外可稳定分化为成熟脂肪细胞,经FFA诱导成为胰岛素抵抗细胞模型;随FFA作用时间延长和浓度增加,胰岛素抵抗程度加重,并以时间和浓度依赖性方式抑制3T3-L1脂肪细胞胰岛素刺激后的葡萄糖特异性转运,高浓度时抑制基础状态下的葡萄糖特异性转运。     

Establishment of the Insulin Resistance Induced by Inflammatory Response in 3T3-L1 Preadipocytes Cell Line

In the light of given recent reports, insulin resistance related to inflammation is characterized by increasing a diverse array of pro-inflammatory cytokines. In this study, hypothesizing that 3T3-L1 non-differentiated preadipocytes cell line as a cell model could be used to investigate this linkage, the aim is to determine whether the preadipocytes induced by different inflammatory responses could cause insulin resistance. This paper has determined the time and concentration-dependent effects of insulin on glucose consumption in the 3T3-L1 non-differentiated preadipocytes. Glucose consumption has also been assayed in the preadipocytes which are treated with LPS and CM originated from LPS-activated RAW264.7. Then protein level of each group has been measured by coomassie brilliant blue protein kit. Furthermore, secretion levels of IL-6 and TNF-alpha are measured by ELISA in the supernatant of RAW264.7 and preadipocytes. Finally, the mRNA expressions for IL-6, TNF-alpha and PPARgamma has been assessed by RT-PCR. The results show that administration of LPS and CM both can increase releases of IL-6 and TNF-alpha, as well as gene expression of IL-6 mRNA; this change is accompanied with suppression of PPARgamma mRNA activation in 3T3-L1 undifferentiated preadipocytes. In conclusion, our results suggest that in preadipocytes, pro-inflammatory cytokines can result in insulin resistance, and deserve further investigation to be helpful for treatment and revealing mechanisms of T2DM.     

性激素对3T3-L1前脂肪细胞和脂肪细胞胰岛素敏感性的影响

目的观察不同浓度雌、雄激素对3T3-L1前脂肪细胞葡萄糖转运的影响,探讨性激素在胰岛素抵抗形成中的意义。方法体外培养3T3-L1前脂肪细胞,并诱导其分化成熟,利用2-脱氧-[3H]-D-葡萄糖掺入法,研究不同浓度的17β雌二醇、睾酮对胰岛素刺激的前脂肪细胞和脂肪细胞葡萄糖摄取能力的影响。结果10-8mol/L的17β雌二醇即能够抑制3T3-L1前脂肪细胞胰岛素刺激状态下的葡萄糖转运,且呈现明显的浓度依赖性抑制;而睾酮为10-8mol/L时3T3-L1前脂肪细胞胰岛素刺激状态下的葡萄糖转运并无明显影响,在浓度达到10-7mol/L开始出现抑制效应,浓度越高抑制效应越明显。结论性激素可以调节3T3-L1前脂肪细胞的胰岛素敏感性。     

小檗碱改善高脂饮食大鼠的胰岛素抵抗

目的:观察小檗碱是否能改善高脂饮食诱导的胰岛素抵抗,以探讨小檗碱干预糖耐量受损(IGT)的可能性。方法:8周龄雄性SD大鼠29只,分为正常组(NC,n=9)和高脂组(HF,n=20)。高脂饲料喂养14周后高脂组分为二组,10只大鼠继续喂养高脂饮食,另一小檗碱组(HF B,n=10)每天灌胃小檗碱150mg/kg体重,治疗6周后进行口服葡萄糖耐量试验和胰岛素耐量试验(ITT),评估小檗碱对胰岛素敏感性的影响。结果:HF组大鼠体重、肝重和附睾脂肪重量均明显高于HF B和NC组(均P<0.01),HF B组空腹血糖和葡萄糖负荷后2h血糖明显低于HF组(分别为5.70±0.52mmol/Lvs6.66±0.51mmol/L和7.88±0.46mmol/Lvs8.85±1.01mmol/L),空腹和葡萄糖负荷后2h胰岛素HF B组也显著低于HF组(分别为0.63±0.25ng/mlvs1.64±0.68ng/ml和1.20±0.21ng/mlvs3.60±0.36ng/ml)。各时间点血糖和胰岛素HF组均显著高于NC组(均P<0.01)。Homa胰岛素抵抗指数HF组明显高于HF B组(P<0.01)。ITT腹腔注射胰岛素后各时间点血糖下降幅度HF B组均高于HF组,15min时HF B组血糖下降23%,而HF组仅下降7%。结论:长期高脂饮食可导致大鼠胰岛素抵抗,小檗碱明显降低高脂大鼠的高胰岛素血症,改善胰岛素抵抗,因此适合于IGT的干预。     

小檗碱激活AMPK抑制3T3-L1脂肪细胞分化

目的 探讨小檗碱对3T3-L1脂肪分化的作用是否与激活腺苷酸活化蛋白激酶（AMPK）有关.方法 在3T3-L脂肪细胞分化全程加入小檗碱,以油红O染色检测3T3-L1脂肪细胞胞浆中脂肪的堆积,实时定量PCR检测过氧化物酶体增殖物激活受体γ2（PPARγ2）、CCAAT增强子结合蛋白α（CEBPα）和AMPK的mRNA表达,以Western印迹法检测AMPK和乙酰辅酶A羧化酶（ACC）的磷酸化水平.结果 小檗碱剂量依赖性地抑制3T3-L1脂肪细胞分化,10 μmol/L小檗碱几乎完全抑制胞浆中脂肪的堆积.5 μmol/L小檗碱在脂肪细胞诱导分化1、3、5、7d后均显著降低CEBPα mRNA表达（P〈0.05或P〈0.01）,诱导分化3、5、7d时显著降低PPARγ2的mRNA表达（P〈0.05或P〈0.01）.AMPK的mRNA水平在分化过程中未受小檗碱的明显影响,而小檗碱明显增加其蛋白磷酸化水平,其下游靶基因ACC磷酸化水平也明显增加.结论 小檗碱抑制3T3-L1脂肪细胞的分化可能与其激活AMPK有关.     

罗格列酮对非糖尿病代谢综合征患者血清脂联素水平和胰岛素抵抗的影响

目的：观察罗格列酮（ROS）对非糖尿病代谢综合征（MS）患者血清脂联素水平和胰岛素抵抗性的影响。方法：选择92例非糖尿病MS患者随机分为两组,A组40例,给予常规治疗;B组52例,在常规治疗上的基础上,加用罗格列酮（ROS）口服。用药前及用药后8周,应用酶联免疫吸附法测定血清脂联素水平、计算胰岛素抵抗指数、胰岛素敏感指数。结果：A组治疗前后脂联素水平（1．49±0．59mg／L vs 1．21±0．66mg／L,P〉0．05）及胰岛素抵抗指数（1．44±0．51 vs 1．32±0．57,P〉0．05）、胰岛素敏感指数（-4．56±0．51vs -4．44±0．57,P〉0．05）比较无显著性差异;B组治疗前后比较,脂联素水平升高（0．89±0．73mg／L vs 2．52±1．37mg／L,P〈0．01）、胰岛素抵抗指数降低（1．50±0．45 vs 0．99±0．35,P〈0．01）、胰岛素敏感指数升高（-4．61±0．45 vs -4．10±0．46,P〈0．01）均有统计学意义。结论：非糖尿病MS患者经口服ROS后脂联素水平明显升高、胰岛素抵抗指数降低、胰岛素敏感指数升高。     

胰岛素抵抗与脑卒中急性期关系的初步研究

目的 :探讨脑血管病患者是否存在胰岛素抵抗 (IR) ,以及IR与患者病情、预后的关系。方法 :测定了 30例脑梗塞、31例脑出血患者和 2 8例健康人的空腹血糖 (FPG)、空腹血清胰岛素 (FINS)、血皮质醇 (F) ,计算胰岛素敏感性指数 (ISI) ,并与神经功能缺损评分和病灶大小进行直线相关分析。结果 :脑卒中患者FPG、FINS及F显著高于对照组 (p<0 .0 0 1) ,ISI较对照组明显降低 (p<0 .0 0 1)。脑卒中轻型组和中重型组的FPG、F、ISI之间也存在明显差异 (p<0 0 0 1、p <0 0 1、p <0 0 5 )。ISI与脑梗塞的面积、脑出血量呈负相关 (r=- 0 372 ,r=- 0 40 6 ,p <0 0 5 )。ISI与神经功能缺损评分亦呈负相关 (r=- 0 32 1,p <0 0 5 )。中重型组的死亡率与病残率高于轻型组。结论 :脑卒中患者存在IR ,其急性期胰岛素水平及IR程度与患者病情与预后有关。建议对血糖水平升高并存在IR与ISI下降者应积极使用胰岛素治疗     

Effects of 4 Weeks Recombinant Human Growth Hormone Administration on Insulin Resistance of Skeletal Muscle in Rats

Purpose

Effect of recombinant human growth hormone (rhGH) administration on lipid storage, and its subsequent effect on insulin sensitivity have not yet been adequately examined. Thus, we investigated the effects of rhGH treatment on muscle triglyceride (TG) and ceramide content, and insulin sensitivity after 4 weeks of rhGH administration in rats.

Materials and Methods

Fourteen rats were randomly assigned to two groups: rhGH injection group (GH, n = 7) and saline injection group (CON, n = 7). GH received rhGH by subcutaneous injections (130 µg·kg^-1·day^-1, 6 days·week^-1) for 4 weeks, while CON received saline injections that were equivalent in volume to GH group. Intramuscular TG and ceramide content and hepatic TG content were measured. To determine insulin sesitivity, oral glucose tolerance test (OGTT) and muscle incubation for glucose transport rate were performed in rats, and used as indicators of insulin sensitivity. We also examined plasm lipid profiles.

Results

After 4 weeks of rhGH treatment, the GH group had higher muscle and liver TG contents than the CON (p < 0.05). Ceramide content in GH was significantly greater than that in CON (p < 0.05). GH also had higher plasma levels of FFA (p < 0.05), glucose and insulin responses during OGTT (p < 0.05), and lower glucose transport rates in submaximal insulin concentration (p < 0.05) as compared with CON. Results indicate that rhGH treatment is associated with insulin resistance in rats.

Conclusion

rhGH treatment elevated muscle TG and ceramide content, and hepatic TG content. Thus, elevation of these compounde by rhGH treatment could contribute to the development of insulin resistance in rats.     

Salicylate Inhibits Macrophage-Secreted Factors Induced Adipocyte Inflammation and Changes of Adipokines in 3T3-L1 Adipocytes

Antidiabetic effects of salicylates have been known for years, however the cellular and molecular mechanisms of the hypoglycemic activity are not well elucidated. We examined the effects of salicylate on inflammation-related changes in gene or/and protein expressions of several adipokines in 3T3-L1 adipocytes and of LPS-induced inflammatory factors in RAW 264.7 cell. Especially, we focused our attention on the cross-talk between the macrophages and adipocytes. Exposure to RAW-CM medium resulted in an increase in the gene expression or/and protein secretion of TNF-α, IL-6 and resistin, and at the same time, a decrease in the gene expression of PPARγ and adiponectin in 3T3-L1 adipocytes. Salicylate effectively reversed these changes, and up-regulated glucose consumption in adipocytes. We also found salicylate inhibited phosphorylation of NF-κB in RAW-CM-stimulated adipocytes. We conclude salicylate blocks inflammatory process in the pathogenesis of inflammation-related insulin resistance.     

甘氨酸对3T3-L1脂肪细胞胰岛素抵抗的影响

目的：探讨甘氨酸对3T3-L1脂肪细胞胰岛素抵抗的影响及其机制。方法:诱导分化3T3-L1脂肪前体细胞为成熟的脂肪细胞，肿瘤坏死因子α（TNF-α）诱导建立脂肪细胞的胰岛素抵抗模型，以罗格列酮为阳性对照，观察甘氨酸干预后胰岛素受体底物-1（IRS-1）和过氧化物酶体增殖物激活受体γ（PPARγ）基因的表达。结果:正常对照组脂肪细胞IRS-1mRNA和PPARγ mRNA的表达最强；TNF-α组IRS-1mRNA和PPARγ mRNA表达显著低于正常对照组；TNF-α加罗格列酮组与TNF-α加甘氨酸组相似，IRS-1mRNA和PPARγ mRNA表达显著高于TNF-α组。结论:甘氨酸对TNF-α诱导的3T3-L1脂肪细胞胰岛素抵抗具有抑制作用，其机制与其增强IRS-1、PPARγ基因的表达有关。     

脂肪酸诱导的3T3-L1脂肪细胞胰岛素抵抗的研究

目的: 观察不同种类、不同浓度脂肪酸对3T3-L1脂肪细胞葡萄糖转运的影响，探讨高脂负荷在胰岛素抵抗形成中的意义，并建立最佳的脂肪酸诱导胰岛素抵抗产生的细胞模型。方法: 以3T3-L1前脂肪细胞和诱导分化成熟的3T3-L1脂肪细胞为研究对象，利用2-脱氧-［³H］-D-葡萄糖掺入法，观察最大葡萄糖摄取率时最佳胰岛素作用浓度和时间；在此基础上研究不同浓度油酸（C18:1）、棕榈酸(C16:0)对前脂肪细胞和脂肪细胞摄取葡萄糖的影响。结果:胰岛素刺激15 min（P<0.05）-1 h（P<0.01），葡萄糖转运呈升高的趋势，至6 h（P>0.05）逐渐下调；胰岛素浓度升高至50 nmol/L时，葡萄糖转运增加336%（P<0.01），100 nmol/L时达最高峰，是基础状态的492%（P<0.01）。0.125 mmol/L油酸或棕榈酸均可明显抑制胰岛素刺激状态下的3T3-L1前脂肪细胞葡萄糖转运（P<0.05），并呈浓度依赖性抑制；油酸及棕榈酸浓度分别达0.5 mmol/L和1.0 mmol/L时，分化成熟脂肪细胞葡萄糖转运显著受抑（P<0.05）。结论: 胰岛素刺激下的3T3-L1脂肪细胞葡萄糖转运有一定的时序性和浓度依赖性，100 nmol/L胰岛素刺激1h，葡萄糖转运率最高。1 mmol/L油酸或棕榈酸作用16-18 h可显著诱导3T3-L1脂肪细胞胰岛素抵抗的发生。     

脂联素、核因子-kB在胰岛素抵抗大鼠表达

目的 观察炎症相关因子脂联素、核因子-kB（NF—kB）在胰岛素抵抗大鼠的表达。方法 20只Wistar大鼠随机分为空白对照组与胰岛素抵抗组，分别给予基础饮食和高糖高脂饮食8周，应用高血浆胰岛素-正常血糖钳夹技术证明胰岛素抵抗的存在。用全自动生化分析仪测定各组血脂、脂联素等，并应用免疫组化技术测定NF-kB在血管内皮细胞的表达。结果 ①应用钳夹技术证明，胰岛素抵抗组存在胰岛素抵抗，而空白对照组未出现胰岛素抵抗；②胰岛素抵抗组甘油三酯、胆固醇、低密度脂蛋白、高密度脂蛋白较空白对照组明显升高（P〈0．05），而保护性因子脂联素浓度则明显降低（P〈0．05）；③免疫组化显示，胰岛素抵抗组大鼠血管内皮细胞NF-kB阳性细胞百分率明显多于空白对照组（P〈0．05）；④脂联素浓度与NF—kB的表达呈明显负相关（r=-0．854，P〈0．05）；结论 胰岛素抵抗时，脂联素浓度降低，NF—kB过表达，二者呈明显负相关。     

参麦注射液改善3T3-L1细胞的胰岛素抵抗

 目的: 探讨参麦注射液改善3T3-L1脂肪前体细胞胰岛素抵抗模型的效果及其作用机制。方法:使用地塞米松等将3T3-L1前脂肪细胞诱导分化为成熟脂肪细胞,使用油红O染色法检测脂肪细胞分化情况;用胰岛素诱导3T3-L1脂肪细胞以建立胰岛素抵抗模型,并使用葡萄糖氧化酶法检测细胞上清液中葡萄糖浓度,以评价模型建立情况。将建立胰岛素抵抗的细胞分为空白对照组、10 μmol/L罗格列酮阳性对照组、25 g/L参麦组和50 g/L参麦组。MTT检测各组药物作用8、16、24和36 h后的细胞活力。药物作用8、16和24 h后测定细胞上清液葡萄糖浓度。免疫印迹检测葡萄糖转运蛋白4(GLUT4)、磷脂酰肌醇3-激酶(PI3K)、AKT和磷酸化AKT(p-AKT)在各组中的蛋白水平。结果:成功建立3T3-L1脂肪细胞胰岛素抵抗模型,葡萄糖浓度数据显示参麦注射液(25、50 g/L)可以改善胰岛素抵抗并可以明显增加3T3-L1细胞GLUT4、PI3K及p-AKT的蛋白水平。结论:参麦注射液可以改善3T3-L1胰岛素抵抗细胞的葡萄糖利用,并且与增加GLUT4、PI3K及p-AKT的蛋白水平有关。     

Relative Effects of Insulin Resistance and Protease Inhibitor Treatment on Lipid and Lipoprotein Metabolism in HIV-Infected Patients

Abstract

Background: The relationship between insulin resistance, dyslipidemia, HIV infection, and antiretroviral therapy remains unclear, and the atherogenic nature of lipid and lipoprotein profiles in HIV-infected patients has not been fully characterized. Method: We measured plasma lipid and lipoprotein subfractions using Vertical Auto Profile-II methodology and directly measured insulin-mediated glucose disposal in 45 protease inhibitor (PI)-treated and non-PI-treated HIV-infected patients. Results: PI-treated patients had higher total, LDL, and narrow-density LDL cholesterol (p < .05) and a trend toward higher triglycerides, whereas HDL cholesterol and LDL particle characteristics were unrelated to PI use or history of lipodystrophy. Insulin sensitivity did not differ on the basis of PI therapy, but decreased insulin sensitivity was associated with lower HDL and HDL-3 cholesterol (p < .01); elevated triglyceride (p < .01), VLDL 1+2, and VLDL 3a+3b lipoproteins (p < .01); and smaller, denser (more atherogenic) LDL particle characteristics (p < .01). Thus, the lipoprotein abnormality associated with PI use was increased LDL cholesterol, whereas changes in TG and HDL metabolism were associated with insulin resistance, independent of PI use. Conclusion: The variables of PI-treatment, dyslipidemia, lipodsytrophy, and insulin resistance do not always cluster together in HIV-infected patients, which suggests that the metabolic phenotype emerging in treated patients results from a complex interplay of drug effects, immune restoration, and baseline insulin sensitivity.     

急性脑梗死患者并发胰岛素抵抗的研究

目的:探讨脑梗死急性期患者是否存在胰岛素抵抗(IR);在急性期血糖升高,是否使用胰岛素治疗.方法:本文测定了50例脑梗死患者和30例健康人的空腹血糖(FPG)、空腹血清胰岛素(FINS)、皮质醇(F),计算胰岛素敏感性指数(ISI),并与神经功能缺损评分和病灶大小进行直接相关分析.结果:脑梗死急性期患者FPG、FINS及F显著高于对照组(P＜0.001),ISI较对照组明显降低(P＜0.001).脑梗死轻型组和中重型组的FPG、F、ISI之间也存在明显差异(P＜0.001、P＜0.01、P＜0.05).ISI与脑梗死的面积呈负相关(r=-0.313,P＜0.05).ISI与神经功能缺损评分也呈负相关(r=-0.317,P＜0.05).中重型组的死亡率与病残率高于轻型组.结论:脑梗死患者急性期存在IR,且急性期胰岛素水平及IR程度与患者病情与预后有关.故在脑梗死急性期对血糖升高的患者应考虑使用胰岛素治疗.     

The Effect of Intraoperative Use of High-Dose Remifentanil on Postoperative Insulin Resistance and Muscle Protein Catabolism: A Randomized Controlled Study

Objective: We investigated the effect of the intraoperative use of a high dose remifentanil on insulin resistance and muscle protein catabolism.Design: Randomized controlled study.Patients and Intervention: Thirty-seven patients undergoing elective gastrectomy were randomly assigned to 2 groups that received remifentanil at infusion rates of 0.1 μg·kg^-1·min^-1 (Group L) and 0.5 μg·kg^-1·min^-1 (Group H).Main outcome measures: Primary efficacy parameters were changes in homeostasis model assessment as an index of insulin resistance (HOMA-IR) and 3-methylhistidine/creatinine (3-MH/Cr). HOMA-IR was used to evaluate insulin resistance, and 3-MH/Cr was used to evaluate the progress of muscle protein catabolism. Intraoperative stress hormones, insulin, and blood glucose were assessed as secondary endpoints.Results: Eighteen patients in Group L and 19 in Group H were examined. HOMA-IR values varied within normal limits in both groups during surgery, exceeding normal limits at 12 h after surgery and being significantly elevated in Group L. There were no significant differences in the 3-MH/Cr values between the 2 groups at any time point. The stress hormones (adrenocorticotropic hormone, cortisol, and adrenaline) were significantly elevated in Group L at 60 min after the start of surgery and at the initiation of skin closure. There were no significant differences in insulin values, but blood glucose was significantly elevated in Group L at 60 min after the start of surgery and at the start of skin closure.Conclusion: Use of high-dose remifentanil as intraoperative analgesia during elective gastrectomy reduced postoperative insulin resistance, although it did not reduce postoperative muscle protein catabolism.     

Association between Serum 25-Hydroxyvitamin D Level and Insulin Resistance in a Rural Population

Purpose

A low serum 25-hydroxyvitamin D [25(OH)D] level in the blood has been correlated with an increased risk of diabetes mellitus; however, the association between serum 25(OH)D level and insulin resistance has not been established in a Korean rural population. The aim of this study was to investigate the independent association between serum 25(OH)D level and insulin resistance in rural Korean adults.

Materials and Methods

This study used data from the Korean Genome Epidemiology Study-Kangwha Study. In the 2011 study, 1200 adults completed health examinations. In an ancillary study, serum 25(OH)D level was measured in a subsample (n=813). After excluding those taking vitamin D supplements, a cross-sectional analysis was carried out on 807 participants (324 men and 483 women) aged 40 to 89 years old. Measured from overnight fasting blood samples, glucose and insulin levels were used to calculate the homeostasis model assessment for insulin resistance (HOMA-IR). Measures of glucose, insulin, and HOMA-IR were log-transformed for parametric tests.

Results

Serum 25(OH)D level was inversely associated with HOMA-IR (β=-0.003, p=0.039) in a univariate analysis. However, the association was not significant after adjustment for sex and age (β=-0.002, p=0.123) or after adjustment for sex, age, body mass index, smoking status, alcohol intake, and regular exercise (β=-0.003, p=0.247).

Conclusion

Our findings suggest that vitamin D is not independently associated with insulin resistance in Korean men and women.     

地菍总黄酮对糖尿病肾病大鼠胰岛素抵抗和肾损害的影响

目的 研究地菍总黄酮对糖尿病肾病(diabetic nephropathy,DN)大鼠胰岛素抵抗和肾损害的影响.方法 在60只大鼠中随机选取10只为正常组,剩余50只均经腹腔注射链脲佐菌素STZ建立DN模型,共建模成功43只,选取40只DN大鼠随机均分为4组每组各10只,分别为模型组以及地菍总黄酮低剂量组150 mg/...     

急诊冠状动脉介入治疗后无复流现象与胰岛素抵抗

目的探讨急性心肌梗死（AMI）急诊经皮冠状动脉介入治疗（PCI）后心肌无复流现象与胰岛素抵抗之间的关系。方法行急诊PCI的ST段抬高型AMI患者109例，其中单光子发射型计算机断层（single photon emission computed tomography，SPECT）心肌灌注显像检测出现心肌无复流现象的22例。测定空腹血糖、空腹胰岛素水平、总胆固醇、甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、肌酐、尿酸水平。评价胰岛素敏感性采用稳态模式评估法（HOMA）及改良的胰岛素敏感性指数（ISI）公式计算。结果AMI无复流组与复流组比较，存在高胰岛素血症（P〈0．05）和胰岛素敏感性的降低（P〈0．05）。结论AMI急诊PCI术后出现心肌无复流现象的患者存在高胰岛素血症和胰岛素抵抗，胰岛素抵抗在心肌无复流现象的发病中可能发挥一定作用。     

Overexpression of LYRM1 induces mitochondrial impairment in 3T3-L1 adipocytes

Homo sapiens LYR motif containing 1 (LYRM1) is a recently discovered gene involved in adipose tissue homeostasis and obesity-associated insulin resistance. The exact mechanism by which LYRM1 induces insulin resistance has not yet been fully elucidated. In this study, we demonstrated that the overexpression of LYRM1 in 3T3-L1 adipocytes resulted in reduced insulin-stimulated glucose uptake, an abnormal mitochondrial morphology, and a decrease in intracellular ATP synthesis and mitochondrial membrane potential. In addition, LYRM1 overexpression led to excessive production of intracellular of reactive oxygen species. Collectively, our results indicated that the overexpression of LYRM1 caused mitochondrial dysfunction in adipocytes, which might be responsible for the development of LYRM1-induced insulin resistance.