非酒精性脂肪性肝病抵抗素、脂联素与肝纤维化相关性研究

目的:研究非酒精性脂肪肝(NAFLD)患者抵抗素、脂联素水平与肝纤维化指标的关系。方法:采用ELASA法检测NAFLD患者和正常对照组的抵抗素、脂联素水平及Ⅲ型前胶原(PCⅢ)、透明质酸(HA)、Ⅳ型胶原(C)、层粘蛋白(LN)水平。结果:NAFLD组脂联素显著低于对照组,抵抗素水平显著高于对照组,抵抗素水平与WHR、BMI、FBG、TG、FINS、HOMA-IRI、PC、PC、HA和LN呈显著正相关,脂联素水平与WHR、BMI、FBG、TG、FINS、HOMA-IRI、PC、PC、HA和LN呈显著负相关,抵抗素与脂联素水平呈显著负相关。结论:NAFLD患者血清抵抗素水平增高,脂联素水平降低,NAFLD患者肝纤维化进程中抵抗素与脂联素可能起重要作用。

盐酸二甲双胍对2型糖尿病中肥胖患者血浆胰高血糖素样肽-1和抵抗素水平的影响

目的:探讨盐酸二甲双胍对2型糖尿病中肥胖患者血浆胰高血糖素样肽-1和抵抗素水平的影响。方法:对60例2型糖尿病(T2DM)中肥胖患者按照年龄、性别、病情、HbA1c,1∶1匹配分为试验组和对照组。试验组口服盐酸二甲双胍500mg,3次/d,疗程8周。对照组口服盐酸二甲双胍250mg,3次/d,疗程8周。采用酶联免疫吸附法(ELISA)分别检测实验组(30例)和对照组(30例)的空腹血清抵抗素、GLP-1,采用氧化酶法分别检测两组空腹血糖(FPG)的水平,采用化学发光法测定空腹胰岛素(FINS)水平。计算体质量指数(BMI)、胰岛素抵抗指数(HOMA-IR)。结果:治疗后两组抵抗素、FINS、FPG、GLP-1水平比较,有明显差异;BMI、HOMA-IR水平无明显差异。试验组治疗前后BMI、HOMA-IR、FPG、FINS、GLP-1、抵抗素水平比较,有明显差异。结论:对于2型糖尿病中肥胖患者来说,盐酸二甲双胍能够改善胰岛素抵抗和胰岛β细胞功能的作用,可能与降低抵抗素水平、升高GLP-1水平的机制有关。

血清抵抗素水平与2型糖尿病患者血管并发症的相关性研究

目的:探讨血清抵抗素水平与2型糖尿病(T2DM)患者血管并发症的关系,及其可能在T2DM血管并发症中所起的作用。方法:选取40例T2DM患者,同时选取20例健康人作为对照组。受试者空腹采血,测定血清抵抗素、一氧化氮(NO)、血管性血友病因子(vWF);行OGTT并测定C肽、胰岛素及生化检查,同时测血压、身高、体重、腰围、体重指数、胰岛素敏感指数、胰岛素抵抗指数等。结果:T2DM患者血清抵抗素、vWF水平均高于正常对照组;NO低于正常对照组。T2DM组抵抗素与vWF呈正相关;与NO呈负相关。结论:T2DM患者血清抵抗素水平增高,且与血管内皮功能相关指标呈正或负相关,提示抵抗素可能与T2DM血管并发症的发生有关,是预测血管并发症的有价值的指标。

2型糖尿病家系血清抵抗素的表达与胰岛素抵抗的相关性及临床意义

目的:研究2型糖尿病(T2DM)家系正常糖耐量一级亲属(一级亲属)血清抵抗素水平的变化,探讨抵抗素与胰岛素抵抗(IR)的关系。方法:收集广西壮族T2DM家系45个,在排除DM和糖耐量损害的前提下,选择一级亲属为观察组(83例),先证者的配偶或其同胞的配偶为正常对照组(76例),检测所有受试者的空腹血糖(FPG)、胰岛素(FINS)、胰岛素原(FPI)、血脂、抵抗素水平。采用稳态模型法(HOMA)计算胰岛素抵抗指数(HOMA-IR)。结果:一级亲属组的甘油三酯(TG)、FPI、FINS、HOMA-IR、抵抗素水平显著高于正常对照组,高密度脂蛋白(HDL)显著低于正常对照组。多元线性逐步回归分析显示:FPG、体质指数(BMI)、抵抗素是影响T2DM家系一级亲属IR的独立危险因素。结论:T2DM家系一级亲属在未发生糖尿病时已存在IR,抵抗素可影响T2DM家系一级亲属IR的程度。

补肾排毒颗粒对维持性血透患者血清抵抗素水平的影响

目的:探讨补肾排毒颗粒对维持性血透患者血清抵抗素水平的影响。方法:选择透析3个月以上的维持性血透患者90例,随机分为3组,常规透析组、补肾排毒颗粒组、立普妥组,每组30例;健康体检的20人作正常对照组。各组分别于服药前、服药4、8、12 W后空腹采血,免疫比浊法测定血清抵抗素(resistin)水平。结果:各透析组患者治疗前血清抵抗素水平均明显高于正常健康组,差异具显著统计学意义(P<0.05);治疗8 W后,补肾排毒颗粒组血清抵抗素水平明显下降(P<0.05);治疗12 W后,立普妥组血清抵抗素水平下降(P<0.05);常规透析组患者抵抗素水平无明显变化(P>0.05)。结论:补肾排毒颗粒可以明显改善维持性血透患者血清抵抗素水平。

养心合剂对慢性心力衰竭利尿剂抵抗病人AVP、AQP2表达的影响

目的观察养心合剂对慢性心力衰竭利尿剂抵抗病人血管加压素(AVP)、水通道蛋白-2(AQP2)表达的影响。方法选取慢性心力衰竭利尿剂抵抗病人60例,随机分为试验组与对照组。对照组给予西医标准化治疗,试验组给予西医标准化治疗加服养心合剂,连续治疗10d后比较两组AVP、AQP2浓度、24h尿量,观察不良反应。结果治疗后试验组血浆AVP及尿液AQP2浓度均较治疗前下降(P <0.05),且低于对照组(P <0.05);治疗后试验组24h尿量较治疗前增加,且优于对照组(P <0.05);养心合剂安全性良好。结论养心合剂可能通过抑制AVP、AQP2的表达,减轻水钠潴留及利尿剂抵抗,进而改善病人心功能,延缓心力衰竭的发展。

Adiponectin Gene Variation -4522C/T Is Associated with Type 2 Diabetic Obesity and Insulin Resistance in Chinese

The authors investigated the possible association of -4522C/T variation of adiponectin gene with coronary heart disease （CHD） and type 2 diabetes mellitus （T2DM）. Genotyping of SNP --4522C/T in 304 patients with CHD, 389 patients with T2DM, and 405 age and sex-matched healthy control subjects was carried out by means of PCR-RFLP approach. No significant difference in the genotype or allele frequencies was found, either between patients with CHD and control subjects, or between patients with T2DM and control subjects. However, in the subgroup analysis, an association of the TAr genotype and T allele with type 2 diabetes combined with obesity （BMI ≥ 25 kg/m2） was found （P = 0.014 and P = 0.034, respectively）. Also the homeostasis model assessment of insulin resistance （HOMA-IR） in T2DM patients with T/T genotype was significantly higher than that in T2DM patients carrying C allele （P = 0.0069）. The authors＇ findings for the first time demonstrated that SNP --4522 in the adiponectin gene was associated with T2DM that combined with obesity and higher insulin resistance index in patients with T2DM. This indicated that the variation might associate with an increased susceptibility to type 2 diabetic obesity and insulin resistance. But -4522C/T polymorphism did not contribute to the susceptibility of CHD.

Effect of Milrinone Induced Insulin Resistance on Glucose and Lipid Metabolism in Rats

Aim To investigate the effects of milrinone (a selective phosphodiesteraseIII inhibitor PDE_3 ) on insulin secretion, blood glucose, plasma free fatty acids (FFA) anddose-response relationship, and assess possible effects of milrinone on glucose metabolism andinsulin sensitivity in conscious rats. Methods The catheterized nonstressed rats were administeredvarious doses of milrinone (1, 5, 25μmoL·kg^(-1)) and were compared with controls. Ahyperinsulinaemic-eugly-caemic clamp was established in counscious rats, andmilrinone(25μmoL·kg^(-1)) and 25% dimethyl sulfoxide (DMSO, as a control) were given at 120 minduring hyperinsulinaemic-euglycaemic clamping. Glucose turnover was determind with by gaschromatograph mass spectrometer (GC-MS). Results After dosing, plasma FFA levels in 3 milrinonegroups significantly increased, compared with the controls and before dosing. The percentages ofelevation of FFA by the different milrinone doses were very similar, 50%, and 52% , 55% for 1, 5,and 25 μmoL·kg^(-1), repectively, at 2 min after dosing. Plasma insulin levels were significantlyelevated in the 5 and 25 μmoL·kg^(-1) groups, and the effect of milrione on glucose concentrationwas detectable only in 25μmoL·kg^(-1) group. During hyperinsulinaemic clamping, there weresignificant increase, in plasma FFA (from 173 +- 15 to 634 +- 87μmoL·kg^(-1)) and hepatic glucoseproduction (HGP), and a significant decrease in glucose infusion rates (GIR) to about 21% and aslight increase in plasma insulin after milrinone treatment. Conclusion Milrinone impaires theability of insulin to suppress lipolysis and HGP, and insulin-mediated glucose utilization inperipheral tissue. Therefore, milrinone administration may induce an acute insulin resistance invivo.

A Study on Exon 17 and 20 of the Insulin Receptor Gene Variations in Patients with Acanthosis Nigricans and Their Close Relatives

Objective: To explore the relationship between the insulin resistance and thedefects or mutations or mutations in insulin receptor (InsR)gene. Methods: Using the single-strandconformation polymorphism(SSCP), mutations and polymorphisms were detected in nine patients withacan-thosis nigricans (AN) and their first degree relatives in exon 17 and 20 of InsR gene. Thepolymorphisms and mutations were confirmed by DNA direct sequencing. Results: Fourteen variant SSCPpat-terns were detected. Direct sequencing revealed seven point mutations and six silentpolymorphisms. Five of the mutations appeared not to be mentioned in the previous literature. Thesemutations were all located within the domain of tyrokinase in InsR. Conclusion: It seem to us thatalmost all the AN patients with severe insulin resistance in this study have mutations in InsRtyrokinase domain.

Molecular mechanism of Radix astragali on improvement of insulin sensitivity of SD rats treated with low dose dexamethasone

Aim To reveal the main active components and the action mechanisms of Radix astragali on insulin sensitivity improvement, we have investigated the effects of polysaccharide portion and saponin portion of Radix astragali extracts on blood biochemical indices and related gene expression of dexamethasone-induced SD rats. Methods SD rats （6 per group） received 2 μg/day subcutaneous dexamethasone for 4 weeks plus same dose （10 g material/kg） of polysaccharide or saponin extracts of Radix astragali. Blood samples, kidney tissues and epididymal fat pads were taken at the end of the experiment. Serum triglyceride （TG）, total cholesterol （TC）, low density lipoprotein cholesterol （LDLC）, high density lipoprotein cholesterol （HDLC）, glucose （GLU） and insulin （INS） levels were measured, respectively, mRNA levels of angiotensinogen in kidney, adiponectin and leptin as well as TNF-α in epididymal fats were determined by RT-PCR assay using GAPDH gene as an internal control. Results Both of polysaccharide and saponin extracts of Radix astragali exhibited positive effects in reducing serum triglycerides, glucose, and insulin levels of dexamethasone-induced SD rats. The saponin group showed more improvements on quantitive insulin sensitivity check index （QUICKI） than the polysaccharide group did. Both of the extracts down-regulated kidney angiotensinogen and fat TNF-α mRNA levels while they were simultaneously up-regulating fat adiponectin and leptin mRNA levels. No significant difference was found between actions of the two extracts. Conclusion Both of polysaccharide and saponin extracts of Radix astragali can improve insulin sensitivity. This action might be closely related to down-regulation of angiotensinogen, TNF-α and up-regulation of adiponectin and leptin expression. The results partly explained the improvement of type Ⅱ diabetes and diabetic nephropathy by Radix astragali. The similar actions of the two crude extracts suggest that unknown key active compounds might exist in both and remain to be discovered.

Effects of over-expressing resistin on glucose and lipid metabolism in mice

Resistin,a newly discovered peptide hormone mainly secreted by adipose tissues,is present at high levels in serum of obese mice and may be a potential link between obesity and insulin resistance in rodents. However,some studies of rat and mouse models have associated insulin resistance and obesity with decreased resistin expression. In humans,no relationship between resistin level and insulin resistance or adiposity was observed. This suggests that additional studies are necessary to determine the specific role of resistin in the regulation of energy metabolism and adipogenesis. In the present study,we investigated the effect of resistin in vivo on glucose and lipid metabolism by over-expressing resistin in mice by intramuscular injection of a recombinant eukaryotic expression vector pcDNA3.1-Retn encoding porcine resistin gene. After injection,serum resistin and serum glucose (GLU) levels were significantly increased in the pcDNA3.1-Retn-treated mice; there was an obvious difference in total cholesterol (TC) level between the experiment and the control groups on Day 30. In pcDNA3.1-Retn-treated mice,both free fatty acid (FFA) and high density lipoprotein (HDL) cholesterol levels were markedly lower than those of control,whereas HDL cholesterol and triglyceride (TG) levels did not differ between the two groups. Furthermore,lipase activity was expressly lower on Day 20. Our data suggest that resistin over-expressed in mice might be responsible for insulin resistance and parameters related to glucose and lipid metabolism were changed accordingly.

High Serum Resistin Level may be an Indicator of the Severity of Coronary Disease in Acute Coronary Syndrome

Objective To investigate the correlation between serum resistin level, cardiovascular risk factors and severity of coronary disease in acute coronary syndrome （ACS）. Methods Alter evaluated by clinical history, electrocardiography, exercise tolerance tests, laboratory tests, and coronary angiography, 220 consecutive patients with suspected chest pain were divided into normal control group, stable angina pectoris （SAP） group, and ACS group, respectively. Baseline clinical characteristics, including height, weight, waist circumference, hip circumference, white blood cell count, high-sensitive C-reactive protein （hsCRP）, total cholesterol, triglyceride, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, were compared among three groups. ELISA was used to detect serum resistin levels. Pearson＇s correlation coefficient analysis was used to assess association between resistin and other traditional cardiovascular risk factors. Multinomial logistic regression analyses were used to define the relationship between serum resistin level and SAP or ACS. Results Serum resistin level in ACS group （1.18±0.48 μg/L） was significantly higher than that in normal control and SAP groups （0.49±0.40 and 0.66±0.40 μg/L; P〈0.01）. Only in ACS group, increased serum resistin level was significantly correlated with hsCRP （r=0.262, P=0.004） and white blood cell count （r=0.347, P=0.001）. Furthermore, serum resistin levels showed a stepwise increase with the number increase of 〉 50% stenosed coronary vessels. Multinomial logistic regression test demonstrated that serum resistin was a strong risk factor for ACS （OR=29.132, 95 % CI： 10.939-77.581, P〈0.001）. Conclusion These findings suggested the potential role of resistin in atherosclerosis and especially its involvement in ACS.

Relationship between resistin level in serum and acute coronary syndrome or stable angina pectoris

Objective： To investigate the relationship between serum resistin level and acute coronary syndrome （ACS） or stable angina pectoris （SAP）. Methods： Sixty-five patients, with coronary artery disease, were enrolled and divided into three subgroups： acute myocardial infarction （AMI）, unstable angina pectoris （UAP） and SAP, and 26 healthy people were recruited as controls in the cross-sectional study. Serum resistin levels were determined by ELISA （enzyme-linked immunosorbent assay）, and WBC （white blood cell count）, hsCRP （high sensitive C-reaction protein）, CKmax （maximum of creatinkinase）, CK-MBmax （maximum of isozyme of creatinkinase） and cTnImax （maximum of troponin） were measured by standard laboratory methods. Results： The serum resistin levels were 4 folds higher in AMI patients, 2.43 folds in UAP patients and I. 12 folds in SAP patients than in the healthy controls （P〈0.05）. The resistin levels were also significantly different between AMI [（8.16±0.79） ng/ml], UAP [（5.59±0.75） ng/ml] and SAP [（3.45±0.56） ng/ml] groups （P〈0.01）; WBC, hsCRP, CK CK-MBmax and cTnlmax were significantly increased in AMI patients over UAP and SAP patients. Spearman analysis showed that serum resistin levels were positively correlated with WBC （r=0.412, P=0.046）, hsCRP （r=0.427,p=0.037）, CK CK-MBmax and cTnImax （r=0.731, 0.678, 0.656; P〈0.01）. Conclusion： Serum resistin levels increased with inflammatory factors and myocardial impairment. The results suggest that human resistin might play an important role in the pathogenesis of atherosclerosis and AMI as an inflammatory factor.

Problems associated with glucose toxicity:Role of hyperglycemia-induced oxidative stress

Glucose homeostasis deficiency leads to a chronic increase in blood glucose concentration. In contrast to physiological glucose concentration, chronic super-physiological glucose concentration negatively affects a large number of organs and tissues. Glucose toxicity means a decrease in insulin secretion and an increase in insulin resistance due to chronic hyperglycemia. It is now generally accepted that glucose toxicity is involved in the worsening of diabetes by affecting the secretion of B-cells. Several mechanisms have been proposed to explain the adverse effects of hyperglycemia. It was found that persistent hyperglycemia caused the functional decline of neutrophils. Infection is thus the main problem resulting from glucose toxicity in the acute phase. In other words, continued hyperglycemia is a life-threatening risk factor, not only in the chronic but also the acute phase, and it becomes a risk factor for infection, particularly in the perioperative period.

Effect of biofilm formation by clinical isolates of Helicobacter pylori on the efflux-mediated resistance to commonly used antibiotics

To evaluate the role of biofilm formation on the resistance of Helicobacter pylori (H. pylori) to commonly prescribed antibiotics, the expression rates of resistance genes in biofilm-forming and planktonic cells were compared.METHODSA collection of 33 H. pylori isolates from children and adult patients with chronic infection were taken for the present study. The isolates were screened for biofilm formation ability, as well as for polymerase chain reaction (PCR) reaction with HP1165 and hp1165 efflux pump genes. Susceptibilities of the selected strains to antibiotic and differences between susceptibilities of planktonic and biofilm-forming cell populations were determined. Quantitative real-time PCR (qPCR) analysis was performed using 16S rRNA gene as a H. pylori-specific primer, and two efflux pumps-specific primers, hp1165 and hefA.RESULTSThe strains were resistant to amoxicillin, metronidazole, and erythromycin, except for one strain, but they were all susceptible to tetracycline. Minimum bactericidal concentrations of antibiotics in the biofilm-forming cells were significantly higher than those of planktonic cells. qPCR demonstrated that the expression of efflux pump genes was significantly higher in the biofilm-forming cells as compared to the planktonic ones.CONCLUSIONThe present work demonstrated an association between H. pylori biofilm formation and decreased susceptibility to all the antibiotics tested. This decreased susceptibility to antibiotics was associated with enhanced functional activity of two efflux pumps: hp1165 and hefA.

A paradox:Insulin inhibits expression and secretion of resistin which induces insulin resistance

AIM: To confirm whether insulin regulates resistinexpression and secretion during differentiation of 3T3-L1preadipocytes and the relationship of resistin with insulinresistance both in vivo and in vitro.METHODS: Supernatant resistin was measured duringdifferentiation of 3T3-L1 preadipocytes. L6 rat myoblastsand hepatoma cell line H4IIE were used to confirm thecellular function of resistin. Diet-induced obese ratswere used as an insulin resistance model to study therelationship of resistin with insulin resistance.RESULTS: Resistin expression and secretion wereenhanced during differentiation 3T3-L1 preadipocytes.This cellular differentiation stimulated resistin expressionand secretion, but was suppressed by insulin. Resistinalso induced insulin resistance in H4IIE hepatocytes andL6 myoblasts. In diet-induced obese rats, serum resistinlevels were negatively correlated with insulin sensitivity,but not with serum insulin.CONCLUSION: Insulin can inhibit resistin expressionand secretion in vitro, but insulin is not a major regulatorof resistin in vivo . Fat tissue mass affects insulinsensitivity by altering the expression and secretion ofresistin.

Adipokines and ghrelin in gastric cancer cachexia

AIM:To investigate the roles of the adipocytokines,ghrelin and leptin in gastric cancer cachexia. METHODS:Resistin,ghrelin,leptin,adiponectin,insulin and insulin-like growth factor(IGF-Ⅰ),were measured in 30 healthy subjects,and 60 gastric cancer patients of which 30 suffered from cancer-induced cachexia and 30 served as a control group. The relationships between hormones,body mass index(BMI) loss ratio,age,gender,and Glasgow Prognostic Score(GPS) were investigated. RESULTS:Cachexia patients had higher tumor stage and GPS when compared with non-cachexia patients(P < 0.05). Ghrelin,resistin,leptin,adiponectin and IGF-Ⅰ,showed a significant correlation with BMI loss ratio and GPS(P < 0.05). A strong correlation was seen between GPS and BMI loss(R = -0.570,P < 0.0001). Multivariate analysis indicated that BMI loss was significantly independent as a predictor of ghrelin,resistin,leptin and IGF-Ⅰ(P < 0.05). Existence of an important significant relationship between resistin and insulin resistance was also noted. CONCLUSION:These results showed that serum ghrelin,leptin,adiponectin,and IGF-Ⅰ play important roles in cachexia-related gastric cancers. No relationshipwas found between resistin and cancer cachexia. Also,because of the correlation between these parameters and GPS,these parameters might be used as a predictor factor.

Hepatitis C virus and type 2 diabetes

This review focuses on the relationship between hepatitis C virus(HCV) infection and glucose metabolism derangements.Cross-sectional and longitudinal studies have shown that the chronic HCV infection is associated with an increased risk of developing insulin resistance(IR) and type 2 diabetes(T2D).The direct effect of HCV on the insulin signaling has been analyzed in experimental models.Although currently available data should be considered as preliminary,HCV seems to affect glucose metabolism via mechanisms that involve cellular pathways that have been implicated in the host innate immune response.IR and T2D not only accelerate the histological and clinical progression of chronic hepatitis C,but also reduce the early and sustained virological response to interferon-alpha-based therapy.Thus,a detailed knowledge of the mechanisms underlying the HCV-associated glucose metabolism derangements is warranted,in order to improve the clinical management of chronic hepatitis C patients.

Molecular detection of Helicobacter pylori antibiotic resistance in stool vs biopsy samples

AIM To compare(1) demographics in urea breath test(UBT) vs endoscopy patients; and(2) the molecular detection of antibiotic resistance in stool vs biopsy samples.METHODS Six hundred and sixteen adult patients undergoing endoscopy or a UBT were prospectively recruited to the study. The Geno Type Helico DR assay was used to detect Helicobacter pylori(H. pylori) and antibiotic resistance using biopsy and/or stool samples from CLOpositive endoscopy patients and stool samples from UBT-positive patients. RESULTS Infection rates were significantly higher in patients referred for a UBT than endoscopy(overall rates: 33% vs 19%; treatment-na?ve patients: 33% vs 14.7%, respectively). H. pylori-infected UBT patients were younger than H. pylori-infected endoscopy patients(41.4 vs 48.4 years, respectively, P < 0.005), with a higher percentage of H. pylori-infected males in the endoscopy-compared to the UBT-cohort(52.6% vs 33.3%, P = 0.03). The Geno Type Helico DR assay was more accurate at detecting H. pylori infection using biopsy samples than stool samples [98.2%(n = 54/55) vs 80.3%(n =53/66), P < 0.005]. Subset analysis using stool and biopsy samples from CLO-positive endoscopy patients revealed a higher detection rate ofresistance-associated mutations using stool samples compared to biopsies. The concordance rates between stool and biopsy samples for the detection of H. pylori DNA, clarithromycin and fluoroquinolone resistance were just 85%, 53% and 35%, respectively. CONCLUSION Differences between endoscopy and UBT patients provide a rationale for non-invasive detection of H. pylori antibiotic resistance. However, the Geno Type Helico DR assay is an unsuitable approach.

Berberine reverses free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ

AIM: To investigate the effects and molecular mechanisms of berberine on improving insulin resistance induced by free fatty acids (FFAs) in 3T3-L1 adipocytes. METHODS: The model of insulin resistance in 3T3-L1 adipocytes was established by adding palmic acid (0.5 mmol/L) to the culture medium. Berberine treatment was performed at the same time. Glucose uptake rate was determined by the 2-deoxy-[3H]-D-glucose method. The levels of IkB kinase beta (IKKβ) Ser181 phosphorylation, insulin receptor substrate-1(IRS-1) Ser307 phosphorylation, expression of IKKβ, IRS-1, nuclear transcription factor kappaB p65 (NF-κB p65), phosphatidylinositol-3-kinase p85 (PI-3K p85) and glucose transporter 4 (GLUT4) proteins were detected by Western blotting. The distribution of NF-κB p65 proteins inside the adipocytes was observed through confocal laser scanning microscopy (CLSM). RESULTS: After the intervention of palmic acid for 24 h, the insulin-stimulated glucose transport in 3T3-L1 adipocytes was inhibited by 67%. Meanwhile, the expression of IRS-1 and PI-3K p85 protein was reduced, while the levels of IKKβ Ser181 and IRS-1 Ser307 phosphorylation, and nuclear translocation of NF-κB p65 protein were increased. However, the above indexes, which indicated the existence of insulin resistance, were reversed by berberine although the expression of GLUT4, IKKβ and total NF-κB p65 protein were not changed during this study. CONCLUSION: Insulin resistance induced by FFAs in 3T3-L1 adipocytes can be improved by berberine. Berberine reversed free-fatty-acid-induced insulin resistance in 3T3-L1 adipocytes through targeting IKKβ.