AIM:To investigate whether nonalcoholic fatty liver disease(NAFLD)affects coronary artery disease(CAD)and identify candidate mediators.METHODS:Patients who underwent coronary angiography were consecutively recruited.T...AIM:To investigate whether nonalcoholic fatty liver disease(NAFLD)affects coronary artery disease(CAD)and identify candidate mediators.METHODS:Patients who underwent coronary angiography were consecutively recruited.The patients were classified into four groups by coronary artery stenosis:A,insignificant;B,one-vessel disease;C,two-vessel disease;and D,three-vessel disease.Abdominal ultrasonography was performed to determine the presence of a fatty liver and categorize by grade:0,no evidence;1,mild;2,moderate;and 3,severe.We measured not only known CAD risk factors,but also serum insulin,HOMA-index,adiponectin,interleukin-6,tumor necrosis factor-αand high-sensitivity C-reactive protein levels.RESULTS:Of the 134 patients who met the inclusion criteria,82(61.2%)had ultrasonographically diagnosed NAFLD.Among the 46 patients with CAD,37(80.4%)had evidence of a fatty liver.The two groups(A vs B-D)were significantly different in terms of age,total cholesterol,triglycerides,low-density lipoprotein levels and fatty liver.Coronary artery stenosis was strongly associated with fatty liver in a grade-dependent manner(P=0.025).In binary logistic regression,NAFLD was a significant independent predictor of CAD(P=0.03,OR=1.685;95%CI:1.051-2.702).Among the candidate mediators,the serum adiponectin level showed a trend toward lowering based on CAD progression(P=0.071).CONCLUSION:NAFLD is an independent risk factor for CAD in a grade-dependent manner.Moreover,adiponectin might be related to the pathogenesis of NAFLD.展开更多
Nonalcoholic fatty liver disease(NAFLD)is a condition in which excess fat accumulates in the liver of a patient with no history of alcohol abuse or other causes for secondary hepatic steatosis.The pathogenesis of NAFL...Nonalcoholic fatty liver disease(NAFLD)is a condition in which excess fat accumulates in the liver of a patient with no history of alcohol abuse or other causes for secondary hepatic steatosis.The pathogenesis of NAFLD and nonalcoholic steatohepatitis(NASH)has not been fully elucidated.The"two-hit"hypothesis is probably a too simplified model to elaborate complex pathogenetic events occurring in patients with NASH.It should be better regarded as a multiple step process,with accumulation of liver fat being the first step,followed by the development of necroinflammation and fibrosis.Adipose tissue,which has emerged as anendocrine organ with a key role in energy homeostasis,is responsive to both central and peripheral metabolic signals and is itself capable of secreting a number of proteins.These adipocyte-specific or enriched proteins,termed adipokines,have been shown to have a variety of local,peripheral,and central effects.In the current review,we explore the role of adipocytokines and proinflammatory cytokines in the pathogenesis of NAFLD.We particularly focus on adiponectin,leptin and ghrelin,with a brief mention of resistin,visfatin and retinol-binding protein 4 among adipokines,and tumor necrosis factor-α,interleukin(IL)-6,IL-1,and briefly IL-18 among proinflammatory cytokines.We update their role in NAFLD,as elucidated in experimental models and clinical practice.展开更多
AIM: To assess significance of serum adipokines to determine the histological severity of non-alcoholic fatty liver disease.METHODS: Patients with persistent elevation in serum aminotransferase levels and well-defined...AIM: To assess significance of serum adipokines to determine the histological severity of non-alcoholic fatty liver disease.METHODS: Patients with persistent elevation in serum aminotransferase levels and well-defined characteristics of fatty liver at ultrasound were enrolled. Individuals with a history of alcohol consumption, hepatotoxic medication, viral hepatitis or known liver disease were excluded. Liver biopsy was performed to confirm nonalcoholic liver disease(NAFLD). The degrees of liver steatosis, lobular inflammation and fibrosis were determined based on the non-alcoholic fatty liver activity score(NAS) by a single expert pathologist. Patients with a NAS of five or higher were considered to have steatohepatitis. Those with a NAS of two or lower were defined as simple fatty liver. Binary logistic regression was used to determine the independent association of adipokines with histological findings. Receiver operating characteristic(ROC) analysis was employed to determine cut-off values of serum adipokines to discriminate the grades of liver steatosis,lobular inflammation and fibrosis. RESULTS: Fifty-four participants aged 37.02 ± 9.82 were enrolled in the study. Higher serum levels of visfatin, IL-8, TNF-α levels were associated independently with steatosis grade of more than 33% [β = 1.08(95%CI: 1.03-1.14), 1.04(95%CI: 1.008-1.07), 1.04(95%CI: 1.004-1.08), P < 0.05]. Elevated serum IL-6 and IL-8 levels were associated independently with advanced lobular inflammation [β = 1.4(95%CI: 1.09-1.8), 1.07(95%CI: 1.003-1.15), P < 0.05]. Similarly, higher TNF-α, resistin, and hepcidin levels were associated independently with advanced fibrosis stage [β = 1.06(95%CI: 1.002-1.12), 19.86(95%CI: 2.79-141.19), 560.72(95%CI: 5.98-5255.33), P < 0.05]. Serum IL-8 and TNF-α values were associated independently with the NAS score, considering a NAS score of 5 as the reference value [β = 1.05(95%CI: 1.01-1.1), 1.13(95%CI: 1.04-1.22), P < 0.05]. CONCLUSION: Certain adipokines may determine the severity of NAFLD histology accurately.展开更多
Background： Many studies have suggested that cigarette smoking and polymorphisms of resi stin and glutathione peroxidase-1 （GPx-1） genes are closely correlated with tile pathogenesis of nonalcoholic lhtty liver dis...Background： Many studies have suggested that cigarette smoking and polymorphisms of resi stin and glutathione peroxidase-1 （GPx-1） genes are closely correlated with tile pathogenesis of nonalcoholic lhtty liver disease （NAFLD）. However, few reports have investigated these associations with respect to NAFLD susceptibility. We, therefore, exalnined the distribution of polymorphisms in GPx-l and resistin genes in NAFLD patients and healthy controls and analyzed the relationship between these polymorphisms and smoking status. Methods： Nine hundred NAFLD patients and 900 healthy controls were selected, and the genetic polymorphisms of resistin gene promoter- 420C/G and GPx- 1 gene Pro 198Leu were analyzed by polymorphism-polymerase chain reaction （PCR） in DNA extracted from peripheral blood leukocytes. Interactions between tile two mutants and the gene-environment interaction with cigarette smoking were also analyzed. Results： Genotype frequencies of 420C/G （GG） and Pro198Leu （LL） were significantly higher in NAFLD cases （49.56% and 50.11%, respectively） compared with healthy controls （23.67% and 24.22%, respectively） （P = 0.0069： P= 0.0072）. Moreover, the risk of NAFLD with 420C/G （GGJ was significantly higher than in controls （odds ratio [OR] =3.1685, 95% confidence interval （（7） 1.9366-5.2073）. Individuals carrying Pro198Leu （LL） had a high risk of NAFLD （OR - 3.1424, 95% C/= 1.7951 5.2367）. Combined analysis of the polymorphisms showed that the -420C/G （GG）/Pro198Leu （LL） genotype was significantly more common in the NAFLD group than in the control group （39.44% vs. 12.78%, respectively, P 0.0054）, while individuals with -420C/G （GG）/Pro198Leu （LL） had a high risk of NAFLD （OR = 5.（1357, 95% CI= 3.1852 7.8106）. Moreover, the cigarette smoking rate in the NAFLD group was significantly higher than in tile control group （OR = 1.8990, P = 0.0083 in the smoking index （SI） _〈400 subgroup： OR = 5.0937, P = 0.0051 in the SI 〉400 subgroup）, and statistical analysis suggested a positive interaction between cigarette smoking and 420C/G （GG） （y = 5.6018 in tile SI≤400 subgroup; γ - 4.4770 in the SI 〉400 subgroup） and Pro198Leu （LL） （y = 5.7715 in the SI ≤400 subgroup： γ 4.5985 in the SI 〉400 subgroup） in increasing the risk of NAFLD. Conclusion： NAFLD risk factors include -420C/G （GG）, Pro198Leu （LL） and cigarette smoking, and these three factors have a significant additive effect on NAFLD risk.展开更多
Background and Aims:Previous studies reported that serum resistin levels were remarkably changed in patients with nonalcoholic fatty liver disease(NAFLD)but the conclusions were inconsistent.The aim of this study was ...Background and Aims:Previous studies reported that serum resistin levels were remarkably changed in patients with nonalcoholic fatty liver disease(NAFLD)but the conclusions were inconsistent.The aim of this study was to investigate accurate serum resistin levels in adult patients with NAFLD.Methods:A complete literature research was conducted in the PubMed,Embase,and Cochrane Library databases,and all the available studies up to 7 May 2020 were reviewed.The pooled standardized mean difference(SMD)values were calculated to investigate the serum resistin levels in patients with NAFLD and healthy controls.Results:A total of 28 studies were included to investigate the serum resistin levels in patients with NAFLD.Patients with NAFLD had higher serum resistin levels than controls(SMD=0.522,95%confidence interval[CI]:0.004–1.040,I2=95.9%).Patients with nonalcoholic steatohepatitis(NASH)had lower serum resistin levels than the healthy controls(SMD=−0.44,95%CI:−0.83–0.55,I2=74.5%).In addition,no significant difference of serum resistin levels was observed between patients with NAFL and healthy controls(SMD=−0.34,95%CI:−0.91–0.23,I2=79.6%)and between patients with NAFL and NASH(SMD=0.15,95%CI:−0.06–0.36,I2=0.00%).Furthermore,subgroup and sensitivity analyses suggested that heterogeneity did not affect the results of meta-analysis.Conclusions:This meta-analysis investigated the serum resistin levels in adult patients with NAFLD comprehensively.Patients with NAFLD had higher serum resistin levels and patients with NASH had lower serum resistin levels than healthy controls.Serum resistin could serve as a potential biomarker to predict the development risk of NAFLD.展开更多
Objective： To investigate the protective effects of Chinese medicine formulation Chaihu Shugan San（柴胡疏肝散, CHSGS） on nonalcoholic fatty liver disease（NAFLD） in rats with insulin resistance（IR） and its molec...Objective： To investigate the protective effects of Chinese medicine formulation Chaihu Shugan San（柴胡疏肝散, CHSGS） on nonalcoholic fatty liver disease（NAFLD） in rats with insulin resistance（IR） and its molecular mechanisms. Methods： Male Sprague-Dawley rats were randomly divided into six groups： the control group, the model group, Dongbao Gantai group（东宝肝泰, DBGT, 0.09 g methionine/kg）, CHSGS high-dose group（CHSG-H, 12.6 g crude drug/kg）, CHSGS medium-dose group（CHSG-M, 6.3 g crude drug/kg）, and CHSGS low-dose group（CHSG-L, 3.15 g crude drug/kg）. After establishing the NAFLD rat model and treatment for 8 weeks, total cholesterol（TC）, triglyceride（TG）, high-density lipoprotein cholesterol（HDL-C）, free fatty acid（FFA）, fasting blood glucose（FBG）, fasting insulin（FINS） contents in blood serum, and TC, TG contents in the hepatic homogenate were measured by an automatic biochemical analyzer, and a homeostasis model assessment was applied to assess the status of IR, insulin sensitivity index（ISI）, and homeostasis model assessment for insulin secretion（HOMA-IS）. The expression levels of adiponectin and leptin mRNA in liver tissue were analyzed by reverse transcription polymerase chain reaction. Pathological changes of livers were observed by hematoxylineosin staining of paraffin section. Results： Compared with the model group, the serum levels of TC, TG, FFA, FBG, FINS, IRI, ISI, and the liver levels of TC and TG in CHSG-H, CHSG-M, CHSG-L groups showed significant declines（P〈0.01 or P〈0.05）; the serum levels of HDL-C, HOMA-IS were significantly increased（P〈0.01 or P〈0.05）; the expression of leptin mRNA was dramatically decreased and the expression of adiponectin mRNA was increased in the hepatic tissue（P〈0.01 or P〈0.05）. The fatty deposition of liver cells could also be alleviated. Conclusion： CHSGS could up-regulate the expression of adiponectin mRNA and down-regulate the expression of leptin mRNA on the liver, suggesting the CHSGS had positive therapeutic effect on NAFLD in rats with IR.展开更多
目的探讨非酒精性脂肪肝性肝病(nonalcoholic fatty live disease,NAFLD)患者血清脂联素(adiponectin,APN)、内脏脂肪素(Visfatin)水平及其与常用血生化学指标相关性。方法选取2014年6月至2017年12月云南省第一医院NAFLD的患者45例作为...目的探讨非酒精性脂肪肝性肝病(nonalcoholic fatty live disease,NAFLD)患者血清脂联素(adiponectin,APN)、内脏脂肪素(Visfatin)水平及其与常用血生化学指标相关性。方法选取2014年6月至2017年12月云南省第一医院NAFLD的患者45例作为观察组,选取健康志愿者32例作为对照组。采用全自动生化检测仪检测各研究对象血生化学指标,通过酶联免疫吸附试验(ELISA)检测各研究对象血清中APN、Visfatin的水平,分析其表达水平与各血生化指标的相关性。结果NAFLD组的BMI、腰围、臀围和腰臀比(WHR)显著高于对照组(P<0.05);NAFLD组血清TG、HDL-c、LDL-c、HbAIC、UA水平显著高于对照组(P<0.05);NAFLD组血清APN、Visfatin的浓度均显著低于对照组(P<0.05)。NAFLD患者血清APN水平与其BMI、WHR、TG、HDL-C、LDL-C、HBAIC、UA水平呈明显负相关,r值分别为-0.231、-0.203、-0.218、-0.249、-0.210、-0.242、-0.235,P均<0.01;NAFLD患者血清Visfatin水平与其BMI、WHR、TG、HBAIC、UA呈明显正相关,r值分别为0.212、0.175、0.186、0.198、0.161,P均<0.05,与HDL-C、LDL-C、APN水平呈明显负相关,r值分别为-0.180、-0.156、-0.200,P值均<0.05。结论NAFLD患者血清APN、Visfatin水平较正常健康人群降低,APN、Visfatin可能参与了NAFLD的发生发展,可作为NAFLD患者诊断和预警的潜在检测指标。展开更多
基金Supported by A 2009 Research Grant from Kangwon National University
文摘AIM:To investigate whether nonalcoholic fatty liver disease(NAFLD)affects coronary artery disease(CAD)and identify candidate mediators.METHODS:Patients who underwent coronary angiography were consecutively recruited.The patients were classified into four groups by coronary artery stenosis:A,insignificant;B,one-vessel disease;C,two-vessel disease;and D,three-vessel disease.Abdominal ultrasonography was performed to determine the presence of a fatty liver and categorize by grade:0,no evidence;1,mild;2,moderate;and 3,severe.We measured not only known CAD risk factors,but also serum insulin,HOMA-index,adiponectin,interleukin-6,tumor necrosis factor-αand high-sensitivity C-reactive protein levels.RESULTS:Of the 134 patients who met the inclusion criteria,82(61.2%)had ultrasonographically diagnosed NAFLD.Among the 46 patients with CAD,37(80.4%)had evidence of a fatty liver.The two groups(A vs B-D)were significantly different in terms of age,total cholesterol,triglycerides,low-density lipoprotein levels and fatty liver.Coronary artery stenosis was strongly associated with fatty liver in a grade-dependent manner(P=0.025).In binary logistic regression,NAFLD was a significant independent predictor of CAD(P=0.03,OR=1.685;95%CI:1.051-2.702).Among the candidate mediators,the serum adiponectin level showed a trend toward lowering based on CAD progression(P=0.071).CONCLUSION:NAFLD is an independent risk factor for CAD in a grade-dependent manner.Moreover,adiponectin might be related to the pathogenesis of NAFLD.
文摘Nonalcoholic fatty liver disease(NAFLD)is a condition in which excess fat accumulates in the liver of a patient with no history of alcohol abuse or other causes for secondary hepatic steatosis.The pathogenesis of NAFLD and nonalcoholic steatohepatitis(NASH)has not been fully elucidated.The"two-hit"hypothesis is probably a too simplified model to elaborate complex pathogenetic events occurring in patients with NASH.It should be better regarded as a multiple step process,with accumulation of liver fat being the first step,followed by the development of necroinflammation and fibrosis.Adipose tissue,which has emerged as anendocrine organ with a key role in energy homeostasis,is responsive to both central and peripheral metabolic signals and is itself capable of secreting a number of proteins.These adipocyte-specific or enriched proteins,termed adipokines,have been shown to have a variety of local,peripheral,and central effects.In the current review,we explore the role of adipocytokines and proinflammatory cytokines in the pathogenesis of NAFLD.We particularly focus on adiponectin,leptin and ghrelin,with a brief mention of resistin,visfatin and retinol-binding protein 4 among adipokines,and tumor necrosis factor-α,interleukin(IL)-6,IL-1,and briefly IL-18 among proinflammatory cytokines.We update their role in NAFLD,as elucidated in experimental models and clinical practice.
文摘AIM: To assess significance of serum adipokines to determine the histological severity of non-alcoholic fatty liver disease.METHODS: Patients with persistent elevation in serum aminotransferase levels and well-defined characteristics of fatty liver at ultrasound were enrolled. Individuals with a history of alcohol consumption, hepatotoxic medication, viral hepatitis or known liver disease were excluded. Liver biopsy was performed to confirm nonalcoholic liver disease(NAFLD). The degrees of liver steatosis, lobular inflammation and fibrosis were determined based on the non-alcoholic fatty liver activity score(NAS) by a single expert pathologist. Patients with a NAS of five or higher were considered to have steatohepatitis. Those with a NAS of two or lower were defined as simple fatty liver. Binary logistic regression was used to determine the independent association of adipokines with histological findings. Receiver operating characteristic(ROC) analysis was employed to determine cut-off values of serum adipokines to discriminate the grades of liver steatosis,lobular inflammation and fibrosis. RESULTS: Fifty-four participants aged 37.02 ± 9.82 were enrolled in the study. Higher serum levels of visfatin, IL-8, TNF-α levels were associated independently with steatosis grade of more than 33% [β = 1.08(95%CI: 1.03-1.14), 1.04(95%CI: 1.008-1.07), 1.04(95%CI: 1.004-1.08), P < 0.05]. Elevated serum IL-6 and IL-8 levels were associated independently with advanced lobular inflammation [β = 1.4(95%CI: 1.09-1.8), 1.07(95%CI: 1.003-1.15), P < 0.05]. Similarly, higher TNF-α, resistin, and hepcidin levels were associated independently with advanced fibrosis stage [β = 1.06(95%CI: 1.002-1.12), 19.86(95%CI: 2.79-141.19), 560.72(95%CI: 5.98-5255.33), P < 0.05]. Serum IL-8 and TNF-α values were associated independently with the NAS score, considering a NAS score of 5 as the reference value [β = 1.05(95%CI: 1.01-1.1), 1.13(95%CI: 1.04-1.22), P < 0.05]. CONCLUSION: Certain adipokines may determine the severity of NAFLD histology accurately.
文摘Background： Many studies have suggested that cigarette smoking and polymorphisms of resi stin and glutathione peroxidase-1 （GPx-1） genes are closely correlated with tile pathogenesis of nonalcoholic lhtty liver disease （NAFLD）. However, few reports have investigated these associations with respect to NAFLD susceptibility. We, therefore, exalnined the distribution of polymorphisms in GPx-l and resistin genes in NAFLD patients and healthy controls and analyzed the relationship between these polymorphisms and smoking status. Methods： Nine hundred NAFLD patients and 900 healthy controls were selected, and the genetic polymorphisms of resistin gene promoter- 420C/G and GPx- 1 gene Pro 198Leu were analyzed by polymorphism-polymerase chain reaction （PCR） in DNA extracted from peripheral blood leukocytes. Interactions between tile two mutants and the gene-environment interaction with cigarette smoking were also analyzed. Results： Genotype frequencies of 420C/G （GG） and Pro198Leu （LL） were significantly higher in NAFLD cases （49.56% and 50.11%, respectively） compared with healthy controls （23.67% and 24.22%, respectively） （P = 0.0069： P= 0.0072）. Moreover, the risk of NAFLD with 420C/G （GGJ was significantly higher than in controls （odds ratio [OR] =3.1685, 95% confidence interval （（7） 1.9366-5.2073）. Individuals carrying Pro198Leu （LL） had a high risk of NAFLD （OR - 3.1424, 95% C/= 1.7951 5.2367）. Combined analysis of the polymorphisms showed that the -420C/G （GG）/Pro198Leu （LL） genotype was significantly more common in the NAFLD group than in the control group （39.44% vs. 12.78%, respectively, P 0.0054）, while individuals with -420C/G （GG）/Pro198Leu （LL） had a high risk of NAFLD （OR = 5.（1357, 95% CI= 3.1852 7.8106）. Moreover, the cigarette smoking rate in the NAFLD group was significantly higher than in tile control group （OR = 1.8990, P = 0.0083 in the smoking index （SI） _〈400 subgroup： OR = 5.0937, P = 0.0051 in the SI 〉400 subgroup）, and statistical analysis suggested a positive interaction between cigarette smoking and 420C/G （GG） （y = 5.6018 in tile SI≤400 subgroup; γ - 4.4770 in the SI 〉400 subgroup） and Pro198Leu （LL） （y = 5.7715 in the SI ≤400 subgroup： γ 4.5985 in the SI 〉400 subgroup） in increasing the risk of NAFLD. Conclusion： NAFLD risk factors include -420C/G （GG）, Pro198Leu （LL） and cigarette smoking, and these three factors have a significant additive effect on NAFLD risk.
基金This study was supported by a grant from the National Natural Science Foundation of China(No.31770837)which plays a significant role in the design of the study and data collection,analysis nor interpretation,nor in the writing of the manuscript.
文摘Background and Aims:Previous studies reported that serum resistin levels were remarkably changed in patients with nonalcoholic fatty liver disease(NAFLD)but the conclusions were inconsistent.The aim of this study was to investigate accurate serum resistin levels in adult patients with NAFLD.Methods:A complete literature research was conducted in the PubMed,Embase,and Cochrane Library databases,and all the available studies up to 7 May 2020 were reviewed.The pooled standardized mean difference(SMD)values were calculated to investigate the serum resistin levels in patients with NAFLD and healthy controls.Results:A total of 28 studies were included to investigate the serum resistin levels in patients with NAFLD.Patients with NAFLD had higher serum resistin levels than controls(SMD=0.522,95%confidence interval[CI]:0.004–1.040,I2=95.9%).Patients with nonalcoholic steatohepatitis(NASH)had lower serum resistin levels than the healthy controls(SMD=−0.44,95%CI:−0.83–0.55,I2=74.5%).In addition,no significant difference of serum resistin levels was observed between patients with NAFL and healthy controls(SMD=−0.34,95%CI:−0.91–0.23,I2=79.6%)and between patients with NAFL and NASH(SMD=0.15,95%CI:−0.06–0.36,I2=0.00%).Furthermore,subgroup and sensitivity analyses suggested that heterogeneity did not affect the results of meta-analysis.Conclusions:This meta-analysis investigated the serum resistin levels in adult patients with NAFLD comprehensively.Patients with NAFLD had higher serum resistin levels and patients with NASH had lower serum resistin levels than healthy controls.Serum resistin could serve as a potential biomarker to predict the development risk of NAFLD.
基金Suppport by the National Natural Science Foundation of China(No.30973913)the Science Foundation of Science and Technology Bureau of Guangdong(No.2008A030101005)
文摘Objective： To investigate the protective effects of Chinese medicine formulation Chaihu Shugan San（柴胡疏肝散, CHSGS） on nonalcoholic fatty liver disease（NAFLD） in rats with insulin resistance（IR） and its molecular mechanisms. Methods： Male Sprague-Dawley rats were randomly divided into six groups： the control group, the model group, Dongbao Gantai group（东宝肝泰, DBGT, 0.09 g methionine/kg）, CHSGS high-dose group（CHSG-H, 12.6 g crude drug/kg）, CHSGS medium-dose group（CHSG-M, 6.3 g crude drug/kg）, and CHSGS low-dose group（CHSG-L, 3.15 g crude drug/kg）. After establishing the NAFLD rat model and treatment for 8 weeks, total cholesterol（TC）, triglyceride（TG）, high-density lipoprotein cholesterol（HDL-C）, free fatty acid（FFA）, fasting blood glucose（FBG）, fasting insulin（FINS） contents in blood serum, and TC, TG contents in the hepatic homogenate were measured by an automatic biochemical analyzer, and a homeostasis model assessment was applied to assess the status of IR, insulin sensitivity index（ISI）, and homeostasis model assessment for insulin secretion（HOMA-IS）. The expression levels of adiponectin and leptin mRNA in liver tissue were analyzed by reverse transcription polymerase chain reaction. Pathological changes of livers were observed by hematoxylineosin staining of paraffin section. Results： Compared with the model group, the serum levels of TC, TG, FFA, FBG, FINS, IRI, ISI, and the liver levels of TC and TG in CHSG-H, CHSG-M, CHSG-L groups showed significant declines（P〈0.01 or P〈0.05）; the serum levels of HDL-C, HOMA-IS were significantly increased（P〈0.01 or P〈0.05）; the expression of leptin mRNA was dramatically decreased and the expression of adiponectin mRNA was increased in the hepatic tissue（P〈0.01 or P〈0.05）. The fatty deposition of liver cells could also be alleviated. Conclusion： CHSGS could up-regulate the expression of adiponectin mRNA and down-regulate the expression of leptin mRNA on the liver, suggesting the CHSGS had positive therapeutic effect on NAFLD in rats with IR.
文摘目的探讨非酒精性脂肪肝性肝病(nonalcoholic fatty live disease,NAFLD)患者血清脂联素(adiponectin,APN)、内脏脂肪素(Visfatin)水平及其与常用血生化学指标相关性。方法选取2014年6月至2017年12月云南省第一医院NAFLD的患者45例作为观察组,选取健康志愿者32例作为对照组。采用全自动生化检测仪检测各研究对象血生化学指标,通过酶联免疫吸附试验(ELISA)检测各研究对象血清中APN、Visfatin的水平,分析其表达水平与各血生化指标的相关性。结果NAFLD组的BMI、腰围、臀围和腰臀比(WHR)显著高于对照组(P<0.05);NAFLD组血清TG、HDL-c、LDL-c、HbAIC、UA水平显著高于对照组(P<0.05);NAFLD组血清APN、Visfatin的浓度均显著低于对照组(P<0.05)。NAFLD患者血清APN水平与其BMI、WHR、TG、HDL-C、LDL-C、HBAIC、UA水平呈明显负相关,r值分别为-0.231、-0.203、-0.218、-0.249、-0.210、-0.242、-0.235,P均<0.01;NAFLD患者血清Visfatin水平与其BMI、WHR、TG、HBAIC、UA呈明显正相关,r值分别为0.212、0.175、0.186、0.198、0.161,P均<0.05,与HDL-C、LDL-C、APN水平呈明显负相关,r值分别为-0.180、-0.156、-0.200,P值均<0.05。结论NAFLD患者血清APN、Visfatin水平较正常健康人群降低,APN、Visfatin可能参与了NAFLD的发生发展,可作为NAFLD患者诊断和预警的潜在检测指标。
