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脂肪组织瘦素基因与非酒精性脂肪肝的研究
引用本文:杨辉,李瑜元,聂玉强,洪勇,江庆澜,沙卫红.脂肪组织瘦素基因与非酒精性脂肪肝的研究[J].中华肝脏病杂志,2006,14(11):828-831.
作者姓名:杨辉  李瑜元  聂玉强  洪勇  江庆澜  沙卫红
作者单位:1. 510180,广州医学院附属市一人民医院消化内科
2. 510180,广州医学院附属市一人民医院普外科
基金项目:广州市卫生机构重点科研基金(20042001)
摘    要:目的探讨非酒精性脂肪肝(NAFLD)患者脂肪组织瘦素mRNA基因表达水平和胰岛素抵抗与血浆瘦素等的相关性。方法行熳性胆囊炎、胃溃疡、腹股沟疝等择期手术的NAFLD患者21例、对照组患者24例,于术中取少许腹部皮下和网膜脂肪组织送检。应用SYBR Green I实时定量逆转录聚台酶链反应法检测瘦素mRNA的表达水平,用稳态模型法计算胰岛素抵抗指数,用酶联免疫吸附法测定血浆瘦素和胰岛素水平。结果NAFLD和对照组瘦素基因表达值分别为1.32±0.12、0.99±0.05,1.10±0.09、0.87±0.13;瘦素基因表达和胰岛素抵抗指数与血浆瘦素浓度直接关联(r值分别为0.72、0.69,P值均<0.05)。结论脂肪组织瘦素基因高表达是高瘦素血症的主要原因,肥胖和非肥胖的NAFLD患者存在瘦素抵抗和胰岛素抵抗,提示瘦素抵抗与胰岛素抵抗一样和NAFLD发病密切相关。

关 键 词:瘦素  脂肪肝  非酒精性  基因表达  瘦素抵抗
收稿时间:2006-04-12
修稿时间:2006年4月12日

Relationship between leptin gene of adipose tissues and nonalcoholic fatty liver disease
YANG Hui,LI Yu-yuan,NIE Yu-qiang,HONG Yong,JIANG Qing-lan,SHA Wei-hong.Relationship between leptin gene of adipose tissues and nonalcoholic fatty liver disease[J].Chinese Journal of Hepatology,2006,14(11):828-831.
Authors:YANG Hui  LI Yu-yuan  NIE Yu-qiang  HONG Yong  JIANG Qing-lan  SHA Wei-hong
Institution:Department of Gastroenterology, First People's Municipal Hospital, Guangzhou Medical College, Guangzhou 510180, China.
Abstract:OBJECTIVE: To investigate leptin mRNA expressions in subcutaneous (SC) and omental (OM) adipose tissues of patients with nonalcoholic fatty liver disease (NAFLD), and their relationships with insulin resistance (IR), blood leptin, blood triglyceride, total blood cholesterol, blood glucose, body weight index and waist-hip ratio. METHODS: SC and OM adipose tissues were obtained from 10 obese and 11 nonobese NAFLD patients and from 11 obese and 13 nonobese patients without NAFLD, who served as controls. Leptin mRNA expression levels in the subcutaneous and omental adipose tissues were measured using SYBR Green I quantitative real-time PCR. IR was estimated using homeostasis assessment (HOMA). The levels of plasma leptin and insulin were measured using ELISA. RESULTS: The relative mRNA expression of leptin, HOMA-IR and blood leptin levels in NAFLD differed significantly from those of the controls (P < 0.05). The leptin/GAPDH ratio of the obese and nonobese NAFLD and control cases were 1.32 +/- 0.12, 0.99 +/- 0.05, 1.10 +/- 0.09, 0.87 +/- 0.13 respectively. The expression levels of SC and OM adipose leptin mRNA in NAFLD patients were positively correlated with HOMA-IR (r=0.72, P < 0.05), blood leptin (r=0.69, P < 0.05), blood triglyceride (r=0.32, P < 0.05), body weight index (r=0.57, P < 0.05) and waist-hip ratio (r=0.50, P <0.05). CONCLUSION: The primary reason for high levels of blood leptin is high leptin mRNA expression in adipose tissues; in both obese and nonobese patients with NAFLD; high levels of blood leptin and the leptin mRNA expression in adipose tissues and IR exist. These findings suggest that leptin resistance exists in patients with NAFLD and leptin resistance is positively correlated with NAFLD, the same as in insulin resistance.
Keywords:Leptin  Fatty liver disease  nonalcoholic  Gene expression  Leptin resistance
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