瘦素抵抗与男性非酒精性脂肪肝的关系

卢震亚; 王群燕; 饶伟强; 蔡卫民

瘦素抵抗与男性非酒精性脂肪肝的关系

详细信息

中图分类号: R575.5
计量
- 文章访问数: 1952
- HTML全文浏览量: 14
- PDF下载量: 835
- 被引次数: 0
出版历程
- 出版日期: 2006-01-20

Relationship between leptin resistance and nonalcoholic fatty liver in male patients.

摘要

摘要: 研究瘦素抵抗和男性非酒精性脂肪肝（nonalcoholic fatty liver,NAFL）的关系。我们用放射免疫法检测52例NAFL患者和45例正常对照者血清中的瘦素水平,分析血清瘦素与男性NAFL患者以及与HOMA-IR（以HOMA模型计算胰岛素抵抗指数）、总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）和低密度脂蛋白胆固醇（LDL-C）等指标的关系。NAFL患者血清中的瘦素水平（6.75±1.32μg/ml）显著高于正常对照组（3.21±0.95μg/ml）,P<0.01,且肥胖的NAFL患者血清中的瘦素水平（7.95±0.85ng/ml）显著高于非肥胖NAFL患者的瘦素水平（6.11±1.21μg/ml）,P<0.01。NAFL患者血清中的FINS、HOMA-IR和TG水平均高于正常对照组,且NAFL患者血清瘦素水平与HOMA-IR呈负相关（r=0.521,P<0.05）,与BMI呈正相关（r=0.718,P<0.00）,与TG呈正相关（r=0.425,P<0.01）。男性NAFL患者存在着明显的瘦素抵抗,提示瘦素抵抗在NAF...
- 非酒精性脂肪肝 /
- 瘦素
Abstract: To study the relationship between leptin resistance and nonalcoholic fatty liver (NAFL) in male patients.52 male patients with NAFL diagnosed by ultrasonographic examination and 45 healthy adults enrolled in study.Serum leptin was determined by radioimmunoassay.Fasting insulin (FINS) , fasting glucose (FPG) , TG, TC, HDL-C and LDL-C were also detected.The correlation between leptin and other parameter were analysised.Leptin levels in NAFL patients was found significantly higher than that in control group (6.75±1.32ng/ml vs 3.21±0.95ng/ml, P<0.01) .Leptin levels in obese patients was significantly higher than that in non-obese patients (7.95±0.85ng/ml VS 6.11±1.21ng/ml P<0.01) .HOMA-IR and Tg were also higher in the NAFL group than the control group.Logistic regression analysis revealed that in NAFL patients leptin concentration was negative correlation to HOMA-IR (r=-0.521, P<0.05) and positive correlation to BMI TG (r=0.781, P<0.01and r=0.425, P<0.05) , but there were no relation with Tc, HDL-C and LDH-C.Conclusion the serum leptin levels were significantly higher in patients with NAFL.It is evidence that patients with leptin resistance.Leptin resistance is avery important contributor to the pathogenesis of NAFL.
- fatty liver /
- leptin

HTML全文

参考文献(13)

[1]Marchesini G, Brizi M, Bianchi G, et al.Metformin in non-alcoholicsteatohepatitis[J].Lancet, 2001, 358 (9285) ∶893-894.

[2]Uygun A, Kadayifci A, Yesilova Z, et al.Serum leptin levels in patientswith nonalcoholic steatohepatitis[J].Am J Gastroenterol, 2000, 95 (12) ∶3584-3589.

[3]Bloks VW, Plosch T, Van-Goor H, et al.Hyperlipidemia andatherosclerosis associated with liver disease in ferrochelatase-deficientmice[J].J Lipid Res, 2001, 42 (1) ∶41-50.

[4]Santos Alvarez J, Goberna R, Sanchez-Margalet V.Human Leptinstimulates proliferation and activation of human circulating monocytes[J].Cell Immunol, 1999, 194 (1) ∶6-11.

[5]Tobe K, Ogura T, Tsukamoto C, et al.Relationship between serum leptinand fatty liver in Japanese male adolescent university students[J].Am JGastroenterol, 1999, 94 (11) ∶3328-3335.

[6]朱惠娟, 史铁蘩, 胡明明, 等.减重治疗逆转超重及肥胖症患者脂肪肝的作用[J].中华内科杂志, 2003, 42 (2) ∶98-102.

[7]Zhang Y, Proenca R, Maffei M, et al.Positional cloning of the mouseobese gene and its human homologue[J].Nature, 1994, 372 (6505) ∶425-432.

[8]Bartek J, Bartos J, Galuska J, et al.Expression of ob gene coding theproduction of the hormone leptin in hepatocytes of liver with steatosis[J].Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub, 2001, 145 (1) ∶15-20.

[9]Lewandowski K, Horn R, Ocallaghan CJ, et al.Free leptin, bound lep-tin, and soluble leptin receptor in normal and diabetic pregnancies[J].JClin Endocrinol Metab, 1999, 84 (1) ∶300-306.

[10] Koteish A, Dieh1 AM.Animal models of steatosis[J].Semin LiverDis, 2001, 21 (1) ∶89-104.

[11]Giannini E, Botta F, Cataldi A, et al.Leptin levels in nonalcoholicsteatohepatitis and chronic hepatitis C[J].Hepatogastroenterology, 1999, 46 (28) ∶2422-2425.

[12]Giannini E, Botta F, Cataldi A, et al.Leptin levels in nonalcoholicsteatohepatitis and chronic C[J].Hepatogastroenterology, 1999, 46 (28) ∶2422-2425.

[13]Chehab FF, Lim ME, Lu R.Correction of the sterility defect in ho-mozygous obese female mice by treatment with the human recombinantleptin[J].Nat Genet, 1996, 12 (3) ∶318-320.

施引文献

资源附件(0)

访问统计