IGF1和IGFBP3在非酒精性脂肪性肝病病程中的表达变化

肝脏 ›› 2019, Vol. 24 ›› Issue (5): 521-525.

IGF1和IGFBP3在非酒精性脂肪性肝病病程中的表达变化

邹琳, 李铁岩, 佘会元

200135 上海宁夏医科大学公利医院培养基地(邹琳);同济大学附属东方医院心脏外科(李铁岩);上海市浦东新区公利医院感染科(佘会元)

收稿日期:2018-09-22 发布日期:2020-04-10
通讯作者: 佘会元,Email:shehuiy@sina.com
作者简介:李铁岩
基金资助:
上海市浦东新区公利医院青年英才基金(GLRq2017-02);上海市浦东新区公利医院青年基金(2017YQNJJ-07);同济大学青年优秀人才培养行动计划(2016KJ063)

Received:2018-09-22 Published:2020-04-10

摘要/Abstract

摘要： 目的比较IGF1、IGFBP3血清水平在单纯性脂肪肝(NAFL)和脂肪性肝炎(NASH)中的表达差异,探讨血清IGF1、IGFBP3水平与非酒精性脂肪性肝病(NAFLD)的疾病进展及与相关代谢参数的关联性。方法选取符合NAFLD诊断标准的患者80例,其中NASH患者50例,30例年龄、性别匹配的NAFL患者,采用酶联免疫分析法(ELISA)测定两组患者血清胰岛素样生长因子1(IGF1)、胰岛素样生长因子结合蛋白3(IGFBP3)表达水平以及相关代谢参数。结果与NAFL组相比,NASH组患者有更高的体质指数(BMI)、腰围、肝酶指标(ALT、AST、γ-GGT)、胰岛素(Insulin)水平、胰岛素抵抗水平(HOMA-IR)、游离脂肪酸水平(FFA),IGF1水平明显下调(149.89+114.94)对(100.78+51.97),(P=0.034);IGFBP3明显上调(10.52+6.44)对(16.66+11.6),(P=0.003)。结论 IGF1、IGFBP3可能与NAFLD疾病进展密切相关。

关键词: 非酒精性脂肪肝病, 单纯性脂肪肝, 脂肪性肝炎, 胰岛素样生长因子1, 胰岛素样生长因子结合蛋白3

邹琳, 李铁岩, 佘会元. IGF1和IGFBP3在非酒精性脂肪性肝病病程中的表达变化[J]. 肝脏, 2019, 24(5): 521-525.

参考文献

[1] Targher G. Non-alcoholic fatty liver disease as driving force in coronary heart disease? Gut, 2017, 66:213.
[2] Ye P, Qu CF, Hu XL. Impact of IGF-1, IGF-1R, and IGFBP-3 promoter methylation on the risk and prognosis of esophageal carcinoma. Tumor Biol, 2016, 37:6893-6904.
[3] Wang J, Li YC, Deng M, et al. Serum insulin-like growth factor 1 and its binding protein 3 as prognostic factors for the incidence, progression, and outcome of hepatocellular carcinoma: a systematic review and meta-analysis. Oncotarget, 2017,8:81098-81108.
[4] Liang S, Cheng X, Hu Y, et al. Insulin-like growth factor 1 and metabolic parameters are with nonalcoholic fatty liver disease in obese children and adolescents. ActaPaediatrica, 2017, 106:298-303.
[5] Völzke H, Nauck M, Rettig R, et al. Association between hepatic steatosis and serum IGF1 and IGFBP-3 levels in a population-based sample. European Journal of Endocrinology, 2009, 161:705-713.
[6] Diehl AM, Day C. Cause, pathogenesis, and treatment of nonalcoholic steatohepatitis. N Engl J Med, 2017, 377:2063-2072.
[7] Yan XD, Yao M, Wang L, et al. Overexpression of insulin-like growth factor-1 receptor as a pertinent biomarker for hepa-tocytes malignant transformation. World J Gastroenterol, 2013, 19:6084-6092.
[8] Svegliatibaroni G, Ridolfi F, Di SA, et al. Insulin and insulin-like growth factor-1 stimulate proliferation and type I collagen accumulation by human hepatic stellate cells: differential effects on signal transduction pathways. Hepatology, 1999, 29:1743-1751.
[9] Takahashi Y, Iida K, Takahashi K, et al. Growth hormone reverses nonalcoholic steatohepatitis in a patient with adult growth hormone deficiency. Gastroenterology, 2007, 132:938-943.
[10] Liu Z, Cordoba-Chacon J, Kineman RD, et al. Growth hormone control of hepatic lipid metabolism. Diabetes, 2016, 65:3598-3609.
[11] Borrelli A, Bonelli P, Tuccillo FM, et al. Role of gut micro-biota and oxidative stress in the progression of non-alcoholic fatty liver disease to hepatocarcinoma: Current and innovative therapeutic approaches. Redox Biol, 2018, 15:467-479.
[12] Puche JE, García-Fernández M, Muntané J, et al. Low doses of insulin-like growth factor-I induce mitochondrial protection in aging rats. Endocrinology, 2008, 149:2620-2627.