黃文森,鄧少雄,吳晴翼,李金塔,李靖云,康錦芬,黃思婧,陳 韻

(1泉州醫(yī)學(xué)高等專科學(xué)校內(nèi)科學(xué)教研室,泉州 362000;2福建醫(yī)科大學(xué)附屬泉州第一醫(yī)院內(nèi)分泌科;*通訊作者,E-mail:drdengsx@126.com)

ApoB/ApoA1比值及non-HDL-C與2型糖尿病合并非酒精性脂肪肝病的相關(guān)性

黃文森1,2,鄧少雄1*,吳晴翼1,李金塔1,李靖云1,康錦芬1,黃思婧1,陳 韻1,2

(1泉州醫(yī)學(xué)高等專科學(xué)校內(nèi)科學(xué)教研室,泉州 362000;2福建醫(yī)科大學(xué)附屬泉州第一醫(yī)院內(nèi)分泌科;*通訊作者,E-mail:drdengsx@126.com)

目的 探討2型糖尿病患者載脂蛋白B(ApoB)和載脂蛋白A1(ApoA1)的比值、非高密度脂蛋白膽固醇(non-HDL-C)與非酒精性脂肪肝病(NAFLD)的關(guān)系。 方法 208例2型糖尿病患者按有無合并非酒精性脂肪肝病分為未合并非酒精性脂肪肝病組(non-NAFLD組)和合并非酒精性脂肪肝病組(NAFLD組),所有患者均檢測空腹血糖、空腹胰島素、血脂、糖化血紅蛋白等指標(biāo),同時記錄糖尿病病程、身高、體質(zhì)量、腰圍等臨床一般資料,計算ApoB/ApoA1比值及non-HDL-C,比較兩組之間的指標(biāo)差異并進(jìn)行Logistic回歸分析及ROC曲線分析。 結(jié)果 NAFLD組的ApoB/ApoA1比值、non-HDL-C、甘油三酯、總膽固醇、低密度脂蛋白膽固醇、空腹血糖、糖化血紅蛋白、體質(zhì)量指數(shù)、腰圍均高于non-NAFLD組,差異有統(tǒng)計學(xué)意義(P<0.05)。Logistic回歸分析結(jié)果顯示，ApoB/ApoA1比值及non-HDL-C均為影響2型糖尿病患者發(fā)生非酒精性脂肪肝病的獨立危險因素。ROC曲線分析結(jié)果顯示，ApoB/ApoA1比值及non-HDL-C預(yù)測合并NAFLD的曲線下面積分別為0.795，0.709(P<0.05);進(jìn)一步比較兩者曲線下面積,行Z檢驗結(jié)果顯示兩者間差異無統(tǒng)計學(xué)意義(P>0.05)。 結(jié)論 ApoB/ApoA1比值、non-HDL-C均為影響2型糖尿病患者發(fā)生非酒精性脂肪肝病的獨立危險因素,兩者對2型糖尿病合并非酒精性脂肪肝病均具有良好的預(yù)測價值。

載脂蛋白B; 載脂蛋白A1; 非高密度脂蛋白膽固醇; 2型糖尿病; 非酒精性脂肪肝病

肝硬化、肝癌等肝臟相關(guān)疾病已經(jīng)發(fā)展成為影響2型糖尿病(type 2 diabetes mellitus,T2DM)患者生存的主要因素之一,而作為代謝綜合征肝臟表現(xiàn)的非酒精性脂肪肝病(non-alcoholic fatty liver disease,NAFLD)也已成為全世界最常見的慢性肝臟疾病,國外研究報道大約25%的成年人患有NAFLD,T2DM患者NAFLD的患病率更是高達(dá)75%,其與肥胖、胰島素抵抗密切相關(guān)[1,2]。載脂蛋白B(apolipoprotein B,ApoB)和載脂蛋白A1(apolipoprotein A1,ApoA1)的比值與非高密度脂蛋白膽固醇(non-high density lipoprotein cholesterol, non-HDL-C)升高均為T2DM患者常見的脂代謝紊亂表現(xiàn),與胰島素抵抗亦密切相關(guān)。Nomikos等[3]通過一項長達(dá)10年的研究發(fā)現(xiàn)ApoB/ApoA1比值和non-HDL-C優(yōu)于低密度脂蛋白膽固醇等其他脂代謝指標(biāo),為預(yù)測心血管疾病風(fēng)險的最佳指標(biāo),但目前關(guān)于ApoB/ApoA1比值及non-HDL-C與T2DM患者合并NAFLD關(guān)系的研究國內(nèi)外尚缺乏。本文旨在通過探討ApoB/ApoA1比值及non-HDL-C與T2DM患者合并NAFLD的相關(guān)性,從而為T2DM患者合并NAFLD的早期預(yù)測和干預(yù)提供一種可能的方法與途徑。

1 資料與方法

1.1 研究對象

選擇208例(男性119例,女性89例)于2014-06～2015-08在福建醫(yī)科大學(xué)附屬泉州第一醫(yī)院(泉州醫(yī)學(xué)高等?？茖W(xué)校教學(xué)醫(yī)院)內(nèi)分泌科就診住院的T2DM患者,所有患者均符合WHO制定的糖尿病的診斷及分型標(biāo)準(zhǔn)[4],其中合并NAFLD(NAFLD組)128例,未合并NAFLD(non-NAFLD組)80例。NAFLD由專門的超聲科主治醫(yī)師根據(jù)中華醫(yī)學(xué)會肝臟病學(xué)分會2010年修訂的非酒精性脂肪肝病診療指南[5]進(jìn)行影像學(xué)診斷。入選者排除標(biāo)準(zhǔn):①合并嚴(yán)重的糖尿病急慢性并發(fā)癥;②妊娠或哺乳期婦女;③酒精性肝病、病毒性肝病、自身免疫性肝病、藥物性肝病、遺傳性肝病;④近2月曾口服他汀類、貝特類等調(diào)脂藥物。

1.2 方法

1.2.1 人體基本指標(biāo)測量 由專門的內(nèi)分泌科護師完成所有入選患者的身高(H)、體質(zhì)量(W)和腰圍(WC)的測量;采用標(biāo)準(zhǔn)汞柱式血壓計測量右上肢肱動脈血壓,記錄收縮壓(SBP)和舒張壓(DBP)數(shù)值,血壓測量前30 min內(nèi)患者禁止飲咖啡濃茶和吸煙,并囑患者排空膀胱、安靜休息15 min。

1.2.2 生化指標(biāo)檢測 所有患者采血前1 d均應(yīng)忌高脂食物和忌酒,禁食10-12 h后于第2天清晨空腹采靜脈血5 ml,1 000×g離心20 min,取其上清由全自動生化儀酶法檢測甘油三酯(TG)、總膽固醇(TC)、高密度脂蛋白膽固醇(HDL-C)、低密度脂蛋白膽固醇(LDL-C)、載脂蛋白A1(ApoA1)、載脂蛋白B(ApoB)、空腹血糖(FPG)并采用化學(xué)發(fā)光法檢測空腹胰島素(FINS)及高壓液相色譜法測定糖化血紅蛋白(HbA1c)。

1.2.3 指標(biāo)計算 體質(zhì)量指數(shù)(BMI)=體質(zhì)量(kg)/身高2(m2);穩(wěn)態(tài)模型評估胰島素抵抗指數(shù)(HOMA-IR)=FPG×FINS/22.5;利用Frost公式non-HDL-C=TC-(HDL-C)計算non-HDL-C含量,計算ApoA1/ApoB比值。

1.3 統(tǒng)計學(xué)處理

2 結(jié)果

2.1 NAFLD組與non-NAFLD組一般資料比較

NAFLD組的BMI、腰圍高于non-NAFLD組,差異有統(tǒng)計學(xué)意義(P<0.05);而兩組間的性別、年齡、糖尿病病程、SBP、DBP差異無統(tǒng)計學(xué)意義(見表1)。

表1 NAFLD組與non-NAFLD組的一般資料比較

Table 1 Comparison of general information between NAFLD group and non-NAFLD group

組別n男/女年齡(歲)糖尿病病程(年)SBP(mmHg)DBP(mmHg)BMI(kg/m2)腰圍(cm)NAFLD組12877/5154.80±12.066.95±3.46130.39±16.7082.20±11.4525.52±3.0093.68±8.17non-NAFLD組8042/3853.88±12.266.29±3.02127.93±18.4879.31±10.3722.98±2.6786.03±8.47 t/χ21.1790.5321.4040.9941.8366.1886.482 P0.2780.5950.1620.3210.0680.0000.000

2.2 NAFLD組與non-NAFLD組的生化指標(biāo)比較

NAFLD組TG、TC、LDL-C、non-HDL-C、ApoB、ApoB/ApoA1、FPG、HOMA-IR及HbA1c均高于non-NAFLD組,而HDL-C、ApoA1低于non-NAFLD組,且差異有統(tǒng)計學(xué)意義(P<0.05,見表2)。

表2 NAFLD組與non-NAFLD組的生化指標(biāo)比較

Table 2 Comparison of biochemical indicators between NAFLD group and non-NAFLD group

組別nTG(mmol/L)TC(mmol/L)LDL-C(mmol/L)HDL-C(mmol/L)non-HDL-C(mmol/L)NAFLD組1282.06±1.105.55±1.263.56±1.131.08±0.334.48±1.23non-NAFLD組801.27±0.905.00±1.353.13±1.141.33±0.403.67±1.25 t5.0322.9772.642-4.8934.558 P0.0000.0030.0090.0000.000組別nApoB(g/L)ApoA1(g/L)ApoB/ApoA1FPG(mmol/L)HOMA-IRHbA1c(%)NAFLD組1281.11±0.291.18±0.270.97±0.249.98±4.105.72±3.4710.09±2.19non-NAFLD組800.90±0.261.37±0.320.69±0.208.55±3.883.75±3.129.04±2.56 t5.278-4.5948.7122.4984.1383.150 P0.0000.0000.0000.0130.0000.002

2.3 T2DM患者合并NAFLD的影響因素Logistic回歸分析

以是否合并NAFLD為因變量,進(jìn)行二分類非條件Logistic回歸分析結(jié)果顯示ApoB/ApoA1、non-HDL-C、BMI、WC作為T2DM患者發(fā)生NAFLD的獨立危險因素。T2DM合并NAFLD的影響因素Logistic回歸分析見表3。

表3 T2DM合并NAFLD的影響因素Logistic回歸分析

Table 3 Logistic regression analysis of influencing factors of NAFLD in T2DM patients

因素βSEWalsPOR95%CI BMI0.1750.0873.9990.0461.1911.003-1.414 WC0.0670.0285.5070.0191.0691.011-1.130 ApoB/ApoA14.3821.02818.1650.00080.02610.666-600.427 non-HDL-C0.9420.4424.5500.0332.5661.079-6.100 常數(shù)-13.6652.53729.0120.0000.000

β:偏回歸系數(shù)值;SE:標(biāo)準(zhǔn)誤;Wals:Wald卡方值;OR:比值比;95% CI:95%可信區(qū)間

2.4 T2DM患者ApoB/ApoA1與non-HDL-C對合并NAFLD的預(yù)測價值

以影響T2DM患者發(fā)生NAFLD的獨立危險因素ApoB/ApoA1、non-HDL-C進(jìn)行ROC曲線分析,結(jié)果顯示ApoB/ApoA1、non-HDL-C預(yù)測合并NAFLD的曲線下面積分別為0.795，0.709(P<0.05，見表4，圖1),兩者均大于0.7提示對合并NAFLD具有良好的預(yù)測價值。而進(jìn)一步對ApoB/ApoA1、non-HDL-C預(yù)測T2DM患者合并NAFLD的曲線下面積進(jìn)行比較,行Z檢驗結(jié)果顯示兩者間差異無統(tǒng)計學(xué)意義(Z=1.753,P=0.079)。

表4 ApoB/ApoA1與non-HDL-C對預(yù)測合并NAFLD的ROC曲線分析結(jié)果

Table 4 The ROC curve analysis results of ApoB/ApoA1 ratio and level of non-HDL-C for predicting NAFLD

指標(biāo)AUCSEP95%CIApoB/ApoA10.7950.0310.0000.734-0.856non-HDL-C0.7090.0380.0000.634-0.784

AUC:ROC曲線下面積;SE:標(biāo)準(zhǔn)誤

圖1 T2DM患者ApoB/ApoA1與non-HDL-C預(yù)測合并NAFLD的ROC曲線Figure 1 The ROC curves of ApoB/ApoA1 ratio and level of non-HDL-C for predicting NAFLD in T2DM patients

3 討論

NAFLD為脂質(zhì)在肝臟的過度沉積所致,疾病譜包括單純性脂肪肝、非酒精性脂肪性肝炎及肝硬化,嚴(yán)重者可進(jìn)一步演變?yōu)楦伟┗蚋嗡ソ?胰島素抵抗、氧化應(yīng)激及代謝性炎癥反應(yīng)參與NAFLD的發(fā)生與進(jìn)展。NAFLD僅次于丙型肝炎已成為美國成年人等待肝臟移植的第二大病因[6],此外國內(nèi)學(xué)者研究發(fā)現(xiàn)NAFLD可顯著增加T2DM患者發(fā)生心血管疾病的風(fēng)險性[7],Targher等[8]學(xué)者的研究亦發(fā)現(xiàn)NAFLD與T2DM患者的持續(xù)性心房顫動的患病率增加密切相關(guān)。NAFLD不僅僅作為T2DM患者代謝紊亂的標(biāo)志物,而且積極參與患者內(nèi)皮功能障礙、動脈粥樣化形成和血栓形成傾向[9]。

本研究通過對208例T2DM患者的研究表明NAFLD組的BMI、腰圍、HOMA-IR明顯高于non-NAFLD組,且BMI、腰圍均為T2DM患者合并NAFLD的獨立危險因素,說明合并NAFLD的T2DM患者胰島素抵抗更明顯,肥胖尤其是腹型肥胖的T2DM患者更容易發(fā)生NAFLD,這與既往的研究結(jié)果相似[10]。

除了胰島素抵抗,脂代謝紊亂也在T2DM患者合并NAFLD發(fā)生發(fā)展過程中起著重要的作用。國外研究表明富含脂肪和膽固醇的膳食是驅(qū)動脂代謝紊亂和NAFLD發(fā)生發(fā)展的主要因素[11],脂代謝紊亂又可導(dǎo)致T2DM患者大量脂質(zhì)在肝臟沉積,進(jìn)一步加劇脂質(zhì)對胰島素的抵抗?fàn)顟B(tài)從而形成惡性循環(huán)[12],而減少NAFLD患者的脂代謝紊亂則可明顯改善肝臟組織學(xué)變化[13]。本研究結(jié)果同樣顯示NAFLD組的T2DM患者相較于non-NAFLD組更易出現(xiàn)脂代謝紊亂,表現(xiàn)為TG、TC、LDL-C、non-HDL-C、ApoB、ApoB/ApoA1升高,而HDL-C、ApoA1降低;Logistic回歸分析進(jìn)一步顯示ApoB/ApoA1、non-HDL-C為T2DM患者發(fā)生NAFLD的獨立危險因素。

ApoB是與non-HDL-C相關(guān)的載脂蛋白,向肝臟外轉(zhuǎn)運膽固醇,可刺激動脈平滑肌增殖具有很強的致動脈粥樣硬化的作用;而ApoA1則是與HDL-C相關(guān)的載脂蛋白,參與向肝臟內(nèi)逆向轉(zhuǎn)運膽固醇,具有清除膽固醇、抗動脈粥樣硬化及防止脂質(zhì)沉積的功能;因此ApoB/ApoA1比值反映肝臟膽固醇轉(zhuǎn)運的平衡[14]。non-HDL-C包括LDL-C、極低密度脂蛋白膽固醇、中間密度脂蛋白膽固醇、乳糜微粒殘粒及脂蛋白a等,均為含ApoB的脂蛋白,較LDL-C更好地反映小而致密LDL-C(sLDL-C)的數(shù)量,而NAFLD與增加的sLDL-C呈獨立相關(guān)[15,16]。ApoB/ApoA1比例的升高意味著Non-HDL-C水平升高和/或HDL-C水平下降,ApoB/ApoA1和non-HDL-C較其他脂質(zhì)指標(biāo)均能從整體上更全面地反映致動脈粥樣硬化脂代謝的紊亂。國內(nèi)學(xué)者研究表明ApoB/ApoA1與NAFLD的患病風(fēng)險增加存在獨立正相關(guān)性[17];而Zelber-Sagi等[18]學(xué)者的研究亦表明non-HDL-C較TG、TC、LDL-C等其他脂質(zhì)指標(biāo)對NAFLD具有更強的預(yù)測能力。在T2DM合并NAFLD患者中,肝臟中LDL-C、極低密度脂蛋白膽固醇等non-HDL-C的含量增加,雖ApoB生成增多但仍處于相對不足,繼而出現(xiàn)non-HDL-C向體內(nèi)肝外組織輸出不足,導(dǎo)致脂質(zhì)在肝細(xì)胞內(nèi)的積累;同時過量的肝細(xì)胞內(nèi)膽固醇會激活肝臟X受體調(diào)節(jié)膽固醇體內(nèi)平衡但也會誘導(dǎo)肝脂肪變性并促進(jìn)肝臟極低密度脂蛋白膽固醇顆粒的分泌,進(jìn)一步損害肝細(xì)胞和促進(jìn)NAFLD的發(fā)生和發(fā)展[19]。而ApoA1缺乏的小鼠也對飲食誘導(dǎo)的肥胖敏感,易出現(xiàn)肝脂質(zhì)沉積導(dǎo)致NAFLD[20]。本研究應(yīng)用ROC曲線分析,結(jié)果顯示ApoB/ApoA1、non-HDL-C預(yù)測T2DM患者合并NAFLD的曲線下面積分別為0.795，0.709,對合并NAFLD具有良好的預(yù)測價值,且兩者之間差異無統(tǒng)計學(xué)意義。

綜上所述,ApoB/ApoA1、non-HDL-C均為影響T2DM患者發(fā)生NAFLD的獨立危險因素,兩者對T2DM患者合并NAFLD均具有良好的預(yù)測價值,對及時發(fā)現(xiàn)和干預(yù)合并NAFLD具有重要臨床意義,但ApoB/ApoA1、non-HDL-C通過哪些具體機制影響T2DM患者發(fā)生NAFLD尚有待進(jìn)一步的深入研究。

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Correlation of ApoB/ApoA1 ratio and non-high density lipoprotein cholesterol with non-alcoholic fatty liver disease in type 2 diabetes mellitus patients

HUANG Wensen1,2,DENG Shaoxiong1*,WU Qingyi1,LI Jinta1,LI Jingyun1,KANG Jinfen1,HUANG Sijing1,CHEN Yun1,2

(1DepartmentofInternalMedicine,QuanzhouMedicalCollege,Quanzhou362000,China;2DepartmentofEndocrinology,FirstHospitalofQuanzhouAffiliatedtoFujianMedicalUniversity;*Correspondingauthor,E-mail:drdengsx@126.com)

ObjectiveTo investigate the relationship between the ratio of apolipoprotein B to apolipoprotein A1(ApoB/ApoA1 ratio), non-high density lipoprotein cholesterol(non-HDL-C) and non-alcoholic fatty liver disease(NAFLD) in type 2 diabetes mellitus(T2DM) patients.MethodsTotally 208 T2DM patients were classified as non-NAFLD group and NAFLD group. Fasting blood glucose, fasting insulin, blood lipid and glycosylated hemoglobin of all the patients were measured. Diabetes duration, height, and waist circumference were recorded. The ApoB/ApoA1 ratio and non-HDL-C were calculated. The indexes between the two groups were compared and analyzed by Logistic regression analysis and ROC curve analysis.ResultsThe ApoB/ApoA1 ratio, non-HDL-C, triglyceride, total cholesterol, low density lipoprotein, fasting blood glucose, glycosylated hemoglobin, body mass index and waist circumference were significantly higher in NAFLD group than in non-NAFLD group(P<0.05). Logistic regression analysis showed that the ApoB/ApoA1 ratio and the level of non-HDL-C were independent risk factors of NAFLD in T2DM patients. The areas under the ROC curve of ApoB/ApoA1 ratio and level of non-HDL-C to predict NAFLD were 0.795 and 0.709,respectively(P<0.05). Further comparison of the areas under the ROC curve using theZtest showed no statistically significant difference between ApoB/ApoA1 ratio and the level of non-HDL-C(P>0.05).ConclusionThe ApoB/ApoA1 ratio and the level of non-HDL-C are the independent risk factors, and may be better markers for predicting NAFLD in T2DM patients.

apolipoprotein B; apolipoprotein A1; non-high density lipoprotein cholesterol; type 2 diabetes mellitus; non-alcoholic fatty liver disease

福建省中青年教師教育科研項目科技A類資助項目(JA13396)

黃文森,男,1981-02生,碩士,副教授,E-mail:vinson170@163.com

2017-04-21

R587.2

A

1007-6611(2017)08-0778-05

10.13753/j.issn.1007-6611.2017.08.005