宋 穎,李啟富,田 波,鐘 立,楊淑敏,夏 偉,畢小云
(重慶醫(yī)科大學(xué)附屬第一醫(yī)院1.內(nèi)分泌科;2.檢驗(yàn)科 400016)
多囊卵巢綜合征患者血清游離脂肪酸水平測定及其相關(guān)因素分析
宋 穎1,李啟富1,田 波1,鐘 立1,楊淑敏1,夏 偉1,畢小云2△
(重慶醫(yī)科大學(xué)附屬第一醫(yī)院1.內(nèi)分泌科;2.檢驗(yàn)科 400016)
目的分析多囊卵巢綜合征(PCOS)患者血清游離脂肪酸(FFAs)水平的變化,并探討其相關(guān)因素?方法 納入133例PCOS患者及116例年齡匹配的健康女性,測量身高?體質(zhì)量?腰圍;行75g無水葡萄糖耐量試驗(yàn),并測空腹血清血脂?空腹胰島素(FINS)?血清FFAs?總睪酮,計(jì)算胰島素抵抗指數(shù)(HOMA-IR);對(duì)101例PCOS患者及20例正常人行高胰島素-正葡萄糖鉗夾術(shù)?結(jié)果PCOS患者血清FFAs水平明顯高于對(duì)照組(P0.01);亞組分析顯示,與兩個(gè)體質(zhì)量匹配的對(duì)照組相比,PCOS患者的FFAs水平也明顯增高(P0.01)?相關(guān)分析顯示,FFAs水平與體質(zhì)量指數(shù)(BMI)?腰圍?總膽固醇(TC)?低密度脂蛋白膽固醇(LDL-c)?總睪酮(r分別為0.20?0.18?0.19?0.18?0.18,P0.05)呈正相關(guān);與高密度脂蛋白膽固醇(HDL-c)?穩(wěn)態(tài)期120~180min葡萄糖代謝率(M120-180)(r分別為-0.17?-0.22,P0.05)呈負(fù)相關(guān)?結(jié)論與年齡匹配的健康婦女相比,PCOS患者血清FFAs水平顯著升高,且與BMI?腰圍?TC?LDL-c?總睪酮水平呈正相關(guān),與 HDL-c?M120-180呈負(fù)相關(guān)?
多囊卵巢綜合征;游離脂肪酸;胰島素抵抗
多囊卵巢綜合征(polycystic ovary syndrome,PCOS)是一種育齡期婦女常見的生殖內(nèi)分泌紊亂疾病,PCOS患者肥胖?糖脂代謝異常的發(fā)生率均較正常人顯著增高?目前,已證實(shí)2型糖尿病和肥胖患者體內(nèi)常有血清游離脂肪酸(free fatty acids,FFAs)水平的增高,并且FFAs與胰島素抵抗(insulin resistance,IR)呈正相關(guān)[1]?雖然已有研究表明,PCOS患者也存在血清FFAs水平的增高及IR[2-3],但目前對(duì)此類人群的研究不多,且缺乏大樣本量及年齡匹配的對(duì)照組的研究?本研究旨在進(jìn)一步分析PCOS患者空腹血清FFAs水平的變化,并探討其相關(guān)因素,從而為進(jìn)一步探討PCOS發(fā)生?發(fā)展的機(jī)制提供重要的理論依據(jù)?
1.1 一般資料 納入重慶地區(qū)2007年11月至2010年1月就診于本院婦科及內(nèi)分泌科的133例PCOS患者及116例年齡匹配的健康婦女作為對(duì)照?受試者均無糖尿病史,未懷孕,絕經(jīng)前或最近至少3個(gè)月未服用過降糖藥和激素類藥物?PCOS的診斷標(biāo)準(zhǔn)參照歐洲人類生殖與胚胎學(xué)會(huì)和美國生殖醫(yī)學(xué)學(xué)會(huì)在鹿特丹會(huì)議上推薦的標(biāo)準(zhǔn)[4],并排除其他引起高雄激素?排卵障礙的內(nèi)分泌疾病,如先天性腎上腺增生?庫欣綜合征?分泌雄激素的腫瘤?高催乳素血癥?甲狀腺疾病等?本研究得到重慶醫(yī)科大學(xué)倫理委員會(huì)的認(rèn)可,所有調(diào)查均取得受試對(duì)象的知情同意?
1.2 研究方法
1.2.1 病史采集及人體學(xué)測量 采用統(tǒng)一制定的健康信息調(diào)查表,由專人對(duì)受試者進(jìn)行病史詢問及體格檢查,身體測量包括:身高?體質(zhì)量?腰圍;按照體質(zhì)量/身高(kg/m2)計(jì)算體質(zhì)量指數(shù)(body mass index,BMI)?
1.2.2 實(shí)驗(yàn)室檢查 (1)所有受試者于月經(jīng)第5~8天(閉經(jīng)者不限時(shí)間)禁食8~12h,次日清晨空腹抽肘靜脈血后行口服75g無水葡萄糖耐量試驗(yàn)(oral glucose tolerance test,OG-TT),并測定空腹胰島素(fasting insulin,FINS)?血清FFAs?總睪酮?總膽固醇(total cholesterol,TC)?三酰甘油(triacylglycerol,TG)?高密度脂蛋白膽固醇(high density lipoprotein cholestorol,HDL-c)?低密度脂蛋白膽固醇(low density lipoprotein cholestorol,LDL-c);另擇日對(duì)其中101例PCOS患者及20例正常人行高胰島素-正葡萄糖鉗夾術(shù)[5],以穩(wěn)態(tài)期120~180 min葡萄糖代謝率(M120-180)評(píng)估胰島素敏感性?(2)血漿葡萄糖測定采用己糖激酶法(邁瑞B(yǎng)S-200全自動(dòng)生化分析儀),試劑盒由中生北控生物科技股份有限公司提供;空腹胰島素和總睪酮測定采用電化學(xué)發(fā)光法,試劑盒由德國羅氏診斷有限公司提供;血脂測定采用OLYMPUS AU5400型全自動(dòng)生化檢測儀,試劑由日本和光純藥工業(yè)株式會(huì)社提供;血清FFAs測定采用酶法測定,試劑由日本積水藥療株式會(huì)社提供?
1.2.3 評(píng)價(jià)標(biāo)準(zhǔn) (1)超重?肥胖的診斷參照《中國成人超重和肥胖癥預(yù)防控制指南》[6],24.0kg/m2≤BMI28.0kg/m2為超重,BMI≥28.0kg/m2為肥胖;中心性肥胖:女性腰圍不低于80cm?(2)IR的診斷參照1999年 WHO的標(biāo)準(zhǔn)[7]以正常對(duì)照組鉗夾術(shù)中M120-180下四分位數(shù)為切點(diǎn)將PCOS組分為IR組(M120-18010.76mg?min-1?kg-1,n=80)和非IR組(M120-180≥10.76mg?min-1?kg-1,n=21)?(3)采用穩(wěn)態(tài)模型計(jì)算胰島素抵抗指數(shù)(homeostasis model assessment-IR,HOMA-IR)評(píng)價(jià)胰島素抵抗:HOMA-IR=FINS×空腹血糖(fasting plasma glucose,FPG)/22.5[8-9]?
1.3 統(tǒng)計(jì)學(xué)處理 使用SPSS13.0統(tǒng)計(jì)軟件進(jìn)行分析?計(jì)量資料以±s表示,偏態(tài)分布的變量[TG?FPG?餐后2小時(shí)血糖(2-hour postprandial blood glucose,2hPG)?FINS?HOMAIR]經(jīng)對(duì)數(shù)轉(zhuǎn)換后呈正態(tài)分布再進(jìn)行分析?兩組間均數(shù)比較采用t檢驗(yàn);多組均數(shù)之間的兩兩比較采用方差分析?以PCOS組的FFAs為應(yīng)變量,以其他因素為自變量行Pearson相關(guān)分析?P0.05為差異有統(tǒng)計(jì)學(xué)意義?
2.1 一般情況 兩組研究對(duì)象年齡差異無統(tǒng)計(jì)學(xué)意義(P0.05),與對(duì)照組相比,PCOS組有更高的 BMI?腰圍?FPG?2hPG?FINS?HOMA-IR?總睪酮?FFAs?TG和更低的 HDL-c?M120-180(P0.05或P0.01),而TC?LDL-c在兩組間的差異無統(tǒng)計(jì)學(xué)意義(P0.05),見表1?
表1 PCOS組與對(duì)照組一般情況及生化指標(biāo)的比較(±s)
表1 PCOS組與對(duì)照組一般情況及生化指標(biāo)的比較(±s)
#:經(jīng)對(duì)數(shù)轉(zhuǎn)換后進(jìn)行統(tǒng)計(jì)分析;*:P0.05,**:P 0.01,與對(duì)照組比較?
項(xiàng)目 PCOS組25.61±4.36 25.92±2.67 BMI(kg/m2) 23.65±4.44** 20.96±2.16腰圍(cm) 78.66±11.11** 70.32±6.10 FPG(mmol/L)# 5.19±0.60** 4.95±0.37 2hPG(mmol/L)# 7.12±1.88** 5.53±1.08 TC(mmol/L) 4.24±0.87 4.38±0.63 TG(mmol/L)# 1.36±1.39** 0.76±0.37 HDL-c(mmol/L) 1.09±0.24** 1.37±0.28 LDL-c(mmol/L) 2.08±0.68 2.09±0.44 FINS(mIU/L)# 10.97±11.01* 7.29±6.68 HOMA-IR# 2.61±2.86* 1.60±1.35 M120-180(mg/min×kg-1) 8.32±2.90** 12.08±1.78總睪酮(ng/dL) 58.35±29.40** 41.77±19.85 FFAs(μmol/L) 893.57±319.60**對(duì)照組年齡(歲)657.55±290.31
2.2 亞組間血清FFAs水平比較 按BMI是否超過了24.0kg/m2重新分組?PCOS組分為正常體質(zhì)量的PCOS組(n=76)和超重/肥胖的PCOS組(n=57);對(duì)照組分為正常體質(zhì)量的對(duì)照組(n=108)和超重/肥胖的對(duì)照組(n=8)?四個(gè)亞組中血清FFAs水平的比較見表2?
表2 四個(gè)亞組間血清FFAs水平的比較
2.3 PCOS的兩個(gè)亞組血清FFAs水平的比較 兩組均高于體質(zhì)量匹配的對(duì)照組(P0.01),但FFAs在PCOS的兩個(gè)亞組間比較,P0.05?以正常對(duì)照組鉗夾術(shù)中 M120-180下四分位數(shù)為切點(diǎn)將PCOS組分為IR組(M120-18010.76mg?min-1?kg-1,n=80,79.2%)和非IR 組(M120-180≥10.76 mg?min-1?kg-1,n=21,20.8%)?PCOS兩個(gè)亞組間血清FFAs水平的比較見表3?PCOS患者的IR組較非IR組有更高的BMI和FFAs濃度?
表3 PCOS患者的兩個(gè)亞組間血清FFAs水平的比較
2.4 血清FFAs水平相關(guān)因素分析 以PCOS患者的FFAs水平為應(yīng)變量,Pearson相關(guān)分析顯示,FFAs水平與BMI?腰圍?TC?LDL-c?總睪酮(r分別為0.20?0.18?0.19?0.18?0.18?0.05)呈 正 相 關(guān);與 HDL-c?M120-180(r分 別 為 -0.17?-0.22,P0.05)呈負(fù)相關(guān);與年齡?FPG?2hPG?FINS?TG?HOMA-IR(r分別 為 0.01?0.09?0.16?0.14?0.13?0.12,P0.05)無相關(guān)性?
本研究顯示,PCOS患者血清FFAs水平明顯高于對(duì)照組(P0.01),與體質(zhì)量匹配的對(duì)照組相比,超重/肥胖的PCOS患者FFAs水平明顯增高(P0.01),PCOS患者的IR組較非IR組也有更高的FFAs濃度;相關(guān)分析提示PCOS患者的FFAs水平分別與BMI?腰圍?TC?LDL-c?總睪酮呈正相關(guān),與HDL-c?M120-180呈負(fù)相關(guān)?
Holte等[10]研究發(fā)現(xiàn),PCOS患者較之體質(zhì)量匹配的正常婦女有更高的血清FFAs水平,本研究結(jié)果與之一致?而肥胖的PCOS患者減輕體質(zhì)量后血清FFAs水平和胰島素敏感性都有一定程度的改善,部分可恢復(fù)排卵[11],具體機(jī)制尚不清楚?另外,肥胖與PCOS患者的IR及糖尿病的發(fā)生相關(guān),且獨(dú)立于糖尿病家族史[12]?本研究中,超重/肥胖的PCOS組患者血清FFAs水平高于體質(zhì)量正常的PCOS組,且PCOS患者血清FFAs水平與BMI?腰圍呈正相關(guān),提示肥胖,特別是中心性肥胖的PCOS患者,其腹部脂肪堆積程度與血清FFAs濃度之間存在一定的相關(guān)性?
報(bào)道顯示,中國南部的PCOS患者中大約46.9%發(fā)生IR[13]?高水平的血清FFAs分別與PCOS患者的IR[2]及2型糖尿病的發(fā)生有關(guān)[14],且胰島素增敏劑對(duì)PCOS患者IR的治療有效[15-16]?本研究PCOS患者中IR的發(fā)生概率為79.2%,明顯高于之前報(bào)道;且IR組與非IR組相比,前者血清FFAs水平明顯高于后者,雖然差異無統(tǒng)計(jì)學(xué)意義,但相關(guān)分析得出血清FFAs水平與M120-180呈負(fù)相關(guān)?目前對(duì)于PCOS患者血清FFAs水平的升高與IR的發(fā)生機(jī)制尚不明確?有研究認(rèn)為[17-20]激素敏感性脂肪酶和脂蛋白脂酶之間的失調(diào)及抗脂解作用減弱,是IR時(shí)FFAs升高的重要原因,但對(duì)于PCOS患者來說,僅FFAs單一因素并不能解釋IR的發(fā)生[21-22]?
另外,研究發(fā)現(xiàn)[23],存在IR的PCOS患者,因白細(xì)胞與內(nèi)皮細(xì)胞的相互作用,損害內(nèi)皮及線粒體氧化功能?而FFAs同時(shí)也是導(dǎo)致氧化應(yīng)激的物質(zhì)之一,受高水平的FFAs刺激,活性氧簇生成增多,氧耗降低?因此,存在高FFAs水平的PCOS患者,炎癥反應(yīng)更明顯,心血管疾病的發(fā)生風(fēng)險(xiǎn)將會(huì)更高?
進(jìn)一步研究發(fā)現(xiàn),短期高水平的FFAs可通過增強(qiáng)肝臟硫酸轉(zhuǎn)移酶的活性致正常體內(nèi)高雄激素血癥[24-25]?而且,胰島素增敏劑可改善PCOS患者高雄激素的臨床特征[26]?Reed等[27]研究發(fā)現(xiàn),居住在倫敦西北部的亞洲婦女其血清FFAs水平與睪酮水平呈正相關(guān)?另外,年輕的PCOS患者中,隨著雄激素水平的增高,其患代謝綜合征的風(fēng)險(xiǎn)增加,且這種作用獨(dú)立于肥胖及IR[28]?本研究也得到了類似的結(jié)果,提示血清FFAs水平增高可能是PCOS發(fā)病的重要機(jī)制之一[22]?此外,對(duì)高加索人[29]?印度人[30]的研究表明,血清高FFAs水平均為糖調(diào)節(jié)受損,向糖尿病進(jìn)展的一個(gè)獨(dú)立危險(xiǎn)因素?本研究尚未得到FFAs與血糖的相關(guān)性,可能與研究對(duì)象的年齡及PCOS的病程有關(guān)?另外,本研究僅為橫斷面研究,關(guān)于FFAs與糖尿病發(fā)生的關(guān)系,還需要進(jìn)行長期隨訪觀察?
綜上所述,與年齡匹配的健康婦女相比,PCOS患者血清FFAs水平顯著升高,并且與肥胖?血脂異常?高雄激素?IR等因素相關(guān)?因此,降低PCOS患者空腹血清FFAs的水平,可能會(huì)有助于PCOS相關(guān)疾病的改善及遠(yuǎn)期并發(fā)癥的預(yù)防,成為治療PCOS的一個(gè)新思路[31]?
[1] 羅四川,李啟富,劉紅梅.清醒狀態(tài)大鼠高胰島素-正常血糖鉗夾術(shù)的建立及其意義[J].重慶醫(yī)科大學(xué)學(xué)報(bào),2004,29(3):334-336.
[2] Macut D,Panidis D,Glisic B,et al.Lipid and lipoprotein profile in women with polycystic ovary syndrome[J].Can J Physiol Pharmacol,2008,86(4):199-204.
[3] Wu Y,Zhang J,Wen Y,et al.Increased acylation-stimulating protein,C-reactive protein,and lipid levels in young women with polycystic ovary syndrome[J].Fertil Steril,2009,91(1):213-319.
[4] Kousta E,Tolis G,Franks S.Polycystic ovary syndrome.Revised diagnostic criteria and long-term health consequences[J].Hormones(Athens),2005,4(3):133-147.
[5] 汪志紅,李啟富,張素華,等.高胰島素-正葡萄糖鉗夾技術(shù)的建立[J].重慶醫(yī)科大學(xué)學(xué)報(bào),2004,29(5):615-617.
[6] 中國肥胖問題工作組.中國成人超重和肥胖癥預(yù)防與控制指南(節(jié)錄)[J].營養(yǎng)學(xué)報(bào),2004,26(1):1-4.
[7] Alberti KG,Zimmet PZ.Definition,diagnosis and classification of diabetes mellitus and its complications.Part 1:diagnosis and classification of diabetes mellitus provisional report of a WHO consultation[J].Diabet Med,1998,15(7):539-553.
[8] Matthews DR,Hosker JP,Rudenski AS,et al.Homeostasis model assessment:insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man[J].Diabetologia,1985,28(7):412-419.
[9] Yajnik CS,Joglekar CV,Lubree HG,et al.Adiposity,inflammation and hyperglycaemia in rural and urban Indian men:Coronary Risk of Insulin Sensitivity in Indian Subjects(CRISIS)Study[J].Diabetologia,2008,51(1):39-46.
[10]Holte J,Bergh T,Berne C.Restored insulin sensitivity but persistently increased early insulin secretion after weight loss in obese women with polycystic ovary syndrome[J].J Clin Endocrinol Metab,1995,80(9):2586-2593.
[11]Kuchenbecker WK,Groen H,van Asselt SJ,et al.In women with polycystic ovary syndrome and obesity,loss of intra-abdominal fat is associated with resumption of ovulation[J].Hum Reprod,2011,26(9):2505-2512.
[12]Kuba VM,Cavalieri PM,Christóforo AC,et al.Insulin resistance and metabolic profile in lean and overweight/obese polycystic ovary syndrome patients[J].Arg Bras Endocrinol Metabol,2006,50(5):1026-1033.
[13]Huang J,Ni R,Chen X,et al.Metabolic abnormalities in adolescents with polycystic ovary syndrome in South China[J].Reprod Biol Endocrinol,2010,8(1):142.
[14]Pankow JS,Duncan BB,Schmidit MI,et al.Fasting plasma free fatty acids and risk of type 2diabetes:the atherosclerosis risk in communities study[J].Diabetes Care,2004,27(1):77-82.
[15]Galindo García CG,Vega Arias Mde J,Hernández Marín I,et al.Mechanism of action of insulin sensitizer agents in the treatment of polycystic ovarian syndrome[J].Ginecol Obstet Mex,2007,75(3):148-154.
[16]Teede HJ,Meyer C,Norman RJ.Insulin-sensitisers in the treatment of polycystic ovary syndrome[J].Expert Opin Pharmacother,2005,6(14):2419-2427.
[17]Haemmerle G,Zimmermann R,Hayn H,et al.Hormonesensitive lipase deficiency in mice causes diglyeride accumulation in adipose tissue,muscle,and testis[J].J Biol Chem,2002,77(7):4806-4815.
[18]Mlinar B,Pfeifer M,Vrtacnik-Bokal E,et al.Decreased lipin 1beta expression in visceral adipose tissue is associated with insulin resistance in polycystic ovary syndrome[J].Eur J Endocrinol,2008,159(6):833-839.
[19]Seow KM,Tsai YL,Hwang JL,et al.Omental adipose tissue overexpression of fatty acid transporter CD36and decreased expression of hormone-sensitive lipase in insulin-resistant women with polycystic ovary syndrome[J].Hum Reprod,2009,24(8):1982-1988.
[20]Rydén M,Jocken J,van Harmelen V,et al.Comparative studies of the role of hormone-sensitive lipase and adipose triglyceride lipase in human fat cell lipolysis[J].Am J Physiol Endocrinol Metab,2007,292(6):E1847-E1855.
[21]Morin-Papunen LC,Vauhkonen I,Koivunen RM,et al.Insulin sensitivity,insulin secretion,and metabolic and hormonal parameters in healthy women and women with polycystic ovarian syndrome[J].Hum Reprod,2000,15(6):1266-1274.
[22]Ciampelli M,Muzj G,Leoni F,et al.Metabolic and endocrine consequences of acute suppression of FFAs by acipimox in polycystic ovary syndrome[J].J Clin Endocrinol Metab,2001,86(11):5324-5329.
[23]Victor VM,Rocha M,Ba?uls C,et al.Induction of oxidative stress and human leukocyte/endothelial cell interactions in polycystic ovary syndrome patients with insulin resistance[J].J Clin Endocrinol Metab,2011,96(10):3115-3122.
[24]Mai K,Bobbert T,Kullmann V,et al.Free fatty acids increase androgen precursors in vivo[J].J Clin Endocrinol Metab,2006,91(4):1501-1507.
[25]Mai K,Bobbert T,Reinecke F,et al.Intravenous lipid and heparin infusion-induced elevation in free fatty acids and triglycerides modifies circulating androgen levels in women:a randomized,controlled trial[J].J Clin Endocrinol Metab,2008,93(10):3900-3906.
[26]Azziz R,Ehrmann D,Legro RS,et al.Troglitazone improves ovulation and hirsutism in the polycystic ovary syndrome:a multicenter,double blind,lacebo-ontrolled trial[J].J Clin Endocrinol Metab,2001,86(4):1626-1632.
[27]Reed MJ,Dunkley SA,Singh A,et al.The role of free fatty acids in regulating the tissue availability and synthesis of sex steroids[J].Prostaglandins Leukot Essent Fatty Acids,1993,48(1):111-116.
[28]Coviello AD,Legro RS,Dunaif A.Adolescent girls with polycystic ovary syndrome have an increased risk of themetabolic syndrome associated with increasing androgen levels independent of obesity and insulin resistance[J].J Clin Endocrinol Metab,2006,91(2):492-497.
[29]Charles MA,Eschwège E,Thibult N,et al.The role of non-esterified fatty acids in the deterioration of glucose tolerence in the Caucasian subjects:Resultsof the Paris Prospective Study[J].Diabetologia,1997,40(9):1101-1106.
[30]Stefan N,Stumvoll M,Bogardus C,et al.Elevated plasma nonesterified fatty acids are associated with deterioration of acute insulin response in IGT but not NGT[J].Am J Physiol Endocrinol Metab,2003,284(6):E1156-E1161.
[31]Douglas CC,Gower BA,Darnell BE,et al.Role of diet in the treatment of polycystic ovary syndrome[J].Fertil Steril,2006,85(3):679-688.
Concentration of serum free fatty acids and its correlation analyses in patients with polycystic ovarian syndrome
ObjectiveTo measure the concentration of free fatty acids(FFAs)and to analyze its associations with correlative factors in the patients with polycystic ovarian syndrome(PCOS).Methods133PCOS women and 116healthy,age-matched controls were recruited.Physical examination and laboratory analysis were performed.All subjects underwent a standard 75-g oral glucose tolerance test.101PCOS women and 20controls underwent hyperinsulinemic euglycemic clamp to assess their insulin sensitivity.IR was also estimated by homeostasis model assessment of insulin resistance(HOMA-IR).ResultsThe levels of serum FFAs in PCOS women were significantly higher as compared with controls(P0.01).Subgroup analysis showed that the levels of serum FFAs in two PCOS subgroups were significantly higher as compared with the two weight-matched control subgroups(P0.01).Correlation analyses showed that in all subjects,FFAs positively correlated with BMI,waist circumference,total cholesterol(TC),LDL-c and total testosterone(r=0.20,r=0.18,r=0.19,r=0.18,r=0.18,P0.05)and negatively correlated with HDL-c and M120-180value(r=-0.17,r=-0.22,P0.05).ConclusionComparing with age-matched healthy women,the levels of serum FFAs in PCOS women are elevated evidently and positively correlated with BMI,waist circumference,TC,LDL-c and total testosterone,negatively correlated with HDL-c and M120-180value.
polycystic ovary syndrome;free fatty acids;insulin resistance
10.3969/j.issn.1671-8348.2012.16.009
A
1671-8348(2012)16-1585-04
△通訊作者,E-mail:bxy20061963@163.com?
2011-10-19
2011-11-22)
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