25.0kg/m2,均未經(jīng)降血糖、降血脂、利尿、降壓、抗尿酸藥物治療。測定血清胰島素及生化指標(biāo),用CT在臍水平測定腹部脂肪分布。結(jié)果直線相關(guān)分析顯示"/>
牟倫盼等
[摘要] 目的 探討男性肥胖患者中血尿酸(SUA)與體脂分布及代謝綜合征(MS)的相關(guān)性。 方法 選取2012—2014年門診就診的133例肥胖患者,體重指數(shù)(BMI)均>25.0 kg/m2,均未經(jīng)降血糖、降血脂、利尿、降壓、抗尿酸藥物治療。測定血清胰島素及生化指標(biāo),用CT在臍水平測定腹部脂肪分布。結(jié)果 直線相關(guān)分析顯示SUA與BMI、腰圍、內(nèi)臟脂肪、內(nèi)臟脂肪/皮下脂肪比值、空腹血糖、HOMA-IR、甘油三酯、血肌酐、收縮壓、舒張壓呈正相關(guān),相關(guān)系數(shù)分別為0.361、0.446、0.634、0.360、0.193、0.287、0.477、0.259、0.280、0.181;多元逐步回歸分析顯示對(duì)SUA影響最大的因素依次為內(nèi)臟脂肪面積、甘油三酯,標(biāo)準(zhǔn)化回歸系數(shù)分別為0.533、0.183;內(nèi)臟脂肪蓄積隨血尿酸水平升高明顯增加,更高的4分位數(shù)血尿酸對(duì)應(yīng)更高的內(nèi)臟脂肪面積(P<0.05)。MS組SUA水平高于非MS組者[(434.6±69.6)umol/L vs(367.0±104.9)umol/L,P<0.01];Spearman秩相關(guān)分析顯示SUA水平隨MS組分?jǐn)?shù)增加而增高(P<0.01)。結(jié)論 SUA水平與內(nèi)臟脂肪蓄積相關(guān);代謝綜合征患者SUA水平更高。
[關(guān)鍵詞] 血尿酸; 內(nèi)臟脂肪面積; 代謝綜合征
[中圖分類號(hào)] R473.74 [文獻(xiàn)標(biāo)識(shí)碼] A [文章編號(hào)] 1674-0742(2014)10(b)-0011-03
Relation Between Serum Uric Acid Level and Body Fat Distribution, Metabolic Syndrome in Obesity
MOU Lunpan1 JIANG Jianjia1 SU Jinbo1 SUN Bingqing2 LIN Zhenzhong3
1.Department of Endocrinology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, Fujian Province, 362000, China;2.Imaging Department, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, Fujian Province, 362000, China;3. Clinical Laboratory, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, Fujian Province, 362000, China
[Abstract] Objective We investigated the relationship between serum uric acid (SUA) and body fat distribution, metabolic syndrome(MS) in obese men. Methods 133 cases of obese outpatients from year 2012 to 2014, with body mass index(BMI)≥25.0 Kg/m2, were enrolled in the study. These patients have never been given hypoglycemic, hypolipidemic, hydragogue, anti-hypertensive or anti-hyperuricemic agents. Body fat distribution was measured by computed tomography (CT) scanning at the umbilical level. Serum insulin and other biochemical parameters were also measured. Results Linear correlation analysis showed that SUA is positively correlated with BMI, waist circumference, visceral fat area, the ratio of visceral fat area with subcutaneous fat area, fasting plasma glucose, HOMA-IR, serum triglyceride, serum creatinine, systolic and diastolic blood pressure, and the above parameter of correlation coefficient was 0.361, 0.446, 0.634, 0.360, 0.193, 0.287, 0.477, 0.259, 0.280, 0.181, respectively. Stepwise multiple regression analysis showed that visceral fat area, and serum triglyceride were significant explanatory variables for SUA levels, and the standardized regression coefficient was 0.533, 0.183 respectively. Visceral fat accumulation increased significantly with the increase of uric acid. A higher quartile of SUA showed a higher visceral fat area (P<0.05). The SUA was significantly higher in metabolic syndrome group than that in the non-metabolic syndrome group (434.6±69.6 umol/l vs 367.0±104.9umol/l, P<0.01). In Spearman rank correlation analysis, the SUA was elevated with increasing metabolic syndrome characteristics (P<0.01). Conclusion The present study indicated that SUA is significantly associated with visceral fat accumulation. Patients with metabolic syndrome revealed a higher SUA.
[Key words] Serum uric acid; Visceral fat area; Metabolic syndrome
高尿酸血癥因嘌呤代謝紊亂及(或)尿酸排泄障礙引起,常與各種生活方式相關(guān)性疾病伴隨出現(xiàn)。流行病學(xué)研究顯示高尿酸血癥是動(dòng)脈粥樣硬化性心血管疾病的危險(xiǎn)因子[1-2]。代謝綜合征(Metabolic Syndrome,MS)全球指南將高尿酸血癥表述為與MS征相關(guān)的代謝紊亂[3]。MS是一些代謝異常的集合,主要包括高血壓、高血糖、血脂紊亂和肥胖,可以明顯增加心腦血管事件的發(fā)生。腹型肥胖據(jù)腹部脂肪蓄積部位不同可區(qū)分為內(nèi)臟型肥胖與皮下型肥胖。該研究旨在探討血尿酸水平與體脂蓄積及代謝綜合癥發(fā)病的相關(guān)性,以2012—2014年首次就診該院內(nèi)分泌科的男性肥胖患者133例為研究對(duì)象,現(xiàn)報(bào)道如下。
1 對(duì)象與方法
1.1 研究對(duì)象
選取首次就診筆者醫(yī)院內(nèi)分泌科的男性肥胖患者133例,平均年齡(40.7±12.4)歲;未經(jīng)降血糖、降壓、降血脂、利尿、抗尿酸藥物治療;無飲酒習(xí)慣。無慢性心肺肝腎疾病。
1.2 研究方法
1.2.1 所有病例均由專人測定身高、體重、腰圍、血壓。
1.2.2 體脂含量及分布 (1)總體脂含量: 以體重指數(shù)(BMI)表示。(2) 腹部體脂含量: ①簡單測量:以腰圍,即腰部骨性胸廓最下緣與髂嵴最上緣連線的中點(diǎn)周徑;②精細(xì)測量:采用螺旋CT于空腹?fàn)顟B(tài)下行腹部掃描,病人仰臥并于掃描過程中屏氣,掃描相當(dāng)于臍水平。機(jī)配軟件計(jì)算內(nèi)臟脂肪面積、皮下脂肪面積。
1.2.3 生化指標(biāo) 生化指標(biāo)以自動(dòng)生化分析儀測定;空腹血清胰島素以放射免疫法測定,批內(nèi)CV<5%,批間CV<6.5%。
1.2.4 胰島素抵抗 用穩(wěn)態(tài)模式評(píng)估法的HOMA-IR 公式[空腹血漿葡萄糖(mmol/L)×空腹血清胰島素(mU/L)/22.5]計(jì)算。
1.2.5 MS的診斷標(biāo)準(zhǔn) 依據(jù)2004年中華醫(yī)學(xué)會(huì)糖尿病分會(huì)關(guān)于MS的診斷標(biāo)準(zhǔn):①BMI≥25 kg/m2;②FBG≥6.1 mmol/L和(或)糖負(fù)荷后2 h血糖≥7.8 mmol/L和(或)糖尿病治療者;③SBP≥140 mmHg和(或)DBP≥90 mmHg,或高血壓病治療者;④空腹甘油三酯(TG)≥1.7 mmol/L和(或)高密度脂蛋白膽固醇(HDL-C)男性<0.9 mmol/L,女性<1.0 mmol/L。符合以上3項(xiàng)或3項(xiàng)以上者診斷為MS。
1.3 統(tǒng)計(jì)方法
計(jì)量資料以(x±s)表示,兩變量間比較用成組t檢驗(yàn);SUA與各臨床指標(biāo)的相關(guān)性分析用Pearson相關(guān)性檢驗(yàn);各臨床指標(biāo)對(duì)SUA的影響用多元逐步回歸分析;代謝綜合征組分對(duì)SUA的影響用Spearman秩相關(guān)分析。
2 結(jié)果
2.1 病例基本特征
共133例受試者,平均年齡(40.7±12.4)歲,BMI(29.8±3.9)kg/m2,腰圍(101.5±11.4)cm,四分位數(shù)血尿酸,Q1:≤375 umol/L,32例;Q2:376~429 umol/L,34例;Q3:430~460 umol/L,32例;Q4:≥461 umol/L,35例。各四分位數(shù)年齡差異無統(tǒng)計(jì)學(xué)意義;Q1組患者腰圍及BMI較其他三組低(均P<0.05),Q2、Q3及Q4的腰圍及BMI差異無統(tǒng)計(jì)學(xué)意義(均P>0.05),見表1。
2.2 血尿酸與體脂分布的相關(guān)性
內(nèi)臟脂肪蓄積隨血尿酸水平升高明顯增加,更高的4分位數(shù)血尿酸對(duì)應(yīng)更高的內(nèi)臟脂肪面積,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)見圖1。
Q1、Q2、Q3、Q4組皮下脂肪面積分別為(238±77)cm2、(240±90)cm2、(266±81)cm2、(248±107)cm2(F=0.66,P>0.05),組間差異無統(tǒng)計(jì)學(xué)意義。
血尿酸與BMI、腰圍、內(nèi)臟脂肪、內(nèi)臟脂肪/皮下脂肪比值、空腹血糖、HOMA-IR、甘油三酯、血肌酐、收縮壓、舒張壓呈正相關(guān);血尿酸與皮下脂肪、總膽固醇、高密度脂蛋白膽固醇、低密度脂蛋白膽固醇無相關(guān)性。在人體測量各參數(shù)中,血尿酸水平與內(nèi)臟脂肪面積相關(guān)系數(shù)最高,相關(guān)性最強(qiáng)(P<0.01)。見表2。
將與血尿酸存在相關(guān)性的各臨床指標(biāo)進(jìn)行多元逐步回歸分析,結(jié)果顯示對(duì)血尿酸影響最大的因素依次為內(nèi)臟脂肪面積、甘油三酯,見表3。
2.3 血尿酸與代謝綜合征的相關(guān)性
代謝綜合征組(85例)血尿酸水平高于非代謝綜合征組(48例)者[(434.6±69.6)umol/Lvs(367.0±104.9)umol/L,P<0.01)。Spearman秩相關(guān)分析顯示血尿酸水平隨代謝綜合征組分?jǐn)?shù)增加而增高,差異有統(tǒng)計(jì)學(xué)意義(P<0.01)。
3 討論
高尿酸血癥、腹型肥胖是動(dòng)脈粥樣硬化性心血管疾病的危險(xiǎn)因子,常與各種生活方式相關(guān)性疾病伴隨出現(xiàn),從而加速動(dòng)脈粥樣硬化進(jìn)展。為此,該研究通過CT檢測肥胖患者內(nèi)臟脂肪與皮下脂肪的分布特征,進(jìn)一步明確血尿酸與體脂分布及代謝綜合征發(fā)病的相關(guān)性。腰圍是判斷腹型肥胖的建議指標(biāo),但它不能準(zhǔn)確地反應(yīng)內(nèi)臟脂肪量的變化,而判斷內(nèi)臟脂肪量的金標(biāo)準(zhǔn)是CT或MRI[4]。該研究采用CT測定腹型肥胖患者的皮下脂肪量及內(nèi)臟脂肪量,并評(píng)估了腹型肥胖患者腹部脂肪分布與血尿酸的相關(guān)性。
該研究結(jié)果顯示各4分位數(shù)SUA病例其年齡相近,除Q1患者腰圍及BMI較小外,其余三組患者腰圍及BMI差異無統(tǒng)計(jì)學(xué)意義,但仍可以看出隨SUA水平升高,腰圍及BMI有增加的趨勢。為此,該研究進(jìn)一步分析了SUA與腰圍、BMI、內(nèi)臟脂肪面積、皮下脂肪面積及內(nèi)/皮面積比值這些與體脂分布相關(guān)各指標(biāo)的相關(guān)性,并得出了SUA與內(nèi)臟脂肪面積相關(guān)性最強(qiáng)的結(jié)論。結(jié)合多元逐步回歸分析可見內(nèi)臟脂肪蓄積隨血尿酸水平升高明顯增加,對(duì)SUA影響最大的因素即為內(nèi)臟脂肪面積,與文獻(xiàn)報(bào)道相近[5]。因內(nèi)臟脂肪面積對(duì)腰圍及BMI的貢獻(xiàn)較小,這很好的解釋了為何隨SUA升高腰圍及BMI增加不明顯。腹部脂肪異常分布,尤其是內(nèi)臟型肥胖與血尿酸水平及MS發(fā)病率的升高密切相關(guān),
內(nèi)臟脂肪蓄積較皮下脂肪蓄積對(duì)血尿酸水平影響大,內(nèi)臟型肥胖血尿酸升高可能與胰島素抵抗引起尿酸排泄低下及內(nèi)臟脂肪蓄積使尿酸合成亢進(jìn)有關(guān)。Quinones等[6]證實(shí)胰島素水平上升降低尿尿酸排泄,Ter Maaten等[7]也證明尿酸排泄與胰島素抵抗呈負(fù)相關(guān)。因此,內(nèi)臟型肥胖者高尿酸水平可能是高胰島素血癥或胰島素抵抗降低腎小管尿酸排泄的結(jié)果。Fabregat等[8]發(fā)現(xiàn)內(nèi)臟型肥胖時(shí)經(jīng)門靜脈運(yùn)送至肝的游離脂肪酸增加,嘌呤經(jīng)磷酸戊糖途徑從頭合成增強(qiáng)而促使尿酸產(chǎn)生增加。無論是胰島素抵抗導(dǎo)致的尿酸排泄減少抑或是游離脂肪酸增加導(dǎo)致的尿酸生產(chǎn)增加,均為內(nèi)臟脂肪蓄積的結(jié)果,
綜上所述,血尿酸水平與內(nèi)臟脂肪蓄積及代謝綜合征密切相關(guān)。
[參考文獻(xiàn)]
[1] Culleton BF,Larson MG,Kannel WB,et al.Serum uric acid and risk for cardiovascular disease and death:The Framingham Heart Study[J].Ann Intern M ed,1999,131:7-13.
[2] Bickel C,Rupprecht HJ,Blankenberg S,et a1.Serum uric acid as an independent predictor of mortality in patients with angiographically proven coronary artery disease[J].Am J Cardiol,2002,89:12-17.
[3] Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome[J]. Lancet, 2005,365(9468):1415-1428.
[4] Wajchenberg B L. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome[J]. Endocr Rev, 2000,21(6):697-738.
[5] Tamba S, Nishizawa H, Funahashi T,et a1. Relationship between the serum uric acid level, visceral fat accumulation and serum adiponectin concentration in Japanese men[J]. Intern Med, 2008,47(13):1175-1180.
[6] Quinones Galvan A, Natali A, Baldi S,et al. Effect of insulin on uric acid excretion in humans[J].Am J Physiol,1995,268: E1-E5.
[7] Ter Maaten JC, Voorburg A, Heine RJ, et al.Renal handling of urate and sodium during acute physiological hyperinsulinaemia in healthy subjects[J].Clin Sci (Lond),1997,92: 51-58.
[8] Fabregat I, Revilla E, Machado A. Short-term control of the pentose phosphate cycle by insulin could be modulated by NADPH/NADP ratio in rat adipocytes and hepatocytes[J]. Biochem Biophys Res, 1987,146:920-925.
(收稿日期:2014-07-05)
內(nèi)臟脂肪蓄積較皮下脂肪蓄積對(duì)血尿酸水平影響大,內(nèi)臟型肥胖血尿酸升高可能與胰島素抵抗引起尿酸排泄低下及內(nèi)臟脂肪蓄積使尿酸合成亢進(jìn)有關(guān)。Quinones等[6]證實(shí)胰島素水平上升降低尿尿酸排泄,Ter Maaten等[7]也證明尿酸排泄與胰島素抵抗呈負(fù)相關(guān)。因此,內(nèi)臟型肥胖者高尿酸水平可能是高胰島素血癥或胰島素抵抗降低腎小管尿酸排泄的結(jié)果。Fabregat等[8]發(fā)現(xiàn)內(nèi)臟型肥胖時(shí)經(jīng)門靜脈運(yùn)送至肝的游離脂肪酸增加,嘌呤經(jīng)磷酸戊糖途徑從頭合成增強(qiáng)而促使尿酸產(chǎn)生增加。無論是胰島素抵抗導(dǎo)致的尿酸排泄減少抑或是游離脂肪酸增加導(dǎo)致的尿酸生產(chǎn)增加,均為內(nèi)臟脂肪蓄積的結(jié)果,
綜上所述,血尿酸水平與內(nèi)臟脂肪蓄積及代謝綜合征密切相關(guān)。
[參考文獻(xiàn)]
[1] Culleton BF,Larson MG,Kannel WB,et al.Serum uric acid and risk for cardiovascular disease and death:The Framingham Heart Study[J].Ann Intern M ed,1999,131:7-13.
[2] Bickel C,Rupprecht HJ,Blankenberg S,et a1.Serum uric acid as an independent predictor of mortality in patients with angiographically proven coronary artery disease[J].Am J Cardiol,2002,89:12-17.
[3] Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome[J]. Lancet, 2005,365(9468):1415-1428.
[4] Wajchenberg B L. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome[J]. Endocr Rev, 2000,21(6):697-738.
[5] Tamba S, Nishizawa H, Funahashi T,et a1. Relationship between the serum uric acid level, visceral fat accumulation and serum adiponectin concentration in Japanese men[J]. Intern Med, 2008,47(13):1175-1180.
[6] Quinones Galvan A, Natali A, Baldi S,et al. Effect of insulin on uric acid excretion in humans[J].Am J Physiol,1995,268: E1-E5.
[7] Ter Maaten JC, Voorburg A, Heine RJ, et al.Renal handling of urate and sodium during acute physiological hyperinsulinaemia in healthy subjects[J].Clin Sci (Lond),1997,92: 51-58.
[8] Fabregat I, Revilla E, Machado A. Short-term control of the pentose phosphate cycle by insulin could be modulated by NADPH/NADP ratio in rat adipocytes and hepatocytes[J]. Biochem Biophys Res, 1987,146:920-925.
(收稿日期:2014-07-05)
內(nèi)臟脂肪蓄積較皮下脂肪蓄積對(duì)血尿酸水平影響大,內(nèi)臟型肥胖血尿酸升高可能與胰島素抵抗引起尿酸排泄低下及內(nèi)臟脂肪蓄積使尿酸合成亢進(jìn)有關(guān)。Quinones等[6]證實(shí)胰島素水平上升降低尿尿酸排泄,Ter Maaten等[7]也證明尿酸排泄與胰島素抵抗呈負(fù)相關(guān)。因此,內(nèi)臟型肥胖者高尿酸水平可能是高胰島素血癥或胰島素抵抗降低腎小管尿酸排泄的結(jié)果。Fabregat等[8]發(fā)現(xiàn)內(nèi)臟型肥胖時(shí)經(jīng)門靜脈運(yùn)送至肝的游離脂肪酸增加,嘌呤經(jīng)磷酸戊糖途徑從頭合成增強(qiáng)而促使尿酸產(chǎn)生增加。無論是胰島素抵抗導(dǎo)致的尿酸排泄減少抑或是游離脂肪酸增加導(dǎo)致的尿酸生產(chǎn)增加,均為內(nèi)臟脂肪蓄積的結(jié)果,
綜上所述,血尿酸水平與內(nèi)臟脂肪蓄積及代謝綜合征密切相關(guān)。
[參考文獻(xiàn)]
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(收稿日期:2014-07-05)