绝经后女性高血压病伴糖耐量减低患者骨密度分析及临床意义
|
摘要
【目的】
在建立双能X线吸收法(DXA)骨密度测量的基础上,分析绝经后女性高血压病(EH)伴糖耐量减低(IGT)患者骨密度的变化,探讨绝经后女性糖耐量减低对骨密度的影响,并探讨其可能发病机制。
[方法]
连续入选2009年1月至2010年1月暨南大学附属第一医院心内科、内分泌科住院与门诊、及附属校门诊部绝经后女性患者(66.82±10.69岁),共107例,详细记录基础资料,常规检测三大常规、血脂、肝肾功能等。参照国际IGT、高血压诊断标准将其分为正常对照组55例、单纯IGT组28例、IGT合并EH组24例,均使用DXA测量全身、局部腰椎(腰椎L1-L4)和股骨近端(包括股骨颈、大转子和Ward's三角)的骨密度(Bone Mineral Density,BMD)。使用SPSS13.0软件进行资料的统计分析。计数资料用均数±标准差表示；x2检验分别比较单纯IGT组和IGT合并EH组总骨质疏松(osteoporosis,OP)、腰椎OP、髋部OP的患病率,协方差分析各部位BMD的差别,使用独立样本t检验分别比较三组间实验室指标与各部位BMD,并使用多元回归方法及直线相关分析各部位BMD与相关危险因素之间的相关性。
[结果]
IGT组中,高血压组腰椎OP患病构成比显著高于非高血压组(P<0.05)；而全身OP、双侧股骨近端OP两组构成比无明显差别(P>0.05)。两组BMD比较,高血压组各部位的BMD均低于非高血压组,其中腰椎L1、L2、L3、L4的BMD显著低于非高血压组(P值分别为0.021、0.033、0.036、0.029),但在校正BMI及餐后2h C肽后P值显著变大,两组BMD均无统计学差异。IGT组(包括单纯IGT组和IGT合并EH组)与正常对照组比较,IGT组收缩压、舒张压、标准OGTT餐后2h血糖、HbAlc水平、C肽水平高于正常对照组(P<0.05)；而TC、TG、HDL-C、LDL-C等指标与正常对照组比较无显著差异(P>0.05)。IGT组腰椎L2、L3、L4、Ward's三角区的BMD明显低于正常对照组(P值分别为0.031、0.026、0.034和0.039)；而全身、腰椎L1、股骨颈、大粗隆的BMD无显著差异(P值分别为0.329、0.374、0.085、0.432)。应用多元回归分析并进行相应的直线相关分析,绝经年限、OGTT餐后2h血糖、体重指数(BMI)和BMD有关系；而在有IGT基础上的高血压与BMD呈明显的负相关。
[结论]
绝经后糖耐量减低女性患者部分腰椎、Ward's三角区的骨密度显著降低。对有糖耐量异常基础的绝经后女性,高血压使腰椎骨密度显著降低,而对Ward's三角区的骨密度影响未见明显。骨密度和绝经年限、餐后血糖水平(PPG)、平均动脉压(MAP)呈直线负相关；与体重指数(BMI)呈正相关。
[Objective]
Based on the precision of the measurements of body composition and bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA), we analyzed changes of BMD in postmenopausal female patients with essential hypertension who is suffering impaied glucose tolerance on the purpose of investigating the effect of IGT on postmenopausal female patients, and exploring the possible mechanism.
107 postmenopausal female patients from section of cardiology and endocrine and outpatient section of the first affiliated hospital of Jinan university were selected and recorded the basic file, then accepted blood test. They were divided into 55 cases of normal control group,28 cases of pure IGT group,24 cases of IGT combined EH group according to the IGT and hypertension diagnostic criteria. BMD of total body、partial lumbar spine (lumbar vertebrae L1-L4) and proximal femur (including the femoral neck, trochanter and Ward's triangle) were determined by DXA. All data had been analyzed by SPSS 13.0. Prevalence of osteoporosis were compared between the IGT two groups using Chi-square test, and BMD was compared using covariance analysis. Among the three groups, BMD and laboratory indicators were compared by independent samples T test respectively. The correlation between BMD and risk factors was analyzed using multiple regression method and linear correlation analysis.
[Results]
In the IGT two groups, The prevalence of lumber osteoporosis in hypertension group were higher than that of the non-hypertension group (P<0.05) while there was no significant difference between the two groups in the whole body OP, bilateral proximal femoral component ratio of OP (P>0.05). All BMDs in the hypertension group were higher than that in the non-hypertension group, and there were significant differences in lumbar L1、L2、L3、L4 BMDs between the two groups (P values were 0.021、0.033、0.036 and 0.029 respectively); however, the difference disappeared after adjustment for the BMI and postprandial 2h C-peptide, the P value also increased remarkably. The level of systolic blood pressure (SBP)、diastolic blood pressure (DBP)、the postprandial 2h plasma glucose, HbAlc and C-peptide in IGT group were significant higher than that in normal control group while there was no significant difference between the two groups in the level of TC, TG, HDL-C, LDL-C and other indicators. BMDs in lumbar L2、L3、L4 and Ward's triangle in IGT group were significantly lower than that in the normal control group (P values were 0.031、0.026、0.034 and 0.039 respectively), while there was no significant difference between the two groups in BMDs in total body、lumbar spine L1、femoral neck and greater trochanter (P values were 0.329、0.374、0.085 and 0.432 respectively) Multiple regression method and linear correlation analysis showed that BMDs were associated with menopause age、OGTT postprandial 2h plasma glucose、body mass index (BMI) and hypertension combined with IGT.
[Conclusion]
BMDs in some lumbar spine and Ward's triangle were significantly reduced in postmenopausal female patients. BMDs in lumbar spine were notably lower in postmenopausal female patients with IGT than those without IGT; while there is no significant differences in Ward's triangle BMDs. BMDs were negatively correlated with postmenopausal age、postprandial plasma glucose and mean arterial pressure but positively with BMI.
在建立双能X线吸收法(DXA)骨密度测量的基础上,分析绝经后女性高血压病(EH)伴糖耐量减低(IGT)患者骨密度的变化,探讨绝经后女性糖耐量减低对骨密度的影响,并探讨其可能发病机制。
[方法]
连续入选2009年1月至2010年1月暨南大学附属第一医院心内科、内分泌科住院与门诊、及附属校门诊部绝经后女性患者(66.82±10.69岁),共107例,详细记录基础资料,常规检测三大常规、血脂、肝肾功能等。参照国际IGT、高血压诊断标准将其分为正常对照组55例、单纯IGT组28例、IGT合并EH组24例,均使用DXA测量全身、局部腰椎(腰椎L1-L4)和股骨近端(包括股骨颈、大转子和Ward's三角)的骨密度(Bone Mineral Density,BMD)。使用SPSS13.0软件进行资料的统计分析。计数资料用均数±标准差表示；x2检验分别比较单纯IGT组和IGT合并EH组总骨质疏松(osteoporosis,OP)、腰椎OP、髋部OP的患病率,协方差分析各部位BMD的差别,使用独立样本t检验分别比较三组间实验室指标与各部位BMD,并使用多元回归方法及直线相关分析各部位BMD与相关危险因素之间的相关性。
[结果]
IGT组中,高血压组腰椎OP患病构成比显著高于非高血压组(P<0.05)；而全身OP、双侧股骨近端OP两组构成比无明显差别(P>0.05)。两组BMD比较,高血压组各部位的BMD均低于非高血压组,其中腰椎L1、L2、L3、L4的BMD显著低于非高血压组(P值分别为0.021、0.033、0.036、0.029),但在校正BMI及餐后2h C肽后P值显著变大,两组BMD均无统计学差异。IGT组(包括单纯IGT组和IGT合并EH组)与正常对照组比较,IGT组收缩压、舒张压、标准OGTT餐后2h血糖、HbAlc水平、C肽水平高于正常对照组(P<0.05)；而TC、TG、HDL-C、LDL-C等指标与正常对照组比较无显著差异(P>0.05)。IGT组腰椎L2、L3、L4、Ward's三角区的BMD明显低于正常对照组(P值分别为0.031、0.026、0.034和0.039)；而全身、腰椎L1、股骨颈、大粗隆的BMD无显著差异(P值分别为0.329、0.374、0.085、0.432)。应用多元回归分析并进行相应的直线相关分析,绝经年限、OGTT餐后2h血糖、体重指数(BMI)和BMD有关系；而在有IGT基础上的高血压与BMD呈明显的负相关。
[结论]
绝经后糖耐量减低女性患者部分腰椎、Ward's三角区的骨密度显著降低。对有糖耐量异常基础的绝经后女性,高血压使腰椎骨密度显著降低,而对Ward's三角区的骨密度影响未见明显。骨密度和绝经年限、餐后血糖水平(PPG)、平均动脉压(MAP)呈直线负相关；与体重指数(BMI)呈正相关。
[Objective]
Based on the precision of the measurements of body composition and bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA), we analyzed changes of BMD in postmenopausal female patients with essential hypertension who is suffering impaied glucose tolerance on the purpose of investigating the effect of IGT on postmenopausal female patients, and exploring the possible mechanism.
107 postmenopausal female patients from section of cardiology and endocrine and outpatient section of the first affiliated hospital of Jinan university were selected and recorded the basic file, then accepted blood test. They were divided into 55 cases of normal control group,28 cases of pure IGT group,24 cases of IGT combined EH group according to the IGT and hypertension diagnostic criteria. BMD of total body、partial lumbar spine (lumbar vertebrae L1-L4) and proximal femur (including the femoral neck, trochanter and Ward's triangle) were determined by DXA. All data had been analyzed by SPSS 13.0. Prevalence of osteoporosis were compared between the IGT two groups using Chi-square test, and BMD was compared using covariance analysis. Among the three groups, BMD and laboratory indicators were compared by independent samples T test respectively. The correlation between BMD and risk factors was analyzed using multiple regression method and linear correlation analysis.
[Results]
In the IGT two groups, The prevalence of lumber osteoporosis in hypertension group were higher than that of the non-hypertension group (P<0.05) while there was no significant difference between the two groups in the whole body OP, bilateral proximal femoral component ratio of OP (P>0.05). All BMDs in the hypertension group were higher than that in the non-hypertension group, and there were significant differences in lumbar L1、L2、L3、L4 BMDs between the two groups (P values were 0.021、0.033、0.036 and 0.029 respectively); however, the difference disappeared after adjustment for the BMI and postprandial 2h C-peptide, the P value also increased remarkably. The level of systolic blood pressure (SBP)、diastolic blood pressure (DBP)、the postprandial 2h plasma glucose, HbAlc and C-peptide in IGT group were significant higher than that in normal control group while there was no significant difference between the two groups in the level of TC, TG, HDL-C, LDL-C and other indicators. BMDs in lumbar L2、L3、L4 and Ward's triangle in IGT group were significantly lower than that in the normal control group (P values were 0.031、0.026、0.034 and 0.039 respectively), while there was no significant difference between the two groups in BMDs in total body、lumbar spine L1、femoral neck and greater trochanter (P values were 0.329、0.374、0.085 and 0.432 respectively) Multiple regression method and linear correlation analysis showed that BMDs were associated with menopause age、OGTT postprandial 2h plasma glucose、body mass index (BMI) and hypertension combined with IGT.
[Conclusion]
BMDs in some lumbar spine and Ward's triangle were significantly reduced in postmenopausal female patients. BMDs in lumbar spine were notably lower in postmenopausal female patients with IGT than those without IGT; while there is no significant differences in Ward's triangle BMDs. BMDs were negatively correlated with postmenopausal age、postprandial plasma glucose and mean arterial pressure but positively with BMI.
引文
[1]钱荣立译.WHO专家咨询报告.关于糖尿病的新诊断标准与分型[J].中国糖尿病蕊2000,8(1)：5-6.
[2]王克安,李天麟,向红丁,等.中国糖尿病流行特点研究[J].中华流行病弓噪志1998,19(5)：282-285.
[3]顾东风,吴锡桂.我国老年人群高血压患病率及影响因素[J].中华心血管病杂志,2003,31(6)：654.
[4]田敏,王爱梅.南阳地区老年人高血压的调查分析[J].第四军医大学学报,2005,26(18)：1723-1724.
[5]卫生部疾病预防控制局.疾病的预防与控制…规划与管理[M].北京：人民卫生出版社,2006：119-128.
[6]Nguyen TV, Pocock N. Eisman JA1[J]. J Clin Densitom,2000,3(2):1072-1191.
[7]Monaco MD, Mautino F, Cavanna A. Femur bone mineral density, age and fracture type in 300 hip-fractured women[J]. Aging Clin Exp Res,2002,14(1):47-51.
[8]Keane BE, et al. Quantitative evaluation of bone mineral by radiographic method [J]. Brit J Radio,1959(32):162.
[9]张智海,沈建雄,刘忠厚.中国人骨质疏松症诊断标准回顾性研究[J].中国骨质疏松杂志,2004,10(3)：255-262.
[10]Pejovic-Milic A, McNeill FE, Prestwich WV et al. Development of an accelerator based determination of aluminum burden in peripheral bone by neutron activation analysis [J] Appli radiation&isotopes.1998,49(5):717-719.
[11]Warden SJ, Bennell KL, Matthews B, et al. Quantitative ultrasound assessment of acute bone loss following spinal cord injury:a longitudinal pilot study[J]. Osteoporos Int,2002,13(7):586-592.
[12]Gregg EW, et al. The epidemiology of quantitative ultrasound:A review of the relationships with bone mass, osteoporosis and fracturerisk[J]. Osteoporosis Int, 1997,7:89-99.
[13]赵文俐,陈贤志,石志峰,等.QCT骨密度测量技术若干问题的探讨[J].中 国骨质疏松杂志2004,10(4)：445-448.
[14]余卫.骨矿含量的测定方法简介及其相关问题[J].国外医学内分泌学分册,2005,25(5)：304-307.
[15]Watts NB. Fundamentals and pitfalls of bone mineral density using dual-energy X-ray absorptiometry(DXA)[J]. Osteoporosis Int,2004,15(11):847-854.
[16]Lozo P, Krpan D, Krvavica A.et al. Bone histology in postmenopausal osteoporosis2variations in cellular activity[J]. Acta MED Croatica,2004,58 (1):5-11.
[17]Zhou S, Turgeman G, Harris SE, et al. Estrogens activate bone morphogenetic protein-2 gene trascription in mouse mesenchymal stem cells[J]. Mol Endocrinol, 2003;17(1):56-66
[18]Bord S, Ireland DC, Beavan SR, et al. The effects of estrogen on osteoprotegerin, RANKL, and estrogen receptor expression in human osetoblast[J]. Bone,2003; 32(2): 136-41.
[19]Tobias JH, Compston JE. Dose estrogen stimulate osteoblast function in post-menopausal women[J]? Bone,1999;24(2):121-4.
[20]Samuels A, Perry MJ, Goodship AE, et al. Is high-dose estrogen-induced osteogenesis in the mouse mediated by an estrogen receptor[J]? Bone,2000; 27(1):41-6.
[21]Yeh JK, Chen MM, Aloia JF. Effects of 17 beta-estradiol administration on cortical and cancellous bone of ovariectomized rats with and without hypophysectomy[J]. Bone,1997,20(5):413-20.
[22]Sibonga JD, Lotinum S, Evans GL, et al. Dose-response effects of 2-methoxyestradiol on estrogen target tissues in the ovariectomized rat[J]. Endocrinology,2003; 144(3):785-92.
[23]Manolagas SC. Birth and death of bone cells:basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis[J]. Endocrine Reviews, 2000,21:115-137.
[24]Kousteni S, Chen JR, Bellido T, et al. Reversal of Bone loss in mice by nongenotrop ic signaling of sex steroids [J]. Science,2002,298:843-846.
[25]Kousteni S, Han L, Chen JR, et al. Kinase-mediated regulation of common transcription factors accounts for the bone-protective effects of sex steroids [J]. J Clin Invest,2003,111:1651-1664.
[26]Chang L, Karin M, Mammalian MAP kinase signalling cascades [J]. Nature, 2001,410:37-40.
[27]Okamoto T, Schlegel A, Scherer PE, et al. Caveolins, a family of scaffolding proteins for organizing "preassembled signaling complexes" at the plasma membrane[J]. J Biol Chem,1998,273:5419-5422.
[28]Kousteni S, Han L, Plotkin L, et al. Non-genotropic regulation of CREB-, C/EBP-, as well as Elk-1-and AP-1-mediated transcription by estrogens:downstream effects of ERK and JNK kinase modulation required for anti-apoptosis[J]. J Bone Miner Res,2002,17:S169.
[29]Lyndon F, Cooper, John C, et al. Estrogen-induced resistance to osteoblast apoptosis is associated with increased hsp27 expression[J]. Journal of Cellular Physiology,2002,185:401-407
[30]Luo XH, Liao EY, Liao HJ, et al. Recombinant matrix metallop roteinase-14 catalytic domain induces apoptosis in human osteoblastic SaOS-2 cells[J]. Journal of Endocrinological Investigation,2003,26:1111-1116.
[31]Zecchi-Orlandini S, Formigli L, Tani A, et al.17beta-estradiol induces apoptosis in the preosteoclastic FLG 29.1 cell line [J]. Biochemical & Biophysical Research Communications,1999,255:680-685.
[32]Kapczuk K, Sowinska-Przepiera E, Friebe Z. Osteoprotegerin/RANKL/RANK system and postmenopausal osteoporosis:The possible therapeutic aspects[J]. Ginekologia Polska,2003,74:323-331.
[33]Shevde NK, Bendixen AC, Dienger KM, et al. Estrogens suppress RANK ligand-induced osteoclast differentiation via a stromal cell independent mechanism involving c-Jun repression [J]. Proc Natl Acad Sci USA,2000,97:7829-7834.
[34]Hofbauer LC, Khoslas S, Dunstan CR, et al.The role of osteoprotegerin and osteoprotegerin ligand in the paracrine regulation of bone resorption[J]. J Bone Miner Res,2000,15(1):2.
[35]Chen JR, Plotkin LI, Aguirre JI, et al. Transient versus sustained phosphorylation and nuclear accumulation of ERKs underlie anti-versus Pro-Apoptotic Effects of Estrogens[J]. J Biol Chem,2005,280:4632-4638.
[36]李秀钧.胰岛素抵抗综合征[M].北京人民卫生出版社,2002：117-124.
[37]郭燕,黄兆民,孟俊非,等.非胰岛素依赖型糖尿病患者骨密度变化的探讨[J].中华放射学杂志,1999,33：705-706.
[38]Balint E, Szabo P, Marshal CP, et al. Glucose-induced inhibition of invitro bone mineralization [J]. Bone,2001,1:21-28.
[39]Fong Y, Edelstein D, Wary ED, et al. Inhibition of matrix-induced bone differentiation by advanced glycation end-products in rats[J]. Diabetologia,1993,36: 802-807.
[40]宋守君.糖耐量减低病人骨代谢生化指标的研究[J].中国基层医药2004,11：215.
[41]Webek B, Baccaria L, Ellsm DE, et al. Bone mass in young patients with type 1 diabetes [J]. Bone Miner,1990,8:22-23.
[42]Wang TM, Hsu JF, Jee WS, et al. Evidence for reduced cancallous bone mass in the spontaneously hypertensive rat [J]. Bone Mineral,1993,20:251-264.
[43]Lee WY, Oh KW, Rhee EJ,.et al. Relationship between subclinical thyroid dysfunction and femoral neck bone mineral density in women[J]. Arch Med Res.2006 May;37(4):511-6.
[44]Caixas A, Tirado R, Vendrell J, et al. Plasma visfatin concentrations increase in both hyper and hypothyroid subjects after normalisation of thyroid function and are not related to insulin resistance, anthropometric or inflammatory parameters [J]. Clin Endocrinol (Oxf). (2009) Feb 16. doi:10.1111/j.1365-2265.2009.03546.x
[45]Welborn TA, Breckenridge A, Rubinstein AH et al. Serum insulin in essential hypertension and peripheral vascular disease[J]. Lancet.1966; 1:1336-1337.
[46]Galderisi M, Caso P, Cicala S.et al. Positive association between circulating free insulin-like growth factor-1 levels and coronary flow reserve in arterial systemic hypertension[J].Am J Hyper tens.2002 Sep; 15(9):766-72.
[47]Tschopp O, Schmid C, Speich R, et al. Pre-transplantation bone disease in patients with primary pulmonary hypertension[J]. Chest,2006,129 (4):1002-1008
[48]Vondracek SF, Voelkel NF, McDermott MT. et al. The relationship between adipokines, body composition, and bone density in men with chronic obstructive pulmonary disease[J]. Int J Chron Obstruct Pulmon Dis.2009;4(2):267-77.
[49]Nakagami H, Morishita R. et. al. Hormones and osteoporosis update:Effect of angiotensin II on bone metabolism[J]. Clin Calcium.2009 Jul;19(7):997-1002.
[50]Shimizu H, Nakagami H, Osako MK. et al. Prevention of osteoporosis by angiotensin-converting enzyme inhibitor in spontaneous hypertensive rats[J]. Hypertens Res.(2009)Jul 10. doi:10.1038/hr.2009.99
[51]The expert committee on the diagnosis and classification of the diabetes mellitus. American Diabetes Association:clinical practice recommendations 2002[J]. Diabetes Care,2002,25(supl 1):sl-sl47
[52]Mancia G, de Backer G, Dominiczak A, et al.2007 Guidelines for the management of arterial hypertension:The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) [J]. Eur Heart J,2007,28 (12):1462-1536.
[53]The Writing Group for the ISCD Position Development Conference. Indications and reporting for dual-energy x-ray absorptiometry[J]. J Clin Densitom,2004,7 (1):37-44.
[54]Kanis JA, Johnell O, Oden A, et al. Ten year probabilities of esteoporotic fractures according to BMD and diagnostic thresholds [J]. Osteoporosis Int,2001,12 (12):989-995.
[55]Almeida M, Han L, Martin-Millan M,et al. Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroids[J]. J Biol Chem,2007,282 (37):27285-27297.
[56]Lin J T, Lane JM. Prevention of hip fractures:medical and Nonmedical Management [J]. Instr Course Lect,2004,53:417-425.
[57]Horiuchi T, Onouchi T, Takahashi M, et al. Effect of soy protein on bone metabolism in postmenopausal Japanese women[J]. Osteoporosis Int,2000,11 (8):7212724.
[58]Wong PK, Christie JJ, Wark JD. The effects of smoking on bone health[J]. Clin Sci (Lond),2007,113 (5):233-241.
[59]Torricelli P, Fini M, Giavaresi G. et al. Intermittent exposure to ethanol vapor affects osteoblast behavior more severely than estrogen deficiency does in vitro study on rat osteoblasts [J]. Toxicology,2007,237 (123):168-176.
[60]Parkhouse WS, Coupland DC, Li C, et al. IGF-1 bioavailability is increased by resistance training in older women with low bone mineral density [J]. Mech Ageing Dev,2000;113(2):75-83.
[61]Kiebzak GM, Leamy LJ, Pierson LM, Nord RH, and Zhang ZY. Measurement of Precision of body composition variables using the Lunar DPX-L densitometer[J]. J Clin Densitometry,2000,3(1):35-41.
[62]Pasco JA, Kotowicz MA, Henry MJ, Panahi S, Seeman E, Nicholson GC. Oral contraceptives and bone mineral density:a population-based study [J]. Am J Obstet Gynecol,2000,182(2):265-269.
[63]朴俊红,庞莲萍,刘忠厚,等.中国人口状况及原发性骨质疏松症诊断标准和发生率[J].中国骨质疏松杂志2002,8(1)：1-7.
[64]曹立,雍宜民,沈惠良.老年股骨颈骨折骨密度、Singh指数的研究[J].中国骨质疏松杂志2001,7(2)：103-106.
[65]胡朝,祝素文,刘加和.糖耐量减低62例骨密度变化[J].中国全科医学2007,10(12)：1025-1026.
[66]Hatton R, Stinpel M, Chanbers TJ. Angiotensin II is generated from angiotensin I by bone cells and stimulates osteoclastic bone resorption invitro[J]. J Endocrinol, 1997,152:5-10.
[67]孙宇,崔燎.心血管疾病与骨质疏松[J].中国骨质疏松杂志,2007,13：520-523.
[68]Dvorak MM, De Joussineau C, Carter DH, Pisit kun T, Knepper MA, Gamba G, et al. Thiazide diuretics directly induce osteoblast differentiation and mineralized nodule formation by interacting wit h a sodium chloride co-transporter in bone [J]. J Am Soc Nephrol,2007,18:2509-2516.
[69]毛惠南,高聪.长效钙拮抗剂对老年高血压患者骨密度的影响研究[J].海南医 学，2005,16：62-63.
[70]Young EW, Morris CD, Holcomb S, McMillan G, McCarron DA. Regulation of parathyroid hormone and vitamin D in essential hypertension[J]. Am J Hyper tens 1995,8 (10 Pt1):957-964.
[71]Antonios TF, MacGregor GA. Deleterious effect s of salt intake other than effects on blood pressure [J]. Clin Exp Pharmacol Physiol,1995,22:180-184.
[72]贺琳,黄力.高血压病与原发性骨质疏松症的相关性研究[J].北京中医药-大学学报(中医临床版,2008,15(2)：1-2
[73]杨荣,刘国平.148例原发性高血压钙代谢失调与骨质疏松的关系[J].内蒙古医学杂志2005,37(1 0)：904-905.
[74]Takagi M, Kasayama S, Yamamoto T, et al. Advanced glycosylation end products stimulate interleukin-6 production by human bone derived cells [J]. Bone Miner Res,2001,12:439.
[1]David M., Mayer B, Ralph A, et al. Impaired Fasting Glucose and Impaired Glucose Tolerance[J]. DIABETES CARE.Mar.2007;Vol 30;No 3.
[2]陈家伦,许曼音.餐后高血糖与心血管疾病[J].中华内分泌代谢杂志2007,22(3)：增录3S-1～增录3S-6.
[3]Cavalot F, Petreli A. Postprandial Blood Glucose Is a stronger Predictor of Cardiovascular Events Than Fasting Blood Glucose in Type 2 Diabetes Mellitus, Particularly in women:Lessons from the San Luigi Gonzaga Diabetes Study[J]. J Clin Endocrinol Metab,2006,91 (3):813-819
[4]Kim SK, Hur KY, Kim HJ, et al. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) [J]. JAMA, 2001,285 (6):2486-2497.
[5]汪俊军,张春妮.胆固醇酯转运蛋白基因变异与血脂和动脉粥样硬化性心血管病的关系[J].医学研究生学报2007,20(1)：76-79.
[6]Iijima R, Nakajima R, Sugi K, et al. Improvement of postprandial hyperglycemia has a positive impact on epicardial flow of entire coronary tree in acute coronary syndromes patients[J]. Circ.2007 Jul;71 (7):1079-85.
[7]Ursula M, Axel MG. Endocrine regulation of energy metabolism:Review of pathobiochemical and clinical chemical aspects of leptin, ghrelin, adiponectin, and resistin [J]. Clini Chemi,2004,50:1511-1625
[8]Hideki Katagiri,Tetsuya Yamada and Yoshitomo Oka. Adiposity and Cardiovascular Disorders:Disturbance of the Regulatory System Consisting of Humoral and Neuronal Signals[J]. Circ. Res.2007;101;27-39.
[9]Amasyali B, Kilic A, Celik T, et al, A new frame in thromboembolic cardiovascular disease:Adipocytokine[J]. Int J Cardiol (2008),doi:10.1016/j. ijcard.2008.06.082
[10]Chenhui Zou, Jianhua Shao. Role of adipocytokines in obesity-associated insulin resistance[J]. Journal of Nutritional Biochemistry,19 (2008) 277-286.
[11]Reilly MP, Lehrke M, Wolfe ML,et al. Bilological backgrand and role of adioponectin as marker for insulin resistance and cardiavascular risk[J]. Circulation,2005,111 (7):932-939.
[12]Sato C, Yasukawa Z, Honda N, et al. Identification and adipocyte differentiation-dependent expression of the unique disialic acid residue in an adipose tissue-specific glycoprotein, adipo Q[J]. J Biol Chem,2001,276(31):28849-56.
[13]Tsao TS, Murrey HE, Hug C,et al. Oligomerization state-dependent activation of NF-kappa B signaling pathway by adipocyte complement-related protein of 30 kDa (Acrp30) [J]. Biol Chem,2002,277 (33):29359-362.
[14]Fukuhara A, Matsuda M, Nishizawa M et al. Visfatin:a protein secreted by visceral fat that mimics the effects of insulin[J]. Science,2005; 307 (5708):426-430.
[15]Ralisch S, Klein J, Lossner U et al. Hormonal regulation of the novel adipocytokine visfatin in 3T3-L1 adipocytes[J]. Endocrinol,2005; 185 (3):R1-R8.
[16]Kloting N, Kloting I. Visfatin:gene expression in isolated adipocytes and sequence analysis in obese WOKW rats compared with lean control rats[J]. Biochem Biophys Res Commun,2005,332:1070-1072.
[17]Zhang YY, Gottardo L, Thompson R, et al. A visfatin promoter polymorphism is associated with low-grade inflammation and type diabetes[J]. Obesity,2006,14(12): 2119-2126.
[18]祝尔建,丁百静,朴云峰,等.内脏素基因多态性与2型糖尿病的关系[J].山东医药，2008,48(7)：27-29
[19]Rajala MW, Qi Y, Patel HR, et al. Regulation of resistin expressionand circulating levels in obesity, diabetes, and fasting[J]. Diabetes,2004,53 (7): 1671-1679.
[20]McTernan CL, McTernan PG, Harte AL, et al. Resistin, central obesity, and type 2 diabetes[J]. Lancet,2002,359 (9300):46-47.
[21]Al-Harithy RN, Al-Ghamdi S. Serum resistin, adiposity and insulin resistance in Saudi women with type 2 diabetes mellitus[J]. Ann SaudiMed,2005,25 (4):283-287.
[22]Meier U, Gressner AM. Endocrine regulation of energy metabolism:review of pathobiochemical and clinical chemic. all aspects of leptin, ghrelin, adiponectin, and resistin[J]. Clinl Chem,2004,50(9):1511-1525.
[23]李慧,邹大进,张乐之,等.血清抵抗素水平与肥胖及2型糖尿病的关系[J].中华糖尿病杂志2004,12(3)：199-201.
[24]郭启煜,高妍.瘦素与胰岛素抵抗[J].国外医学内分泌学分册,2002,22(5)313-316.
[25]Tamer L, Ercan B, Unlu A, et al. The relationship between leptin and lipid in atherosclerosis[J]. Indian Heart J,2002; 54(6):692-6.
[26]Boucher J, Masri B, Daviaud D, et al. Apelin,a newly identified adipokine up-regulated by insulin and obesity [J]. Endocrinology,2005,146(4):1764-1771.
[27]Wei L, Hou X, Tatemoto K. Regulation of apelin mRNA expression by insulin and glucocorticoids in mouse 3T3-L1 adipocytes[J].Regul.Pept,2005,132 (123):27-32.
[28]Ashley EA, Powers J,Chen M, et al. The endogenous peptide apelin potently improves cardiac contractility and reduces cardiac loading in vivo[J].Cardiovasc Res,2005,65 (1):73-82.
[29]Nagpal S, Patel S, Jacobe H, et al. Tazarotene-induced gene 2 (TIG2), a novel retinoid-responsive gene in skin[J]. JInvestDer matol,1997,109 (1):91-95.
[30]TakahashiM, Takahashi Y, Takahashi K, et al. Chemerin enhances insulin signaling and potentiates insulin-stimulated glucose up take in 3T3-L1 adipocytes[J]. FEBS Lett,2008,582 (5):573-578.
[31]Bozaoglu K, Bolton K, McMillan J, et al. Chemerin is a novel adipokine associated with obesity and metabolic syndrome [J]. Endocrinology,2007,148 (10): 4687-4694.
[32]徐炯,李晓惠,顾继安.肿瘤坏死因子α与2型糖尿病关系的探讨[J].上海医学2001,24(4)：227-229.
[33]Akiko Hishinuma, Mitsuru Majima, Hitoshi Kurabayashi. Insulin Resistance in Patients with Stroke is Related to Visceral Fat Obesity and Adipocytokines[J] Journal of Stroke and Cerebrovascular Diseases.2008, Vol.17, No.4:175-180.
[2]王克安,李天麟,向红丁,等.中国糖尿病流行特点研究[J].中华流行病弓噪志1998,19(5)：282-285.
[3]顾东风,吴锡桂.我国老年人群高血压患病率及影响因素[J].中华心血管病杂志,2003,31(6)：654.
[4]田敏,王爱梅.南阳地区老年人高血压的调查分析[J].第四军医大学学报,2005,26(18)：1723-1724.
[5]卫生部疾病预防控制局.疾病的预防与控制…规划与管理[M].北京：人民卫生出版社,2006：119-128.
[6]Nguyen TV, Pocock N. Eisman JA1[J]. J Clin Densitom,2000,3(2):1072-1191.
[7]Monaco MD, Mautino F, Cavanna A. Femur bone mineral density, age and fracture type in 300 hip-fractured women[J]. Aging Clin Exp Res,2002,14(1):47-51.
[8]Keane BE, et al. Quantitative evaluation of bone mineral by radiographic method [J]. Brit J Radio,1959(32):162.
[9]张智海,沈建雄,刘忠厚.中国人骨质疏松症诊断标准回顾性研究[J].中国骨质疏松杂志,2004,10(3)：255-262.
[10]Pejovic-Milic A, McNeill FE, Prestwich WV et al. Development of an accelerator based determination of aluminum burden in peripheral bone by neutron activation analysis [J] Appli radiation&isotopes.1998,49(5):717-719.
[11]Warden SJ, Bennell KL, Matthews B, et al. Quantitative ultrasound assessment of acute bone loss following spinal cord injury:a longitudinal pilot study[J]. Osteoporos Int,2002,13(7):586-592.
[12]Gregg EW, et al. The epidemiology of quantitative ultrasound:A review of the relationships with bone mass, osteoporosis and fracturerisk[J]. Osteoporosis Int, 1997,7:89-99.
[13]赵文俐,陈贤志,石志峰,等.QCT骨密度测量技术若干问题的探讨[J].中 国骨质疏松杂志2004,10(4)：445-448.
[14]余卫.骨矿含量的测定方法简介及其相关问题[J].国外医学内分泌学分册,2005,25(5)：304-307.
[15]Watts NB. Fundamentals and pitfalls of bone mineral density using dual-energy X-ray absorptiometry(DXA)[J]. Osteoporosis Int,2004,15(11):847-854.
[16]Lozo P, Krpan D, Krvavica A.et al. Bone histology in postmenopausal osteoporosis2variations in cellular activity[J]. Acta MED Croatica,2004,58 (1):5-11.
[17]Zhou S, Turgeman G, Harris SE, et al. Estrogens activate bone morphogenetic protein-2 gene trascription in mouse mesenchymal stem cells[J]. Mol Endocrinol, 2003;17(1):56-66
[18]Bord S, Ireland DC, Beavan SR, et al. The effects of estrogen on osteoprotegerin, RANKL, and estrogen receptor expression in human osetoblast[J]. Bone,2003; 32(2): 136-41.
[19]Tobias JH, Compston JE. Dose estrogen stimulate osteoblast function in post-menopausal women[J]? Bone,1999;24(2):121-4.
[20]Samuels A, Perry MJ, Goodship AE, et al. Is high-dose estrogen-induced osteogenesis in the mouse mediated by an estrogen receptor[J]? Bone,2000; 27(1):41-6.
[21]Yeh JK, Chen MM, Aloia JF. Effects of 17 beta-estradiol administration on cortical and cancellous bone of ovariectomized rats with and without hypophysectomy[J]. Bone,1997,20(5):413-20.
[22]Sibonga JD, Lotinum S, Evans GL, et al. Dose-response effects of 2-methoxyestradiol on estrogen target tissues in the ovariectomized rat[J]. Endocrinology,2003; 144(3):785-92.
[23]Manolagas SC. Birth and death of bone cells:basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis[J]. Endocrine Reviews, 2000,21:115-137.
[24]Kousteni S, Chen JR, Bellido T, et al. Reversal of Bone loss in mice by nongenotrop ic signaling of sex steroids [J]. Science,2002,298:843-846.
[25]Kousteni S, Han L, Chen JR, et al. Kinase-mediated regulation of common transcription factors accounts for the bone-protective effects of sex steroids [J]. J Clin Invest,2003,111:1651-1664.
[26]Chang L, Karin M, Mammalian MAP kinase signalling cascades [J]. Nature, 2001,410:37-40.
[27]Okamoto T, Schlegel A, Scherer PE, et al. Caveolins, a family of scaffolding proteins for organizing "preassembled signaling complexes" at the plasma membrane[J]. J Biol Chem,1998,273:5419-5422.
[28]Kousteni S, Han L, Plotkin L, et al. Non-genotropic regulation of CREB-, C/EBP-, as well as Elk-1-and AP-1-mediated transcription by estrogens:downstream effects of ERK and JNK kinase modulation required for anti-apoptosis[J]. J Bone Miner Res,2002,17:S169.
[29]Lyndon F, Cooper, John C, et al. Estrogen-induced resistance to osteoblast apoptosis is associated with increased hsp27 expression[J]. Journal of Cellular Physiology,2002,185:401-407
[30]Luo XH, Liao EY, Liao HJ, et al. Recombinant matrix metallop roteinase-14 catalytic domain induces apoptosis in human osteoblastic SaOS-2 cells[J]. Journal of Endocrinological Investigation,2003,26:1111-1116.
[31]Zecchi-Orlandini S, Formigli L, Tani A, et al.17beta-estradiol induces apoptosis in the preosteoclastic FLG 29.1 cell line [J]. Biochemical & Biophysical Research Communications,1999,255:680-685.
[32]Kapczuk K, Sowinska-Przepiera E, Friebe Z. Osteoprotegerin/RANKL/RANK system and postmenopausal osteoporosis:The possible therapeutic aspects[J]. Ginekologia Polska,2003,74:323-331.
[33]Shevde NK, Bendixen AC, Dienger KM, et al. Estrogens suppress RANK ligand-induced osteoclast differentiation via a stromal cell independent mechanism involving c-Jun repression [J]. Proc Natl Acad Sci USA,2000,97:7829-7834.
[34]Hofbauer LC, Khoslas S, Dunstan CR, et al.The role of osteoprotegerin and osteoprotegerin ligand in the paracrine regulation of bone resorption[J]. J Bone Miner Res,2000,15(1):2.
[35]Chen JR, Plotkin LI, Aguirre JI, et al. Transient versus sustained phosphorylation and nuclear accumulation of ERKs underlie anti-versus Pro-Apoptotic Effects of Estrogens[J]. J Biol Chem,2005,280:4632-4638.
[36]李秀钧.胰岛素抵抗综合征[M].北京人民卫生出版社,2002：117-124.
[37]郭燕,黄兆民,孟俊非,等.非胰岛素依赖型糖尿病患者骨密度变化的探讨[J].中华放射学杂志,1999,33：705-706.
[38]Balint E, Szabo P, Marshal CP, et al. Glucose-induced inhibition of invitro bone mineralization [J]. Bone,2001,1:21-28.
[39]Fong Y, Edelstein D, Wary ED, et al. Inhibition of matrix-induced bone differentiation by advanced glycation end-products in rats[J]. Diabetologia,1993,36: 802-807.
[40]宋守君.糖耐量减低病人骨代谢生化指标的研究[J].中国基层医药2004,11：215.
[41]Webek B, Baccaria L, Ellsm DE, et al. Bone mass in young patients with type 1 diabetes [J]. Bone Miner,1990,8:22-23.
[42]Wang TM, Hsu JF, Jee WS, et al. Evidence for reduced cancallous bone mass in the spontaneously hypertensive rat [J]. Bone Mineral,1993,20:251-264.
[43]Lee WY, Oh KW, Rhee EJ,.et al. Relationship between subclinical thyroid dysfunction and femoral neck bone mineral density in women[J]. Arch Med Res.2006 May;37(4):511-6.
[44]Caixas A, Tirado R, Vendrell J, et al. Plasma visfatin concentrations increase in both hyper and hypothyroid subjects after normalisation of thyroid function and are not related to insulin resistance, anthropometric or inflammatory parameters [J]. Clin Endocrinol (Oxf). (2009) Feb 16. doi:10.1111/j.1365-2265.2009.03546.x
[45]Welborn TA, Breckenridge A, Rubinstein AH et al. Serum insulin in essential hypertension and peripheral vascular disease[J]. Lancet.1966; 1:1336-1337.
[46]Galderisi M, Caso P, Cicala S.et al. Positive association between circulating free insulin-like growth factor-1 levels and coronary flow reserve in arterial systemic hypertension[J].Am J Hyper tens.2002 Sep; 15(9):766-72.
[47]Tschopp O, Schmid C, Speich R, et al. Pre-transplantation bone disease in patients with primary pulmonary hypertension[J]. Chest,2006,129 (4):1002-1008
[48]Vondracek SF, Voelkel NF, McDermott MT. et al. The relationship between adipokines, body composition, and bone density in men with chronic obstructive pulmonary disease[J]. Int J Chron Obstruct Pulmon Dis.2009;4(2):267-77.
[49]Nakagami H, Morishita R. et. al. Hormones and osteoporosis update:Effect of angiotensin II on bone metabolism[J]. Clin Calcium.2009 Jul;19(7):997-1002.
[50]Shimizu H, Nakagami H, Osako MK. et al. Prevention of osteoporosis by angiotensin-converting enzyme inhibitor in spontaneous hypertensive rats[J]. Hypertens Res.(2009)Jul 10. doi:10.1038/hr.2009.99
[51]The expert committee on the diagnosis and classification of the diabetes mellitus. American Diabetes Association:clinical practice recommendations 2002[J]. Diabetes Care,2002,25(supl 1):sl-sl47
[52]Mancia G, de Backer G, Dominiczak A, et al.2007 Guidelines for the management of arterial hypertension:The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) [J]. Eur Heart J,2007,28 (12):1462-1536.
[53]The Writing Group for the ISCD Position Development Conference. Indications and reporting for dual-energy x-ray absorptiometry[J]. J Clin Densitom,2004,7 (1):37-44.
[54]Kanis JA, Johnell O, Oden A, et al. Ten year probabilities of esteoporotic fractures according to BMD and diagnostic thresholds [J]. Osteoporosis Int,2001,12 (12):989-995.
[55]Almeida M, Han L, Martin-Millan M,et al. Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroids[J]. J Biol Chem,2007,282 (37):27285-27297.
[56]Lin J T, Lane JM. Prevention of hip fractures:medical and Nonmedical Management [J]. Instr Course Lect,2004,53:417-425.
[57]Horiuchi T, Onouchi T, Takahashi M, et al. Effect of soy protein on bone metabolism in postmenopausal Japanese women[J]. Osteoporosis Int,2000,11 (8):7212724.
[58]Wong PK, Christie JJ, Wark JD. The effects of smoking on bone health[J]. Clin Sci (Lond),2007,113 (5):233-241.
[59]Torricelli P, Fini M, Giavaresi G. et al. Intermittent exposure to ethanol vapor affects osteoblast behavior more severely than estrogen deficiency does in vitro study on rat osteoblasts [J]. Toxicology,2007,237 (123):168-176.
[60]Parkhouse WS, Coupland DC, Li C, et al. IGF-1 bioavailability is increased by resistance training in older women with low bone mineral density [J]. Mech Ageing Dev,2000;113(2):75-83.
[61]Kiebzak GM, Leamy LJ, Pierson LM, Nord RH, and Zhang ZY. Measurement of Precision of body composition variables using the Lunar DPX-L densitometer[J]. J Clin Densitometry,2000,3(1):35-41.
[62]Pasco JA, Kotowicz MA, Henry MJ, Panahi S, Seeman E, Nicholson GC. Oral contraceptives and bone mineral density:a population-based study [J]. Am J Obstet Gynecol,2000,182(2):265-269.
[63]朴俊红,庞莲萍,刘忠厚,等.中国人口状况及原发性骨质疏松症诊断标准和发生率[J].中国骨质疏松杂志2002,8(1)：1-7.
[64]曹立,雍宜民,沈惠良.老年股骨颈骨折骨密度、Singh指数的研究[J].中国骨质疏松杂志2001,7(2)：103-106.
[65]胡朝,祝素文,刘加和.糖耐量减低62例骨密度变化[J].中国全科医学2007,10(12)：1025-1026.
[66]Hatton R, Stinpel M, Chanbers TJ. Angiotensin II is generated from angiotensin I by bone cells and stimulates osteoclastic bone resorption invitro[J]. J Endocrinol, 1997,152:5-10.
[67]孙宇,崔燎.心血管疾病与骨质疏松[J].中国骨质疏松杂志,2007,13：520-523.
[68]Dvorak MM, De Joussineau C, Carter DH, Pisit kun T, Knepper MA, Gamba G, et al. Thiazide diuretics directly induce osteoblast differentiation and mineralized nodule formation by interacting wit h a sodium chloride co-transporter in bone [J]. J Am Soc Nephrol,2007,18:2509-2516.
[69]毛惠南,高聪.长效钙拮抗剂对老年高血压患者骨密度的影响研究[J].海南医 学，2005,16：62-63.
[70]Young EW, Morris CD, Holcomb S, McMillan G, McCarron DA. Regulation of parathyroid hormone and vitamin D in essential hypertension[J]. Am J Hyper tens 1995,8 (10 Pt1):957-964.
[71]Antonios TF, MacGregor GA. Deleterious effect s of salt intake other than effects on blood pressure [J]. Clin Exp Pharmacol Physiol,1995,22:180-184.
[72]贺琳,黄力.高血压病与原发性骨质疏松症的相关性研究[J].北京中医药-大学学报(中医临床版,2008,15(2)：1-2
[73]杨荣,刘国平.148例原发性高血压钙代谢失调与骨质疏松的关系[J].内蒙古医学杂志2005,37(1 0)：904-905.
[74]Takagi M, Kasayama S, Yamamoto T, et al. Advanced glycosylation end products stimulate interleukin-6 production by human bone derived cells [J]. Bone Miner Res,2001,12:439.
[1]David M., Mayer B, Ralph A, et al. Impaired Fasting Glucose and Impaired Glucose Tolerance[J]. DIABETES CARE.Mar.2007;Vol 30;No 3.
[2]陈家伦,许曼音.餐后高血糖与心血管疾病[J].中华内分泌代谢杂志2007,22(3)：增录3S-1～增录3S-6.
[3]Cavalot F, Petreli A. Postprandial Blood Glucose Is a stronger Predictor of Cardiovascular Events Than Fasting Blood Glucose in Type 2 Diabetes Mellitus, Particularly in women:Lessons from the San Luigi Gonzaga Diabetes Study[J]. J Clin Endocrinol Metab,2006,91 (3):813-819
[4]Kim SK, Hur KY, Kim HJ, et al. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) [J]. JAMA, 2001,285 (6):2486-2497.
[5]汪俊军,张春妮.胆固醇酯转运蛋白基因变异与血脂和动脉粥样硬化性心血管病的关系[J].医学研究生学报2007,20(1)：76-79.
[6]Iijima R, Nakajima R, Sugi K, et al. Improvement of postprandial hyperglycemia has a positive impact on epicardial flow of entire coronary tree in acute coronary syndromes patients[J]. Circ.2007 Jul;71 (7):1079-85.
[7]Ursula M, Axel MG. Endocrine regulation of energy metabolism:Review of pathobiochemical and clinical chemical aspects of leptin, ghrelin, adiponectin, and resistin [J]. Clini Chemi,2004,50:1511-1625
[8]Hideki Katagiri,Tetsuya Yamada and Yoshitomo Oka. Adiposity and Cardiovascular Disorders:Disturbance of the Regulatory System Consisting of Humoral and Neuronal Signals[J]. Circ. Res.2007;101;27-39.
[9]Amasyali B, Kilic A, Celik T, et al, A new frame in thromboembolic cardiovascular disease:Adipocytokine[J]. Int J Cardiol (2008),doi:10.1016/j. ijcard.2008.06.082
[10]Chenhui Zou, Jianhua Shao. Role of adipocytokines in obesity-associated insulin resistance[J]. Journal of Nutritional Biochemistry,19 (2008) 277-286.
[11]Reilly MP, Lehrke M, Wolfe ML,et al. Bilological backgrand and role of adioponectin as marker for insulin resistance and cardiavascular risk[J]. Circulation,2005,111 (7):932-939.
[12]Sato C, Yasukawa Z, Honda N, et al. Identification and adipocyte differentiation-dependent expression of the unique disialic acid residue in an adipose tissue-specific glycoprotein, adipo Q[J]. J Biol Chem,2001,276(31):28849-56.
[13]Tsao TS, Murrey HE, Hug C,et al. Oligomerization state-dependent activation of NF-kappa B signaling pathway by adipocyte complement-related protein of 30 kDa (Acrp30) [J]. Biol Chem,2002,277 (33):29359-362.
[14]Fukuhara A, Matsuda M, Nishizawa M et al. Visfatin:a protein secreted by visceral fat that mimics the effects of insulin[J]. Science,2005; 307 (5708):426-430.
[15]Ralisch S, Klein J, Lossner U et al. Hormonal regulation of the novel adipocytokine visfatin in 3T3-L1 adipocytes[J]. Endocrinol,2005; 185 (3):R1-R8.
[16]Kloting N, Kloting I. Visfatin:gene expression in isolated adipocytes and sequence analysis in obese WOKW rats compared with lean control rats[J]. Biochem Biophys Res Commun,2005,332:1070-1072.
[17]Zhang YY, Gottardo L, Thompson R, et al. A visfatin promoter polymorphism is associated with low-grade inflammation and type diabetes[J]. Obesity,2006,14(12): 2119-2126.
[18]祝尔建,丁百静,朴云峰,等.内脏素基因多态性与2型糖尿病的关系[J].山东医药，2008,48(7)：27-29
[19]Rajala MW, Qi Y, Patel HR, et al. Regulation of resistin expressionand circulating levels in obesity, diabetes, and fasting[J]. Diabetes,2004,53 (7): 1671-1679.
[20]McTernan CL, McTernan PG, Harte AL, et al. Resistin, central obesity, and type 2 diabetes[J]. Lancet,2002,359 (9300):46-47.
[21]Al-Harithy RN, Al-Ghamdi S. Serum resistin, adiposity and insulin resistance in Saudi women with type 2 diabetes mellitus[J]. Ann SaudiMed,2005,25 (4):283-287.
[22]Meier U, Gressner AM. Endocrine regulation of energy metabolism:review of pathobiochemical and clinical chemic. all aspects of leptin, ghrelin, adiponectin, and resistin[J]. Clinl Chem,2004,50(9):1511-1525.
[23]李慧,邹大进,张乐之,等.血清抵抗素水平与肥胖及2型糖尿病的关系[J].中华糖尿病杂志2004,12(3)：199-201.
[24]郭启煜,高妍.瘦素与胰岛素抵抗[J].国外医学内分泌学分册,2002,22(5)313-316.
[25]Tamer L, Ercan B, Unlu A, et al. The relationship between leptin and lipid in atherosclerosis[J]. Indian Heart J,2002; 54(6):692-6.
[26]Boucher J, Masri B, Daviaud D, et al. Apelin,a newly identified adipokine up-regulated by insulin and obesity [J]. Endocrinology,2005,146(4):1764-1771.
[27]Wei L, Hou X, Tatemoto K. Regulation of apelin mRNA expression by insulin and glucocorticoids in mouse 3T3-L1 adipocytes[J].Regul.Pept,2005,132 (123):27-32.
[28]Ashley EA, Powers J,Chen M, et al. The endogenous peptide apelin potently improves cardiac contractility and reduces cardiac loading in vivo[J].Cardiovasc Res,2005,65 (1):73-82.
[29]Nagpal S, Patel S, Jacobe H, et al. Tazarotene-induced gene 2 (TIG2), a novel retinoid-responsive gene in skin[J]. JInvestDer matol,1997,109 (1):91-95.
[30]TakahashiM, Takahashi Y, Takahashi K, et al. Chemerin enhances insulin signaling and potentiates insulin-stimulated glucose up take in 3T3-L1 adipocytes[J]. FEBS Lett,2008,582 (5):573-578.
[31]Bozaoglu K, Bolton K, McMillan J, et al. Chemerin is a novel adipokine associated with obesity and metabolic syndrome [J]. Endocrinology,2007,148 (10): 4687-4694.
[32]徐炯,李晓惠,顾继安.肿瘤坏死因子α与2型糖尿病关系的探讨[J].上海医学2001,24(4)：227-229.
[33]Akiko Hishinuma, Mitsuru Majima, Hitoshi Kurabayashi. Insulin Resistance in Patients with Stroke is Related to Visceral Fat Obesity and Adipocytokines[J] Journal of Stroke and Cerebrovascular Diseases.2008, Vol.17, No.4:175-180.