The metabolic syndrome: metabolic changes with vascular consequences

European Journal of Clinical Investigation - Tập 37 Số 1 - Trang 8-17 - 2007
Annemarie M.J. Wassink1, Jobien K. Olijhoek2, Frank L.J. Visseren2
1Department of Vascular Medicine, University Medical Centre, Utrecht, The Netherlands
2University Medical Centre,, Utrecht, the Netherlands

Tóm tắt

AbstractDespite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor‐alpha (TNF‐α) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF‐α are produced in abundance by adipocytes, whereas the production of adiponectin, an anti‐inflammatory adipokine, is reduced. This imbalanced production of pro‐ and anti‐inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. The role of several recently discovered adipokines such as resistin, visfatin and retinol‐binding protein (RBP)‐4 in the pathogenesis of insulin resistance is increasingly understood. Insulin resistance induces several metabolic changes, including hyperglycaemia, dyslipidaemia and hypertension, all leading to increased cardiovascular risk. In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF‐α concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. Adipocyte dysfunction could therefore be regarded as the common antecedent of both insulin resistance and atherosclerosis and functions as the link between obesity and cardiovascular disease. Targeting the dysfunctional adipocyte may reduce the risk for both cardiovascular disease and the development of type 2 diabetes. Although lifestyle intervention remains the cornerstone of therapy in improving insulin sensitivity and its associated metabolic changes, medical treatment might prove to be important as well.

Từ khóa


Tài liệu tham khảo

10.1001/jama.285.19.2486

10.2337/diabetes.52.11.2652

10.2337/diab.46.2.S9

10.1093/aje/kwf145

10.2337/diacare.26.11.3153

10.2337/diabetes.52.5.1210

10.2337/diacare.24.4.683

10.1001/jama.288.21.2709

10.2337/dc05-2307

10.2337/diacare.28.9.2289

10.2337/dc06-0671

10.1002/(SICI)1096-9136(199807)15:7<539::AID-DIA668>3.0.CO;2-S

10.1016/S0140-6736(05)67402-8

Balkau B, 1999, Comment on the provisional report from the WHO consultation, European Group for Study Insulin Resistance (EGIR) Diabet Med, 16, 442

10.1161/CIRCULATIONAHA.105.169404

10.1016/j.ecl.2004.03.005

10.1001/jama.287.3.356

10.1046/j.1365-2362.32.s3.2.x

10.1007/s001250051387

10.1001/archinte.163.4.427

10.1016/j.metabol.2004.04.017

10.1161/CIRCULATIONAHA.106.625848

10.1016/j.tem.2005.08.004

10.1097/01.hco.0000221579.25878.11

10.1126/science.7678183

10.1172/JCI117495

10.1126/science.271.5249.665

10.1074/jbc.271.22.13018

10.1016/S0021-9258(18)54714-1

10.1007/s001250050350

10.1210/en.139.12.4928

10.2337/diab.46.1.3

10.1016/S0002-9149(02)02554-7

10.1172/JCI10583

10.1172/JCI115399

10.1172/JCI117252

10.1172/JCI118742

10.2337/diabetes.48.9.1836

10.1161/01.HYP.0000163475.04421.e4

10.1046/j.1365-2362.32.s3.3.x

10.1172/JCI5479

10.2337/diabetes.50.4.810

10.1161/01.CIR.67.5.968

10.1053/euhj.2001.2889

10.1016/S0140-6736(05)67663-5

10.1046/j.1365-2362.32.s3.4.x

10.1016/S1043-2760(00)00301-5

10.5551/jat.10.234

10.2337/diabetes.52.7.1779

10.1172/JCI117899

10.1172/JCI117936

10.1210/jc.84.1.272

10.1152/ajpendo.2001.280.5.E745

10.1006/bbrc.1999.0255

10.1161/01.ATV.20.6.1595

10.2337/diabetes.51.6.1884

10.2337/diabetes.52.2.239

10.1210/jcem.86.5.7463

10.2337/diabetes.51.10.2968

10.1016/S0140-6736(02)09335-2

10.1161/01.ATV.0000208363.85388.8f

10.2337/diacare.26.8.2442

10.1530/eje.0.1480293

10.1038/35053000

10.1111/j.1462-8902.2004.00334.x

10.1161/01.CIR.0000155620.10387.43

10.1126/science.1097243

10.2337/diabetes.54.10.2911

10.1056/NEJMoa054862

10.1038/nature03711

10.1016/j.ecl.2004.12.001

10.2337/diacare.14.3.173

10.1056/NEJM198708063170605

10.1056/NEJM199602083340607

10.2337/diacare.26.3.805

Haffner SM, 1996, Metabolic precursors of hypertension, The San Antonio Heart Study Arch Intern Med, 156, 1994

10.2337/diabetes.47.2.270

10.1097/00004872-199917080-00017

Vaccaro O, 1996, Does impaired glucose tolerance predict hypertension? A prospective analysis, Diabetologia, 39, 70, 10.1007/BF00400415

10.1210/jcem-62-6-1302

10.1172/JCI111776

10.1007/BF00274259

10.1007/BF00405088

10.1161/01.HYP.0000052314.95497.78

10.1161/CIRCULATIONAHA.105.568055

10.1007/s00125-005-1824-1

Landsberg L, 1986, Diet, obesity and hypertension: an hypothesis involving insulin, the sympathetic nervous system, and adaptive thermogenesis, Q J Med, 61, 1081

10.1161/01.HYP.17.5.669

10.1161/01.HYP.21.2.136

Baron AD, 1994, Hemodynamic actions of insulin, Am J Physiol, 267, E187

10.1046/j.1365-2796.2000.00671.x

10.1111/j.1365-2362.2004.01412.x

10.1152/ajpheart.00092.2005

10.1161/01.HYP.0000036448.44066.53

Eckel RH, 1995, Alterations in lipoprotein lipase in insulin resistance, Int J Obes Relat Metab Disord, 19, S16

10.1161/01.ATV.15.11.1819

10.2337/diab.45.3.S27

10.1007/BF00401766

10.1172/JCI116541

10.1016/j.jacc.2003.10.061

10.1016/j.amjcard.2003.09.028

10.1093/aje/152.10.897

10.1016/j.ecl.2004.03.002

10.1007/s00125-002-0800-2

10.1161/01.CIR.96.9.3042

10.1161/01.HYP.0000083488.67550.B8

10.1016/j.jacc.2005.06.082

10.1161/01.ATV.20.10.2205

10.1161/01.CIR.101.18.2149

10.1161/01.RES.73.1.205

10.1161/01.ATV.0000065195.22904.FA

10.1093/eurheartj/ehl079

10.1161/01.CIR.100.25.2473

Eck SL, 1993, Inhibition of phorbol ester‐induced cellular adhesion by competitive binding of NF‐kappa B in vivo, Mol Cell Biol, 13, 6530

10.1097/00041433-199608000-00008

10.1007/BF00405009

10.2337/diacare.14.6.461

10.2337/diacare.2.2.131

10.2337/diacare.2.2.154

10.1136/hrt.71.3.293

10.1056/NEJM199604113341504

10.2337/diabetes.45.6.736

10.1001/archinte.160.8.1160

10.1046/j.1365-2796.2003.01064.x

10.1007/s00125-004-1433-4

10.1007/s11892-003-0018-9

10.1172/JCI114644

10.2337/diabetes.49.7.1231

10.1161/01.ATV.0000164044.42910.6b

10.1161/01.CIR.102.11.1296

10.1161/01.CIR.103.8.1057

10.1161/01.CIR.0000018622.84402.FF

10.1074/jbc.M307878200

10.1210/jc.2003-031012

10.1161/01.ATV.0000048856.22331.50

10.1001/jama.291.14.1730

10.1681/ASN.V131134

10.1016/S0140-6736(02)09335-2

10.1210/jc.2005-0825

10.1161/CIRCULATIONAHA.106.618918

Thông tin
Thông tin xuất bản

European Journal of Clinical Investigation

Tập 37 Số 1

8-17

Thông tin tác giả