The metabolic syndrome

被引:5791
作者
Eckel, RH
Grundy, SM
Zimmet, PZ
机构
[1] Univ Colorado, Div Endocrinol Diabet & Metab, Aurora, CO 80045 USA
[2] Hlth Sci Ctr, Aurora, CO 80045 USA
[3] Univ Texas, SW Med Ctr Dallas, Dallas, TX 75235 USA
[4] Int Diabet Inst, Melbourne, Vic, Australia
关键词
D O I
10.1016/S0140-6736(05)66378-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The metabolic syndrome is a common metabolic disorder that results from the increasing prevalence of obesity. The disorder is defined in various ways, but in the near future a new definition(s) will be applicable worldwide. The pathophysiology seems to be largely attributable to insulin resistance with excessive flux of fatty acids implicated. A proinflammatory state probably contributes to the syndrome. The increased risk for type 2 diabetes and cardiovascular disease demands therapeutic attention for those at high risk. The fundamental approach is weight reduction and increased physical activity; however, drug treatment could be appropriate for diabetes and cardiovascular disease risk reduction.
引用
收藏
页码:1415 / 1428
页数:14
相关论文
共 166 条
[11]   Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S [J].
Ballantyne, CM ;
Olsson, AG ;
Cook, TJ ;
Mercuri, MF ;
Pedersen, TR ;
Kjekshus, J .
CIRCULATION, 2001, 104 (25) :3046-3051
[12]   Metabolic syndrome and renal sodium handling in three ethnic groups living in England [J].
Barbato, A ;
Cappuccio, FP ;
Folkerd, EJ ;
Strazzullo, P ;
Sampson, B ;
Cook, DG ;
Alberti, KGMM .
DIABETOLOGIA, 2004, 47 (01) :40-46
[13]  
Bays Harold E, 2003, Prev Cardiol, V6, P179, DOI 10.1111/j.1520-037X.2003.03142.x
[14]   Simvastatin does not have a clinically significant pharmacokinetic interaction with fenofibrate in humans [J].
Bergman, AJ ;
Murphy, G ;
Burke, J ;
Zhao, JJ ;
Valesky, R ;
Liu, L ;
Lasseter, KC ;
He, WL ;
Prueksaritanont, T ;
Qiu, Y ;
Hartford, A ;
Vega, JM ;
Paolini, JE .
JOURNAL OF CLINICAL PHARMACOLOGY, 2004, 44 (09) :1054-1062
[15]   Free fatty acids in obesity and type 2 diabetes:: defining their role in the development of insulin resistance and β-cell dysfunction [J].
Boden, G ;
Shulman, GI .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 2002, 32 :14-23
[16]   The Metabolic Syndrome is an independent predictor of cardiovascular disease in Type 2 diabetic subjects. Prospective data from the Verona Diabetes Complications Study [J].
Bonora, E ;
Targher, G ;
Formentini, G ;
Calcaterra, F ;
Lombardi, S ;
Marini, F ;
Zenari, L ;
Saggiani, F ;
Poli, M ;
Perbellini, S ;
Raffaelli, A ;
Gemma, L ;
Santi, L ;
Bonadonna, RC ;
Muggeo, M .
DIABETIC MEDICINE, 2004, 21 (01) :52-58
[17]   Biochemical mechanism of lipid-induced impairment of glucose-stimulated insulin secretion and reversal with a malate analogue [J].
Boucher, A ;
Lu, DH ;
Burgess, SC ;
Telemaque-Potts, S ;
Jensen, MV ;
Mulder, H ;
Wang, MY ;
Unger, RH ;
Sherry, AD ;
Newgard, CB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (26) :27263-27271
[18]   INCREASED APO-A-I AND APO-A-II FRACTIONAL CATABOLIC RATE IN PATIENTS WITH LOW HIGH-DENSITY LIPOPROTEIN-CHOLESTEROL LEVELS WITH OR WITHOUT HYPERTRIGLYCERIDEMIA [J].
BRINTON, EA ;
EISENBERG, S ;
BRESLOW, JL .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 87 (02) :536-544
[19]   Bariatric surgery and long-term control of morbid obesity [J].
Brolin, RE .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2002, 288 (22) :2793-2796
[20]   A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance [J].
Bruning, JC ;
Michael, MD ;
Winnay, JN ;
Hayashi, T ;
Horsch, D ;
Accili, D ;
Goodyear, LJ ;
Kahn, CR .
MOLECULAR CELL, 1998, 2 (05) :559-569