covid
Buscar en
Endocrinología y Nutrición
Toda la web
Inicio Endocrinología y Nutrición Síndrome metabólico
Información de la revista
Vol. 54. Núm. 9.
Páginas 473-478 (noviembre 2007)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 54. Núm. 9.
Páginas 473-478 (noviembre 2007)
Revisiones
Acceso a texto completo
Síndrome metabólico
Metabolic syndrome
Visitas
31824
Amaya Aleixandre
Autor para correspondencia
amaya@med.ucm.es

Correspondencia: Dra. M.A. Aleixandre. Departamento de Farmacología. Facultad de Medicina. Universidad Complutense. 28040 Madrid. España.
, Marta Miguel
Departamento de Farmacología. Facultad de Medicina. Universidad Complutense. Madrid. España
Este artículo ha recibido
Información del artículo
Resumen
Bibliografía
Descargar PDF
Estadísticas

El síndrome metabólico se considera una asociación de problemas de salud que tienen como componente patogénico fundamental la resistencia a la insulina. El diagnóstico implica 3 o más de los siguientes factores de riesgo: obesidad abdominal, triglicéridos altos, colesterol de las lipoproteínas de alta densidad bajo, hipertensión e hiperglucemia en ayunas. El síndrome se relaciona con cambios en la proliferación del músculo liso vascular y con crecimiento y disfunción endotelial. Los adipocitos de estos pacientes segregan ácidos grasos libres y moléculas biológicamente activas; entre ellas, factor de necrosis tumoral alfa, leptina y adiponectina. El paciente debe enfrentarse con un cambio de hábitos en su alimentación y actividad física. Para la dislipemia se utilizan estatinas y fibratos; para mejorar la sensibilidad a la insulina, biguanidas y tiazolidinedionas. Como antihipertensivos se recomienda fármacos que inhiban la formación o los receptores de la angiotensina II.

Palabras clave:
Síndrome metabólico
Resistencia a la insulina
Diabetes
Dislipemia
Obesidad
Hipertensión

Metabolic syndrome is described as a group of health problems whose fundamental pathogenic component is insulin resistance. Diagnosis involvesthe presence of 3 or more of the following risk factors: abdominal obesity, high triglyceride levels, low high-density lipoprotein cholesterol, hypertension, and fasting hyperglycemia. This syndrome is associated with changes in vascular smooth muscle proliferation, stimulus of endothelial growth, and endothelial dysfunction. The adipocytes of patients with metabolic syndrome segregate free fatty acids and biologically active molecules, such as tumor necrosis factor-alpha, leptin and adiponectin. These patients should alter their eating and exercise habits. Statins and fibrates are administered for dyslipidemia. To improve insulin sensitivity, biguanides and thiazolidinediones are used. The recommended anti-hypertensive agents are angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor antagonists.

Key words:
Metabolic syndrome
Insulin resistance
Diabetes
Dyslipidemia
Obesity
Hypertension
El Texto completo está disponible en PDF
Bibliografía
[1.]
G. Reaven.
Role of insulin resistance in human disease.
Diabetes, 37 (1988), pp. 1595-1607
[2.]
N.M. Kaplan.
The deadly quartet. Upper-body obesity, glucose intolerance, hypertriglyceridemia, and hypertension.
Arch Intern Med, 149 (1989), pp. 1514-1520
[3.]
I. Zavaroni, E. Bonora, M. Pagliara, E. Dall’Aglio, L. Luchetti, G. Buonanno.
Risk factors for coronary artery disease in healthy persons with hypersinulinemia and normal glucose tolerance.
N Engl J Med, 320 (1989), pp. 702-706
[4.]
WHO consultation: Definition, diagnosis and classification of diabetes mellitus and its complications WHO/NCD/NCS/99.2;31-3.
[5.]
F. Facchini, Y.-D.I. Chen, C.B. Hollenbeck, G.M. Reaven.
Relationship between resistance to insulin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration.
JAMA, 266 (1991), pp. 3008-3011
[6.]
G.M. Reaven, Y.-D.I. Chen, J. Jeppesen, P. Maheux, R.M. Krauss.
Insulin resistance and hyperinsulinemia in individuals with small, dense, low density lipoprotein particles.
J Clin Invest, 92 (1993), pp. 141-146
[7.]
J.S. Yudkin.
Abnormalities of coagulation and fibrinolysis in insulin resistance.
Diabetes Care, 22 (1999), pp. C25-C30
[8.]
P.A. Sarafidis, P.M. Nilsson.
The metabolic syndrome: a glance at its history.
[9.]
L. Groop, M. Orho-Melander.
The dysmetabolic syndrome.
J Intern Med, 250 (2001), pp. 105-120
[10.]
P.J. Anderson, J.A. Critchley.
Factor analysis of the metabolic syndrome: obesity vs. insulin resistance as the central abnormality.
Int J Obes Relat Metab Disord, 25 (2001), pp. 1782-1788
[11.]
D.W. Erkelens.
Insulin resistance syndrome and type 2 diabetes mellitus.
Am J Cardiol, 88 (2001), pp. J38-J42
[12.]
Third report of the National Cholesterol Education Program (NCEP) Expert Panel on the detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment panel III). Executive summary. NIH Publication 01. JAMA. 2001;285:2486-97.
[13.]
H.F. Lebovitz.
Insulin resistance: definition and consequences.
Exp Clin End Diabetes, 109 (2001), pp. 135-148
[14.]
K.K. Berneis, R.M. Krauss.
Metabolic origins and clinical significance of LDL heterogeneity.
J Lipid Res, 43 (2002), pp. 363-379
[15.]
H. Ueno.
Blood flow regulates the development of vascular hypertrophy, smooth muscle cell proliferation, and endothelial cell oxide synthase in hypertension.
Hypertension, 36 (2000), pp. 8993
[16.]
G. Arcaro, A. Cretti.
Insulin causes endothelial dysfunction in humans: Sites and mechanisms.
Circulation, 105 (2002), pp. 576-582
[17.]
A.D. Liese, H.W. Hense, A. Doring.
Microalbuminuria, central adiposity and hypertension in the non-diabetic urban population of the MONICA Augsburg Survey 1994/95.
J Human Hypertens, 5 (2001), pp. 799-804
[18.]
E.D. Crook.
The genetics of human hypertension.
Semin Nephrol, 22 (2002), pp. 27-34
[19.]
J.P. Despres.
Health consequences of visceral obesity.
Ann Med, 3 (2001), pp. 534-541
[20.]
K. Maeda, K. Okubo, I. Shimomura, K. Mizuno, Y. Matsuzawa, K. Matsubara.
Analysis of an expression profile of genes in the human adipose tissue.
Gene, 190 (1997), pp. 227-235
[21.]
T. Funahashi, T. Nakamura, I. Shimomura, K. Maeda, H. Kuriyama, M. Takahashi, et al.
Role of adipocytokines on the pathogenesis of atherosclerosis in visceral obesity.
Int Med, 38 (1999), pp. 202-206
[22.]
G.F. Adami, G. Ravera.
Metabolic syndrome in severely obese patients.
Obes Surg, 11 (2001), pp. 543-545
[23.]
K.N. Frayn.
Adipose tissue and the insulin resistance syndrome.
Proc Nutr Soc, 60 (2001), pp. 375-380
[24.]
G.S. Hotamisligil, N.S. Shargill, B.M. Spiegelman.
Adipose expression of tumor necrosis factor-alpha: direct role in obesitylinked insulin resistance.
Science, 259 (1993), pp. 87-91
[25.]
Y. Zhang, R. Proenca, M. Maffei, M. Barone, L. Leopold, J.M. Friedman.
Positional cloning of the mouse obese gene and its human homologue.
Nature, 372 (1994), pp. 425-432
[26.]
M. Takahasi, T. Funahashi, I. Shimomura, K. Miyaoka, Y. Matsuzawa.
Plasma leptin and body fat distribution.
Horm Metab Res, 28 (1996), pp. 751-752
[27.]
F. Leyva, I.F. Godsland.
Hyperleptinemia as a component of a Metabolic Syndrome of cardiovascular risk.
Arterioscler Throm Vasc Biol, 18 (1998), pp. 928-933
[28.]
P. Zimmet, E.J. Buyku.
Etiology of the metabolic syndrome: potential role of insuline resistance, leptin resistance and other players.
Ann NY Acad Sci, 892 (1999), pp. 25-44
[29.]
K. Maeda, K. Okubo, I. Shimomura, T. Funahashi, Y. Matsuzawa, Matsubara.
CDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (Adipose Mose Abundant gene transcript 1).
Biochem Biophys Res Comun, 221 (1996), pp. 286-289
[30.]
J. Malik, V. Melenovsky, D. Wichterle, T. Heast, J. Simek, R. Ceska, et al.
Both fenofibrate and atorvastatin improve vascular reactivity in combined hyperlipemia.
Cardiovasc Res, 52 (2001), pp. 290-298
[31.]
UK Prospective Diabetes Study (UKPDS) Group.
Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34).
Lancet, 352 (1998), pp. 854-865
[32.]
A.C. Robinson, J. Burke, S. Robinson.
The effects of metformin on glycemic control and serum lipids in isulin-treated NIDDM patients with sub optimal metabolic control.
Diabetes Care, 21 (1998), pp. 701-705
[33.]
C.A. Reasner.
Where thiazolinediones will fit.
Diabetes Metab Res Rev, 8 (2002), pp. 530-535
[34.]
A.G. Pittas, A.S. Greenberg.
Thiazolidinediones in the treatment of diabetes.
Expert Opin Pharmacother, 3 (2002), pp. 529-540
[35.]
F.M. Marters, F.L. Visseren.
Metabolic and additional vascular effects of thiazolinediones.
Drug, 62 (2002), pp. 1463-1480
[36.]
R. Feldman.
ACE inhibitors versus AT1 blockers in the treatment of hypertension and Syndrome X.
J Cardiol, 16 (2000), pp. E41-E44
Copyright © 2007. Sociedad Española de Endocrinología y Nutrición
Opciones de artículo
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos