Buscar en
Endocrinología y Nutrición
Toda la web
Inicio Endocrinología y Nutrición Relación de la hipertrigliceridemia posprandial con la resistencia a la insulin...
Información de la revista
Vol. 53. Núm. 4.
Páginas 237-241 (Abril 2006)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 53. Núm. 4.
Páginas 237-241 (Abril 2006)
Originales
Acceso a texto completo
Relación de la hipertrigliceridemia posprandial con la resistencia a la insulina en pacientes con síndrome metabólico
Association between postprandial hypertriglyceridemia and insulin resistance in patients with the metabolic syndrome
Visitas
8430
F. Cardonaa,b, M. Gonzalo-Marínc, F.J. Tinahonesa,
Autor para correspondencia
fjtinahones@terra.es

Correspondencia: Dr. F.J. Tinahones. Pabellón 5 Sótano. Laboratorio de Investigación. Hospital Civil. Pza. Hospital Civil, s/n. 29009 Málaga. España.
a Servicio de Endocrinología y Nutrición. Hospital Clínico Virgen de la Victoria. Málaga. España
b Fundación IMABIS. Málaga. España
c Servicio de Endocrinología y Nutrición. Hospital Regional Universitario Carlos Haya. Málaga. España
Este artículo ha recibido
Información del artículo
Introducción

Evidencias indican que la hipertrigliceridemia posprandial está relacionada con la resistencia a la insulina. En este estudio se evalúa la relación de la hipertrigliceridemia posprandial con componentes del síndrome metabólico en pacientes no diabéticos con síndrome metabólico.

Pacientes y método

Se estudió a 35 sujetos no diabéticos con síndrome metabólico. Se analizaron la glucosa, el colesterol, los triglicéridos, la creatinina, el colesterol ligado a lipoproteínas de alta densidad, el colesterol ligado a lipoproteínas de baja densidad y el ácido úrico plasmático; se determinó el índice de masa corporal, el índice cintura-cadera, además del aclaramiento de ácido úrico y la fracción excretora de ácido úrico en muestras de orina de 24 h. Se determinaron los triglicéridos posprandiales a las 4 h tras la sobrecarga oral grasa (55 g de lípidos). La resistencia a la insulina se calculó usando el Homeostasis Model Assessment (HOMA).

Resultados

Los triglicéridos posprandiales se correlacionaron con el ácido úrico (r=0,49, p<0,001), el índice de resistencia (r=0,54, p<0,001) y el de secreción a la insulina (r=0,49, p<0,001). El análisis de regression múltiple indicó que los triglicéridos posprandiales son la variable que mejor explica la varianza de la resistencia y la secreción de la insulina (el 32% de la variabilidad de la varianza), desplazando a los otros componentes del síndrome metabólico. El índice de masa corporal y los triglicéridos posprandiales explicaron el 45% de la varianza del HOMA de la resistencia a la insulina.

Conclusión

Se demuestra que los triglicéridos posprandiales explican mejor la variabilidad de los índices HOMA que otros componentes del síndrome metabólico en pacientes con esta enfermedad.

Palabras clave:
Hipertrigliceridemia posprandial
Resistencia a la insulina
Síndrome metabólico
Background

There is evidence indicating that postprandial hypertriglyceridemia might be related to insulin resistance. We studied the association between postprandial hypertriglyceridemia and factors involved in metabolic syndrome in a group of non-diabetic patients with this syndrome.

Patients and method

Thirty-five nondiabetic persons with metabolic syndrome were studied. Plasma levels of glucose, cholesterol, triglycerides, creatinine, high density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, and uric acid. We also measured height and weight, waist-to-hip ratio, uric acid clearance and its excretion fraction in 24 hour urine samples. Postprandial triglycerides were determined 4 hours after fat overload (55 g of lipids). Insulin resistance was calculated using the homeostasis model assessment (HOMA).

Results

Postprandial triglycerides were correlated with uric acid (r=0.49, p<0.001), insulin resistance index (r=0.54, p<0.001) and insulin secretion index (r=0.49, p<0.001). Multiple regression analysis showed that postprandial triglycerides were the variable that best accounted for the variance in insulin resistance and insulin secretion (32% of the variability in the variance), displacing the other components of the metabolic syndrome. Body mass index and postprandial triglycerides accounted for 45% of the variance in insulin resistance measured by the HOMA.

Conclusions

This study demonstrates that postprandial triglycerides play a greater role in variability in the HOMA indices than other components of the metabolic syndrome in patients with this syndrome.

Key words:
Postprandial hypertriglyceridemia
Insulin resistance
Metabolic syndrome
El Texto completo está disponible en PDF
Bibliografía
[1.]
L. Groop, M. Orho-Melander.
The dysmetabolic syndrome.
J Intern Med, 250 (2001), pp. 105-120
[2.]
B. Balkau, M.A. Charles.
Comment on the provisional report from the WHO consultation. European Group for the Study of Insulin Resistance (EGIR).
Diabet Med, 16 (1999), pp. 442-443
[3.]
K. Alberti, P. Zimmet, W. Consultation.
Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1. Diagnosis and classification of diabetes mellitus, provisional report of a WHO consultation.
[4.]
F.H. De Man, M.C. Cabezas, H.H. Van Barlingen, D.W. Erkelens, T.W. De Bruin.
Triglyceride-rich lipoproteins in non-insulin-dependent diabetes mellitus: post-prandial metabolism and relation to premature atherosclerosis.
Eur J Clin Invest, 26 (1996), pp. 89-108
[5.]
M.A. Austin.
Plasma triglyceride and coronary heart disease.
Arterioscler Thromb, 11 (1991), pp. 2-14
[6.]
S.A. Brown, L.E. Chambless, A.R. Sharrett, A.M. Gotto Jr, W. Patsch.
Postprandial lipemia: reliability in an epidemiologic field study.
Am J Epidemiol, 136 (1992), pp. 538-545
[7.]
D.B. Zilversmit.
Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins.
Clin Chem, 41 (1995), pp. 153-158
[8.]
J.R. Patsch, G. Miesenbock, T. Hopferwieser, V. Muhlberger, E. Knapp, J.K. Dunn, et al.
Relation of triglyceride metabolism and coronary artery disease. Studies in the postprandial state.
Arterioscler Thromb, 12 (1992), pp. 1336-1345
[9.]
M. Nikkila, T. Solakivi, T. Lehtimaki, T. Koivula, P. Laippala, B. Astrom.
Postprandial plasma lipoprotein changes in relation to apolipoprotein E phenotypes and low density lipoprotein size in men with and without coronary artery disease.
Atherosclerosis, 106 (1994), pp. 149-157
[10.]
J.S. Cohn, J.R. McNamara, S.D. Cohn, J.M. Ordovas, E.J. Schaefer.
Postprandial plasma lipoprotein changes in human subjects of different ages.
J Lipid Res, 29 (1988), pp. 469-479
[11.]
J.C. Cohen, T.D. Noakes, A.J. Benade.
Serum triglyceride responses to fatty meals: effects of meal fat content.
Am J Clin Nutr, 47 (1988), pp. 825-827
[12.]
G.F. Lewis, N.M. O’Meara, P.A. Soltys, J.D. Blackman, P.H. Iverius, A.F. Druetzler, et al.
Postprandial lipoprotein metabolism in normal and obese subjects: comparison after the vitamin A fatloading test.
J Clin Endocrinol Metab, 71 (1990), pp. 1041-1050
[13.]
J.E. Ryu, G. Howard, T.E. Craven, M.G. Bond, A.P. Hagaman, J.R. Crouse 3rd.
Postprandial triglyceridemia and carotid atherosclerosis in middle-aged subjects.
Stroke, 23 (1992), pp. 823-828
[14.]
M. Cassader, R. Gambino, G. Ruiu, S. Marena, P. Bodoni, G. Pagano.
Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.
Aging (Milano), 8 (1996), pp. 421-428
[15.]
M. Syvanne, M.R. Taskinen.
Lipids and lipoproteins as coronary risk factors in non-insulin-dependent diabetes mellitus.
Lancet, 350 (1997), pp. SI20-SI23
[16.]
N.M. O’Meara, G.F. Lewis, V.G. Cabana, P.H. Iverius, G.S. Getz, K.S. Polonsky.
Role of basal triglyceride and high density lipoprotein in determination of postprandial lipid and lipoprotein responses.
J Clin Endocrinol Metab, 75 (1992), pp. 465-471
[17.]
B. Eliasson, N. Mero, M.R. Taskinen, U. Smith.
The insulin resistance syndrome and postprandial lipid intolerance in smokers.
Atherosclerosis, 129 (1997), pp. 79-88
[18.]
J. Jeppesen, C.B. Hollenbeck, M.Y. Zhou, A.M. Coulston, C. Jones, Y.D. Chen, et al.
Relation between insulin resistance, hyperinsulinemia, postheparin plasma lipoprotein lipase activity, and postprandial lipemia.
Arterioscler Thromb Vasc Biol, 15 (1995), pp. 320-324
[19.]
J. Schrezenmeir, S. Fenselau, I. Keppler, J. Abel, B. Orth, C. Laue, et al.
Postprandial triglyceride high response and the metabolic syndrome.
Ann N Y Acad Sci, 827 (1997), pp. 353-368
[20.]
E.S. Ford, W.H. Giles, W.H. Dietz.
Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey.
JAMA, 287 (2002), pp. 356-359
[21.]
D.R. Matthews, J.P. Hosker, A.S. Rudenski, B.A. Naylor, D.F. Treacher, R.C. Turner.
Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.
Diabetologia, 28 (1985), pp. 412-419
[22.]
Consensus Development Conference Report Consensus Development Conference on Insulin Resistance. 5-6 November 1997. American Diabetes Association. Diabetes Care. 1998;21:310-4.
[23.]
S.M. Grundy, G.L. Vega.
Two different views of the relationship of hypertriglyceridemia to coronary heart disease. Implications for treatment.
Arch Intern Med, 152 (1992), pp. 28-34
[24.]
F. Cardona, S. Morcillo, M. Gonzalo-Marín, F.J. Tinahones.
The apolipoprotein E genotype predicts postprandial hypertriglyceridemia in patients with the metabolic syndrome.
J Clin Endocrinol Metab, 90 (2005), pp. 2972-2975
[25.]
S.M. Haffner, E. Kennedy, C. González, M.P. Stern, H. Miettinen.
A prospective analysis of the HOMA model. The Mexico City Diabetes Study.
Diabetes Care, 19 (1996), pp. 1138-1141
[26.]
S.M. Haffner, H. Miettinen, M.P. Stern.
The homeostasis model in the San Antonio Heart Study.
Diabetes Care, 20 (1997), pp. 1087-1092
[27.]
E. Bonora, G. Targher, M. Alberiche, R.C. Bonadonna, F. Saggiani, M.B. Zenere, et al.
Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity.
Diabetes Care, 23 (2000), pp. 57-63
[28.]
D. Panarotto, P. Remillard, L. Bouffard, P. Maheux.
Insulin resistance affects the regulation of lipoprotein lipase in the postprandial period and in an adipose tissue-specific manner.
Eur J Clin Invest, 32 (2002), pp. 84-92
[29.]
M. Axelsen, U. Smith, J.W. Eriksson, M.R. Taskinen, P.A. Jansson.
Postprandial hypertriglyceridemia and insulin resistance in normoglycemic first-degree relatives of patients with type 2 diabetes.
Ann Intern Med, 131 (1999), pp. 27-31
[30.]
G. Boden.
Interaction between free fatty acids and glucose metabolism.
Curr Opin Clin Nutr Metab Care, 5 (2002), pp. 545-549
[31.]
G. Boden.
Role of fatty acids in the pathogenesis of insulin resistance and NIDDM.
Diabetes, 46 (1997), pp. 3-10
[32.]
P.D. Dworatzek, R.A. Hegele, T.M. Wolever.
Postprandial lipemia in subjects with the threonine 54 variant of the fatty acid-binding protein 2 gene is dependent on the type of fat ingested.
Am J Clin Nutr, 79 (2004), pp. 1110-1117
[33.]
P. Arner.
Insulin resistance in type 2 diabetes: role of fatty acids.
Diabetes Metab Res Rev, 18 (2002), pp. S5-S9

Este estudio fue financiado con una beca predoctoral Fundación Hospital Carlos Haya, con la Red de Centros de Metabolismo y Nutrición (RCMN C03/08) del Instituto de Salud Carlos III. Madrid. España.

Copyright © 2006. Sociedad Española de Endocrinología y Nutrición
Opciones de artículo
Herramientas
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