Determinar los factores de riesgo y el régimen nutricional en pacientes con síndrome metabólico por resistencia a la insulina
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https://doi.org/10.23857/dc.v10i1.3700Palabras clave:
Resistencia a la insulina, síndrome metabólico, etiopatogenia, insulinemia, glicemiaResumen
El síndrome de resistencia a la insulina, actualmente más conocido como síndrome metabólico (SM), se produce cuando las células de los músculos, grasa e hígado no responden bien a la insulina y no pueden absorber la glucosa de la sangre fácilmente, siendo una condición que puede desencadenar enfermedades cardiovasculares y diabetes, por lo que se debe realizar una detección precoz y un manejo oportuno. La resistencia a la insulina (RI) es una condición metabólica central en la etiopatogenia del SM y su diagnóstico puede efectuarse con mediciones de insulinemia y glicemia en ayuno o con la prueba de tolerancia oral a la glucosa con curva de insulinemia. En su mayor parte el control de este problema de salud se logra con cambios en estilo de vida, incluyendo modificaciones en la dieta y en el patrón de actividad física junto con reducción en el peso y grasa corporal, como también así algunas terapias farmacológicas orientadas a mejorar la sensibilidad a la insulina han sido recomendadas en consensos internacionales, cuando fracasan las terapias no farmacológicas.
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Diet, nutrition and the prevention of chronic World. diseases Health Organ Tech Rep Ser, 916 (2003), pp. i-viii 1-149, backcover
Encuesta Nacional de Salud (ENS) Chile 2009 – 2010. Ministerio de Salud. Reaven G.M.. Role of insulin resistance in human disease. Diabetes, 37 (1988), pp. 1595-1607 Banting lecture 1988
Alberti K.G., Zimmet P.Z.. Definition, diagnosis and classifcation of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med, 15 (1998), pp. 539-553
Gami A.S., Witt B.J., Howard D.E., et al. (2007). Metabolic syndrome and risk of incident cardiovascular events and death: a systematic review and metaanalysis of longitudinal studies. J Am Coll Cardiol, 49 (2007), pp. 403-414
Mottillo S., Filion K.B., Genest J., et al. The metabolic syndrome and cardiovascular risk a systematic review and meta-analysis. J Am Coll Cardiol, 56 (2010), pp. 1113-1132
Ford E.S., Li C., Sattar N. Metabolic syndrome and incident diabetes: current state of the evidence. Diabetes Care, 31 (2008), pp. 1898-1904
Qiao Q., Gao W., Zhang L., Nyamdorj R., Tuomilehto J.. (2008), Metabolic syndrome and cardiovascular disease. Ann Clin Biochem, 44 (2007), pp. 232-263
Alberti K.G., Zimmet P., Shaw J.The metabolic syndrome--a new worldwide definition. Lancet, 366 (2005), pp. 1059-1062
Grundy S.M., Cleeman J.I., Daniels S.R., et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement.
Alberti K.G., Eckel R.H., Grundy S.M., et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.
Kahn R., Buse J., Ferrannini E., Stern M.The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care, 28 (2005), pp. 2289-2304
Orci L.The insulin factory: a tour of the plant surroundings and a visit to the assembly line. The Minkowski lecture 1973 revisited. Diabetologia, 28 (1985), pp. 528-546
Itoh N., Okamoto H.Translational control of proinsulin synthesis by glucose. Nature, 283 (1980), pp. 100-102
McGarry J.D.What if Minkowski had been ageusic? An alternative angle on diabetes. Science, 258 (1992), pp. 766-770
Galgani J.E., Ravussin E. (2012), Postprandial whole-body glycolysis is similar in insulin-resistant and insulin-sensitive non-diabetic humans. Diabetologia, 55 (2012), pp. 737-742
DeFronzo R.A., Tobin J.D., Andres R. (2012), Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am J Physiol, 237 (1979), pp. E214-23
Muniyappa R., Lee S., Chen H., Quon M.J. Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am J Physiol Endocrinol Metab, 294 (2008), pp. E15-26
Matthews D.R., Hosker J.P., Rudenski A.S., Naylor B.A., Treacher D.F., Turner R.C.. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia, 28 (1985), pp. 412-419
Bonora E., Kiechl S., Willeit J., et al. Prevalence of insulin resistance in metabolic disorders: the Bruneck Study. Diabetes, 47 (1998), pp. 1643-1649
Acosta A.M., Escalona M., Maiz A., Pollak F., Leighton F.Determination of the insulin resistance index by the Homeostasis Model Assessment in a population of Metropolitan Region in Chile.
McAuley K.A., Williams S.M., Mann J.I., et al. Diagnosing insulin resistance in the general population. Diabetes Care, 24 (2001), pp. 460-464
Laakso M. How good a marker is insulin level for insulin resistance?. Am J Epidemiol, 137 (1993), pp. 959-965
Ascaso J.F., Merchante A., Lorente R.I., Real J.T., Martinez-Valls J., Carmena R. A study of insulin resistance using the minimal model in nondiabetic familial combined hyperlipidemic patients. Metabolism, 47 (1998), pp. 508-513
Eschwege E., Richard J.L., Thibult N., et al. Coronary heart disease mortality in relation with diabetes, blood glucose and plasma insulin levels. The Paris Prospective Study, ten years later. Horm Metab Res Suppl, 15 (1985), pp. 41-46
Matsuda M., DeFronzo R.A. Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Diabetes Care, 22 (1999), pp. 1462-1470
Bergman R.N., Ider Y.Z., Bowden C.R., Cobelli C. Quantitative estimation of insulin sensitivity. Am J Physiol Endocrinol Metab Gastrointest Physiol, 236 (1979), pp. E667-E677
Galgani J.E., de Jonge L., Rood J.C., Smith S.R., Young A.A., Ravussin E. Urinary C-peptide excretion: a novel alternate measure of insulin sensitivity in physiological conditions. Obesity, 18 (2010), pp. 1852-1857
Manley S.E., Stratton I.M., Clark P.M., Luzio S.D. Comparison of 11 human insulin assays: implications for clinical investigation and research. Clin Chem, 53 (2007), pp. 922-932
Staten M.A., Stern M P., Miller W.G., Steffes M.W., Campbell S.E. Insulin Standardization Workgroup. Insulin assay standardization: leading to measures of insulin sensitivity and secretion for practical clinical care. Diabetes Care, 33 (2010), pp. 205-206
Ghanim H., Aljada A., Hofmeyer D., Syed T., Mohanty P., Dandona P. (2010), Circulating mononuclear cells in the obese are in a proinflammatory state. Circulation, 110 (2004), pp. 1564-1571
Hotamisligil G.S. Inflammation and metabolic disorders. Nature, 444 (2006), pp. 860-867
Schenk S., Saberi M., Olefsky J.M. Insulin sensitivity: modulation by nutrients and inflammation. J Clin Invest, 118 (2008), pp. 2992-3002
McGarry J.D. Banting lecture 2001: dysregulation of fatty acid metabolism in the etiology of type 2 diabetes. Diabetes, 51 (2002), pp. 7-18
Samuel V.T., Petersen K.F., Shulman G.I. Lipid-induced insulin resistance: unravelling the mechanism. Lancet, 375 (2010), pp. 2267-2277
Bachmann O.P., Dahl D.B., Brechtel K., et al. Effects of intravenous and dietary lipid challenge on intramyocellular lipid content and the relation with insulin sensitivity in humans. Diabetes, 50 (2001), pp. 2579-2584
Petersen K.F., Dufour S., Befroy D., Garcia R., Shulman G.I.Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. N Engl J Med, 350 (2004), pp. 664-671
Galgani J.E., Moro C., Ravussin E. Metabolic flexibility and insulin resistance.Am J Physiol Endocrinol Metab, 295 (2008), pp. E1009-17
Samuel V.T., Shulman G.I. Mechanisms for insulin resistance: common threads and missing links. Cell, 148 (2012), pp. 852-871
Holloszy J.O. Skeletal muscle “mitochondrial deficiency” does not mediate insulin resistance. Am J Clin Nutr, 89 (2009), pp. 463S-466S
Moro C., Galgani J.E., Luu L., et al. Influence of gender, obesity, and muscle lipase activity on intramyocellular lipids in sedentary individuals. J Clin Endocrinol Metab, 94 (2009), pp. 3440-3447
Galgani J.E., Vasquez K., Watkins G., Dupuy A., Bertrand-Michel J., Levade T., Moro C. Enhanced skeletal muscle lipid oxidative efficiency in insulin-resistant vs insulin-sensitive nondiabetic, nonobese humans. J Clin Endocrinol Metab, 98 (2013), pp. E646-53
Shi H., Kokoeva M V., Inouye K., Tzameli I., Yin H., Flier J.S. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest, 116 (2006), pp. 3015-3025
Konner A.C., Bruning J.C.Toll-like receptors: linking inflammation to metabolism. Trends Endocrinol Metab, 22 (2011), pp. 16-23
Jaworski K., Sarkadi-Nagy E., Duncan R.E., Ahmadian M., Sul H.S.Regulation of triglyceride metabolism. I V. Hormonal regulation of lipolysis in adipose tissue. Am J Physiol Gastrointest Liver Physiol, 293 (2007), pp. G1-4
Smith J., Al-Amri M., Dorairaj P., Sniderman A. The adipocyte life cycle hypothesis. Clin Sci, 110 (2006), pp. 1-9
Reyes M. Características biológicas del tejido adiposo: el adipocito como célula endocrina. Rev Med Clin Condes, 23 (2012), pp. 136-144
Weisberg S.P., Hunter D., Huber R., Lemieux J., Slaymaker S., Vaddi K., et al. CCR2 modulates inflammatory and metabolic effects of high-fat feeding. J Clin Invest, 116 (2006), pp. 115-124
Fain J.N. Release of interleukins and other inflammatory cytokines by human adipose tissue is enhanced in obesity and primarily due to the nonfat cells. Vitam Horm, 74 (2006), pp. 443-477
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