Importancia del control glucémico posprandial en el paciente con diabetes mellitus tipo 2

Autores/as

  • A Benítez Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción
  • G Benítez Ministerio de Salud Pública
  • L Barriocanal Clínica Integral de Diabetes
  • E Bueno Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción
  • A Caballero Clínica Integral de Diabetes
  • F Cañete Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción
  • JT Jiménez Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción
  • S Logwin Sanatorio La Costa
  • C Menoni Instituto de Previsión Social
  • M Palacios Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción
  • E Valinotti Instituto de Previsión Social
  • R Veja Sanatorio Metropolitano

Palabras clave:

Diabetes, incretinas, hiperglucemia posprandial, riesgo cardiovascular, agonistas de receptores de GLP-1

Resumen

La hiperglucemia postprandial es frecuente en personas con diabetes mellitus, incluso cuando el control metabólico general parece adecuado, según los niveles de hemoglobina glucosilada. Estudios han demostrado la relación entre los valores de glucemia postprandial y enfermedad cardiovascular, independientemente de los valores de glucemia plasmática en ayunas. La diabetes mellitus tipo 2 es una patología progresiva y las fluctuaciones postprandiales de la glucemia parecen desempeñar un papel significativo en sus complicaciones vasculares. Las diferentes Guías de Práctica Clínica hacen énfasis en la individualización de la propuesta terapéutica y enfatizan la necesidad de sacar al paciente rápidamente del estado de hiperglucemia, combinando precozmente cambios del estilo de vida con farmacoterapia, en una progresión rápida a doble y triple terapia no insulínica o instalación temprana de insulinoterapia, combinada con otros fármacos. Un enfoque racional basado en la fisiopatología de la enfermedad ha permitido un notable desarrollo de la oferta fármaco-terapéutica. Es importante analizar las opciones de intervención terapéutica sobre la hiperglucemia postprandial, dadas las experiencias negativas relacionadas con la optimización del control y las dudas sobre la seguridad de los medicamentos. Analizadas todas las alternativas para el control de la glucemia postprandial, en el momento actual las intervenciones más eficaces serían los incretinomiméticos (GLP1ag y DPP-4I) con mayores beneficios sobre la GPP, la HbA1c y el peso. El objetivo general para los pacientes con DMT2 es una HbA1c ≤ 7%, con el fin de disminuir el riesgo de complicaciones, pero es razonable individualizar el tratamiento, balanceando riesgos, beneficios y costos de la terapéutica planteada.

 

Descargas

Los datos de descargas todavía no están disponibles.

Biografía del autor/a

A Benítez, Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción

 

G Benítez, Ministerio de Salud Pública

 

L Barriocanal, Clínica Integral de Diabetes

 

 

E Bueno, Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción

 

A Caballero, Clínica Integral de Diabetes

 

F Cañete, Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción

 

JT Jiménez, Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción

 

S Logwin, Sanatorio La Costa

 

C Menoni, Instituto de Previsión Social

 

M Palacios, Hospital de Clínicas, Facultad de Ciencias Médicas, Universidad Nacional de Asunción

 

E Valinotti, Instituto de Previsión Social

 

R Veja, Sanatorio Metropolitano

 

Citas

Facultad de Ciencias Médicas. Boletín informativo 2002. Editorial.

International Diabetes Federation. Guía para el control de la glucosa posprandial. Disponible en: http://www.idf.org.

Erlinger TP y FL Brancati. Postchallenge hyperglycemia in a national sample of U.S. adults with type 2 diabetes. Diabetes Care. 2001; 24:1734-1738.

Bonora E, Corrao G, Bagnardi V, Ceriello A, Comaschi M, Montanari P et al. Prevalence and correlates of post-prandial hyperglycaemia in a large sample of patients with type 2 diabetes mellitus. Diabetologia. 2006; 49:846-854.

American Diabetes Association. Posprandial blood glucose. (Consensus Statement). Diabetes Care. 2001; 24:775-778.

Pecoraro RE, Chen MS, Porte Jr. D. Glycosylated haemoglobin and fasting plasma glucose in the assessment of outpatient glycemic control in NIDDM. Diabetes Care. 1982; 5:592-599.

Raz I, Wilson PWF, Strojek K, Kowalska I, Bozikov V, Gitt AK et al. Effects of prandial versus fasting glycemia on cardiovascular outcomes in type 2 diabetes: The HEART2D trial. Diabetes Care. 2009; 32:381-386.

Woerle HJ, Neumann C, Zschau S, Tenner S, Irsigler A, Schirra J et al. Impact of fasting and postprandial glycemia on overall glycemic control in type 2 diabetes. Importance of postprandial glycemia to achieve target HbA1c levels. Diabetes Res Clin Pract. 2007;77:280-285.

Cavalot F, Petrelli A, Traversa M, Bonomo K, Fiora E, Conti M et al. Postprandial blood glucose is a stronger predictor of cardiovascular events than fasting blood glucose in type 2 diabetes mellitus, particularly in women: lessons from the San Luigi Gonzaga Diabetes Study. J Clin Endocrinol Metab. 2006; 9:813-819.

Pyörälä K, Savolainen E, Lehtovirta E, Punsar S, Siltanen P. Glucose tolerance and coronary heart disease. Helsinki Policeman Study. J Chronic Dis. 1979; 32:729-745.

Donahue RP, Abbot RD, Reed DM, Yano K. Post challenge glucose concentration and coronary heart disease in men of Japanese ancestry: Honolulu Heart Program. Diabetes. 1987; 36:689-692.

Jackson CA, Yudkin JS, Forrest RD. A comparison of the relationships of the glucose tolerance test and the glycated haemoglobin assay with diabetes vascular disease in the community: the Islington Diabetes Survey. Diabetes Res Clin Pract. 1992;17:111-123.

Lowe LP, Liu K, Greenland P, Metzger BE, Dyer AR, Stamler J. Diabetes asymptomatic hyperglycaemia, and 22-year mortality in black and white men: the Chicago Heart Association Detection Project in Industry Study. Diabetes Care. 1997; 20:163-169.

Barrett-Connor E y A. Ferrara. Isolated post challenge hyperglycaemia and the risk of total cardiovascular disease in older women and men: the Rancho Bernardo Study. Diabetes Care. 1998; 21:1236-1239.

De Vegt F, Dekker M, Ruhè HG, Stehouwer CD.A, Nijpels GBL.M, Heine RJ. Hyperglycaemia is associated with all-cause and cardiovascular mortality in the Hoorn population: the Hoorn Study. Diabetologia. 1999; 42:926-931.

DECODE Study Group. Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med. 2001; 161:397-405.

.Sharrett AR, Chambless LE, Heiss G, Paton CC, Patsch W, for the ARIC investigators. Association of posprandial triglyceride and retinyl palmitate responses with asymptomatic carotid artery atherosclerosis in middle-aged men and women: the Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb Vasc Biol. 1995; 15:2122-2129.

Axelsen M, Smith U, Eriksson JW, Taskinen M, Jansson P-A. Posprandial hypertriglyceridemia and insulin resistance in normoglycemic first-degree relatives of patients with type 2 diabetes. Ann Intern Med. 1999; 131:27-31.

Evans M, Anderson RA, Graham J, Ellis GR, Morris K, Davies S et al. Ciprofibrate therapy improves endothelial function and reduces postprandial lipemia and oxidation stress in type 2 diabetes mellitus. Circulation. 2000; 101:1773-1779.

Wolffenbuttel BH. Postprandial glucose peaks in the pathogenesis of cardiovascular disease in diabetes mellitus. Ned Tijdschr Geneeskd. 2002; 146:654-658.

Shishehbor MH, Avilés RJ, Brennan ML, Fu X, Goormastic M, Pearce GL et al. Association of nitrotyrosine levels with cardiovascular disease and modulation by statin therapy. JAMA. 2003; 289:1675-1680.

Marfella R, Quagliaro L, Nappo F, Ceriello A, Giugliano D. Acute hyperglycaemia induces an oxidative stress in healthy subjects. J Clin Invest. 2001; 108:635-636.

Ceriello A, Giugliano D, Quatraro A, Dello Russo P, Marchi E, Torella R. Hyperglycaemia may determine fibrinopeptid A plasma level increase in humans. Metabolism. 1989; 38: 1162-1163.

Ceriello A, Giugliano D, Quatraro A, Dello Russo P, Torella R. Blood glucose may condition factor VII levels in diabetic and normal subjects. Diabetologia. 1988; 31:889-891.

Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000; 321:405-412.

Kunt T. Current strategies for controlling posprandial hyperglycaemia. Int J Clin Pract Suppl. 2001; 123:19-23.

Izucchi SE, Bergensatal RM, Buse JB, Diamart M, Ferrannini E, Nauck M et al. European Association for the Study of Diabetes (EASD). Management of hyperglycemia in type 2 diabetes: a patient-centered approach position statement of the American Diabetes Association (ADA) and the European Association for the Study of Daibetes (EASD). Diabetes Care. 2012; 35:1364-1379.

Wolever TM, Yang M, Zeng XY, Atkinson F, Brand-Miller JC. Food glycemic index, as given in glycemic index tables, is a significant determinant of glycemic responses elicited by composite breakfast meals. Am J Clin Nutr. 2006; 83:1306-1312.

Sheard NF, Clark NG, Brand-Miller JC, Franz MJ, Pi-Sunyer FX, Mayer-Davis E et al. Dietary carbohydrate (amount and type) in the prevention and management of diabetes: a statement by the American Diabetes Association. Diabetes Care. 2004; 27:2266-2271.

Inson S y J Brand-Miller. Glycemic index, postprandial glycaemia and cardiovascular disease. Curr Opin Lipidol. 2005; 16:69-75.

Kazda C, Hulstrunk H, Helsberg K, Langer F, Forst T, Hanefeld M. Prandial insulin substitution with insulin lispro or insulin lispro mid mixture vs. basal therapy with insulin glargine: a randomized controlled trial in patients with type 2 diabetes beginning insulin therapy. J Diabetes Complications. 2006; 20:145-152.

Goke B y C Herrmann-Rinke. The evolving role of alpha-glucosidase inhibitors. Diabetes Metab Rev. 1998; 14 Suppl 1:S31-S38.

Owens DR, Luzio SD, Ismail I, Bayer T. Increased prandial insulin secretion after administration of a single preprandial oral dose of repaglinide in patients with type 2 diabetes. Diabetes Care. 2000; 23:518-523.

Drucker DJ. Glucagon-like peptide-1 and the islet beta-cell: augmentation of cell proliferation and inhibition of apoptosis. Endocrinology. 2003; 144:5145-5148.

Saad MF, Knowler WC, Pettitt DJ, Nelson RG, Mott DM, Bennett PH. The natural history of impaired glucose tolerance in the Pima Indians. N Engl J Med. 1988; 319:1500-1505.

Powers AC. Diabetes mellitus. En: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18a ed. New York, NY: McGraw-Hill; 2012. http://www.accessmedicine.com/content.aspx?aID=9141196. [Acceso el 6 de marzo del 2012].

DeFronzo RA. Banting lecture: from the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes. 2009; 58:773-795.

Monnier L, Colette C, Dunseath GJ, Owens DR. The loss of postprandial glycemic control precedes stepwise degradation of fasting with worsening diabetes. Diabetes Care. 2007; 30:263–269.

Bolli GB y JE Gerich. The dawn phenomenon: a common occurrence in both non-insulin-dependent and insulin-dependent diabetes mellitus. N Engl J Med. 1984; 310:746–750.

Rayner CK, Samsom M, Jones KL, Horowitz M. Relationships of upper gastrointestinal motor and sensory function with glycemic control. Diabetes Care. 2001; 24:371-381.

Quigley EMM, Hasler W, Parkman HP. AGA technical review on nausea and vomiting. Gastroenterology. 2001; 120:263-286.

Kreymann B, Williams G, Ghatei MA, Bloom SR. Glucagon-like peptide-1 [7-36]: a physiological incretin in man. Lancet. 1987; 2:1300–1304.

Knop FK, Vilsboll T, Hojberg P, Larsen S, Madsbad S. Reduced Incretin Effect in Type 2 Diabetes, Cause or Consequence of the Diabetic State? Diabetes. 2007; 56.

Nauck MA, El-Ouaghlidi A, Gabrys B, Hücking K, Holst JJ, Deacon CF et al. Secretion of incretin hormones (GIP and GLP-1) and incretin effect after oral glucose in first-degree relatives of patients with type 2 diabetes. Regul Pept. 2004; 122:209–217.

Ørskov C, Rabenhøj L, Wettergren A, Kofod H, Holst JJ. Tissue and plasma concentrations of amidated and glycineextended glucagon-like peptide 1 in humans. Diabetes. 1994; 43:535–539.

Feinglos MN, Saad MF, Pi-Sunyer FX, An B, Santiago O a nombre del Liraglutide Doisis-response Study Group. Effects of liraglutide (NN2211), a long-acting GLP-1 analogue, on glucaemic control and bodyweight in subjects with type 2 diabetes. Diabet Med. 2005; 22:1016-1023.

Meier JJ y MA Nauck. Glucose-dependent insulinotropic polypeptide/gastric inhibitory polypeptide. Best Pract Res Clin Endocrinol Metab. 2004; 18:587–606.

Kolterman OG, Kim DD, Shen L, Ruggles JA, Nielsen LL, Fineman MS et al. Pharmacokinetics, pharmacodynamics and safety of exenatide in patients with type 2 diabetes mellitus. Am J Health Syst Pharm. 2005; 62:173-181.

Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007; 87:1409–1439.

Vilsboll T. On the role of the incretin hormones GIP and GLP-1 in the pathogenesis of type 2 diabetes mellitus. Dan Med Bull. 2004; 5:364–370.

The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care. 2003; 26(Suppl 1): S5– S20.

Monnier L, Lapinski H, Colette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: variations with increasing levels of HbA(1c). Diabetes Care. 2003; 26:881-885.

Raccah D, Bretzel R, Owens D, Riddle M. When basal insulin therapy in type 2 diabetes mellitus is not enough - what next? Diabetes Metab. Res. Rev. 2007; 23:257–264.

Harris S, Kapor J, Lank C, Willan A, Houston T. Clinical inertia in patients with T2DM requiring insulin in family practice. Can Fam. Physician. 2010; 56:e418–e424.

UK Prospective Diabetes Study (UKPDS) Group. Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998; 352:837–853.

Patel A, MacMahon S, Chalmers J, Neal B, Billot L, Woodward M et al; for the ADVANCE Collaborative Group. Intensive blood glucose control and vascular outcomes inpatients with type 2 diabetes. N Engl J Med. 2008; 358:2560–2572.

The Writing Team for the Diabetes Control and Complications Trial/DCCT, Epidemiology of Diabetes Interventions and Complications Research Group. Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus. JAMA. 2002; 287:2563–2569.

Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M et al. (INTERHEART Study investigators). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries: case-control study. Lancet. 2004; 364:937-952.

Dale AC, Vatten LJ, Nilsen TI, Midthjell K, Wiseth R. Secular decline in mortality from coronary heart disease in adults with diabetes mellitus: cohort study. BMJ. 2008; 337:a236.

Giugliano D, Ceriello A, Paolisso G. Oxidative stress and diabetic vascular complications. Diabetes Care. 1996; 19:257-267.

Schmidt AM, Yan SD, Wautier JL, Stern D. Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis. Circ Res. 1999; 84:489-497.

Gerich JE. Clinical significance, pathogenesis, and management of postprandial hyperglycemia. Arch Intern Med. 2003; 163:1306–1316.

Andreozzi F, Gastaldelli A, Mannino GC, Sciacqua A, Succurro E, Arturi F et al.Increased carotid intima-media thickness in the physiologic range is associated with impaired postprandial glucose metabolism, insulin resistance and beta cell dysfunction. Atherosclerosis. 2013; 229:277-281. doi:10.1016/j.atherosclerosis.2013.05.028

Kannel W y D McGee. Diabetes and cardiovascular risk factors: the Framingham Study. Circulation. 1979; 59:8-13.

Gubitosi-Klug RA, DCCT/EDIC Research Group. The diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: summary and future directions. Diabetes Care. 2014; 37:44-49. doi: 10.2337/dc13-2148

Hanefeld M, Fischer S, Julius U, Schulze J, Schwanebeck U, Shmechel H et al. Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11-year follow-up. Diabetologia. 1996; 39:1577-1583.

Hanenfeld M, Koehler C, Schaper F, Fuecker K, Henkel E, Temelkova-Kurktschiev T. Postprandial plasma glucose is an independent risk factor for increased carotid intima-media thickness in non-diabetic individuals. Atherosclerosis. 1999; 144:229-235.

Tominaga M, Eguchi H, Manaka H, Igarashi K, Kato T, Sekikawa A, for the Funagata Diabetes Study. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. Diabetes Care. 1999; 22:920–924.

Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M, the STOP-NIDDM Trial Research Group. Acarbose for prevention of type 2 diabetes: the STOP-NIDDM randomized trial. Lancet. 2002; 359:2072-2077.

Esposito K, Giugliano D, Nappo F, Marfella R, for the Campanian Post-prandial Hyperglycemia Study Group. Regression of carotid atherosclerosis by control of postprandial hyperglycemia in type 2 diabetes mellitus. Circulation. 2004; 110:214-219.

Turner RC, Cull CA, Frighi V, Holman RR, UK Prospective Diabetes Study (UKPDS) Group. Glycemic control with diet, sulfonylurea, metformin, or insulin in patients with type 2 diabetes mellitus: progressive requirement for multiple therapies (UKPDS 49). JAMA. 1999; 281:2005-2012.

Gerstein HC, Miller ME, Byington RP, Goff DC Jr, The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008; 358:2545-2559.

Duckworth W1, Abraira C, Moritz T, Reda D, The Investigators for the VADT. Glucose control and vascular complications in veterans with type 2 diabetes. N Engl J Med. 2009; 360:129-139.

American Association of Clinical Endocrinologists (AACE) Comprehensive Diabetes Management. Consensus Statement 2013. 2013; 19 (Suppl 2).

Nishida Y, Tokuyama K, Nagasaka S, Higaki Y, Shirai Y, Kiyonaga A et al. Effect of moderate exercise training on peripheral glucose effectiveness, insulin sensitivity, and endogenous glucose production in healthy humans estimated by two-compartment-labeled minimal model. Diabetes. 2004; 53:315-320.

Xingguang Z, Xiuping X, Xiumin J, Jinxiao W, Shujing Z, Xiaofeng LV. The Effects of Glucose Fluctuation on the Severity of Coronary Artery Disease in Type 2 Diabetes Mellitus. J Diabetes Res. 2013.

Gong S. Impact of Admission Glycemic Variability, Glucose, and Glycosylated Hemoglobin on Major Adverse Cardiac Events After Acute Myocardial Infarction, Diabetes Care. 2013; 36:1026–1032.

White W. Alogliptin after Acute Coronary Syndrome in Patients with Type 2 Diabetes. NEngl J Med. 2013; 369:1327-1335.

Cefalu W, Butler P, Elashoff M, Elashoff R, Gale E. A Critical Analysis of the Clinical Use of Incretin-Based Therapies. Diabetes Care. 2013; 36:2118-2125.

Ahrén B, Leguízamo DA, Miossec P, Saubadu S, Aronson R. Efficacy and Safety of Lixisenatide Once-Daily Morning or Evening Injections in Type 2 Diabetes Inadequately Controlled on Metformin (GetGoal-M). Diabetes Care. 2013; 36:2543-2550.

Gerich J. Pathogenesis and management of postprandial hyperglycemia: role of incretin-based therapies. Int J Gen Med 2013; 6 877–895.

Barnett A, Huisman H, Jones R, von Eynatten M, Patel S, Woerle HJ. Linagliptin for patients aged 70 years or older with type 2diabetes inadequately controlled with common antidiabetes treatments: a randomised, double-blind, placebo-controlled trial. Lancet. 2013; 382:1413–1423.

Bloomgarden ZT. Aspects of insulin treatment. Diabetes Care. 2010; 33:e1-e6.

Raz I .Guideline Approach to Therapy in Patients With Newly Diagnosed Type 2 Diabetes Diabetes Care. 2013; 36:S139-S144.

Hanefeld M, Bouter KP, Dickinson S, Guitard C. Rapid and Short-Acting Mealtime Insulin Secretion With Nateglinide Controls Both Prandial and Mean Glycemia. Diabetes Care. 2000; 23:202–207.

Schramm TK, Gislason GH, Vaag A, Rasmussen JN, Folke F, Hansen ML et al. Mortality and cardiovascular risk associated with different insulin secretagogues compared with metformin in type 2 diabetes, with or without a previous myocardial infarction: a nation wide study. Eur Heart J. 2011; 32:1900–1908.

Ryan G, Briscoe T, Jobe L. Review of pramlintide as adjunctive therapy in treatment of type 1 and type 2 diabetes. Drug Des Devel Ther. 2009; 2:203-214.

Van de Laar F, Lucassen P, Akkermans RP, Van de Lisdonk EH, Rutten GE, Van Weel C. α-Glucosidase Inhibitors for Patients With Type 2 Diabetes. Results from a Cochrane systematic review and meta-analysis. Diabetes Care. 2005; 28:166–175.

Polidori D, Sha S, Mudaliar S, Ciaraldi TP, Ghosh A, Vaccaro N et al. Canagliflozin Lowers Postprandial Glucose and Insulin by Delaying Intestinal Glucose Absorption in Addition to Increasing Urinary Glucose Excretion. Diabetes Care. 2013; 36:2154–2161.

Defronzo RA. Characterization of Renal Glucose Reabsorption in Response to Dapagliflozin in Healthy Subjects and Subjects With Type 2 Diabetes. Diabetes Care. 2013; 36:3169–3176.

Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002; 346:393-403.

Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM et al. Glycolic index of foods: a physiological basis for carbohydrates. Am J Clin Nutr. 1981; 34:362-366.

Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr. 2002; 76:5-56.

Green D, Maiorana A, O’Driscoll G, Taylor R. Effect of exercise training on endothelium-derived nitric oxide function in humans. J Physiol. 2004; 561:1-25.

Short KR, Vittone JL, Bigelow ML, Proctor DN, Rizza RA, Coenen-Schimke JM et al. Impact of aerobic exercise training on age-related changes in insulin sensitivity and muscle oxidative capacity. Diabetes. 2003; 52:1888-1896.

Descargas

Publicado

2015-06-01

Cómo citar

Benítez, A., Benítez, G., Barriocanal, L., Bueno, E., Caballero, A., Cañete, F., … Veja, R. (2015). Importancia del control glucémico posprandial en el paciente con diabetes mellitus tipo 2. Anales De La Facultad De Ciencias Médicas, 48(1), 83–100. Recuperado a partir de https://revistascientificas.una.py/index.php/RP/article/view/2032

Número

Sección

Articulo de Revisión