Información del artículo
La arteriosclerosis es la causa más frecuente de morbilidad y mortalidad cardiovascular en pacientes con diabetes mellitus tipo 2. En los últimos años, estudios epidemiológicos y de intervención han identificado el estado posprandial, caracterizado por un aumento rápido y prolongado de los valores de glucosa en sangre, como un factor de riesgo directo e independiente de arteriosclerosis que contribuye al desarrollo de la enfermedad cardiovascular. La hiperglucemia posprandial podría tener un efecto tóxico directo sobre el endotelio vascular mediado por el estrés oxidativo, lo que favorecería el desarrollo de la disfunción endotelial, una condición protrombótica y proinflamatoria, a través de la producción de radicales libres. Este efecto es independiente de otros factores de riesgo cardiovascular, como la hiperlipidemia. El control y la corrección de los valores de glucemia posprandial es una estrategia muy importante en la prevención de la enfermedad cardiovascular asociada a la diabetes. En esta revisión se han examinado los estudios epidemiológicos y de intervención que asocian la hiperglucemia posprandial con el riesgo de enfermedad cardiovascular, los mecanismos involucrados en estos efectos y las diferentes estrategias terapéuticas para controlar la hiperglucemia posprandial, que incluyen cambios en el estilo de vida y fármacos como los secretagogos de corta duración, los inhibidores de las alfaglucosidasas intestinales, los análogos de insulina de acción rápida y nuevos agentes en desarrollo, como el análogo de amilina, pramlintida; la hormona insulinotrópica GLP-1 y sus homólogos como la exendina, los inhibidores de la dipeptidilpeptidasa IV (DPPIV) o la insulina inhalada.
Palabras clave:
Glucosa posprandial
Riesgo cardiovascular
Diabetes mellitus tipo 2
Atherosclerosis is the most frequent cause of the increased cardiovascular morbidity and mortality observed in type 2 diabetic patients. Over the past few years, epidemiological and preliminary intervention studies have identified that the posprandial state, characterized by a rapid and large increase in blood glucose levels, is a direct and independent risk factor for atherosclerosis and a contributing factor to the development of cardiovascular disease. Posprandial hyperglycemia may have a direct toxic effect on the vascular endothelium, mediated by oxidative stress, which favors the development of endothelial dysfunction, a prothrombotic and proinflammatory condition, through the production of free radicals. This effect is independent of other cardiovascular risk factors such as hyperlipidemia. The control and correction of posprandial glucose levels is an important strategy in the prevention of diabetes-related cardiovascular disease. In this review, epidemiological and intervention studies that associate posprandial hyperglycemia with cardiovascular risk, the mechanisms involved in this effect, and the distinct therapeutic strategies to control posprandial hyperglycemia are reviewed. These therapeutic strategies include lifestyle changes, drugs such as short-acting secretagogues, alpha-glucosidase inhibitors, fast-acting insulin analogues, and new agents under development, such as the synthetic human amylin analogue pramlintide, the insulinotropic hormone GLP-1, a homologue of GLP-1-exendin, dipeptidylpeptidase IV inhibitors (DPPIV) and inhaled insulin formulations.
Key words:
Posprandial glucose
Cardiovascular risk
Type 2 diabetes mellitus
El Texto completo está disponible en PDF
Bibliografía
[1.]
W.B. Kannel, D.L. Mc Gee.
Diabetes and cardiovascular disease: the Framingham Study.
JAMA, 241 (1979), pp. 2035-2038
[2.]
M. Laakso.
Hyperglycemia and cardiovascular disease in type 2 diabetes.
Diabetes, 48 (1999), pp. 937-942
[3.]
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, 352 (1998), pp. 837-853
[4.]
L. Jovanovic.
Rationale for prevention and treatment of posprandial glucose-mediated toxicity.
Endocrinologist, 9 (1999), pp. 87-92
[5.]
A. Avignon, A. Radauceanu, L. Monnier.
Non-fasting plasma glucose is a better marker of diabetic control than fasting plasma glucose in type 2 diabetes.
Diabetes Care, 20 (1997), pp. 1822-1826
[6.]
E. Bonora, M. Muggeo.
Posprandial blood glucose as a risk factor for cardiovascular disease in type II diabetes: the epidemiological evidence.
Diabetologia, 44 (2001), pp. 2107-2114
[7.]
A. Ceriello.
The possible role of posprandial hyperglycaemia in the pathogenesis of diabetic complications.
Diabetologia, 46 (2003), pp. M9-M16
[8.]
American Diabetes Association.
Posprandial blood glucose.
Diabetes Care, 24 (2001), pp. 775-778
[9.]
P.J. Lefebvre, A.J. Scheen.
Glucose metabolism and the posprandial state.
Eur J Clin Invest, 29 (1999), pp. 1-6
[10.]
A.J. Scheen, N. Paquot, B. Jandrain, P.J. Lefebvre.
Posprandial hyperglycemia. I. Physiopathology, clinical consequences and dietary management.
Rev Med Liege, 57 (2002), pp. 138-141
[11.]
H. Gin, V. Rigalleau.
Posprandial hyperglycemia, posprandial hyperglycemia and diabetes.
Diabetes Metab, 26 (2000), pp. 265-272
[12.]
T.M.S. Wolever, J.L. Chiasson, A. Csima, J.A. Hunt, C. Palmason, S.A. Ross, et al.
Variation of podtprandial plasma glucose, palatability, and symptoms associated with a standardized mixed meal versus 75 g oral glucose.
Diabetes Care, 21 (1998), pp. 336-340
[13.]
V. Poitout, R.P. Robertson.
An integrated view of beta-cell dysfunction in type-II diabetes.
Annu Rev Med, 47 (1996), pp. 69-83
[14.]
A. Mitrakou, D. Kelley, M. Mokan, T. Veneman, T. Pangburn, J. Reilly, et al.
Role of reduced suppression of glucose production and diminished early insulin release in impaired glucose tolerance.
N Engl J Med, 326 (1992), pp. 22-29
[15.]
L. Mandarino, B. Baker, R. Rizza, J. Genest, J. Gerich.
Infusion of insulin impairs human adipocyte glucose metabolism in vitro without decreasing adipocyte insulin receptor binding.
Diabetologia, 27 (1984), pp. 358-363
[16.]
L. Rossetti, A. Giaccari, R.A. De Fronzo.
Glucose toxicity.
Diabetes Care, 13 (1990), pp. 610-630
[17.]
J.M. Chehade, A.D. Mooradian.
A rational approach to drug therapy of type 2 diabetes mellitus.
Drugs, 60 (2000), pp. 95-113
[18.]
R.E. Pecoraro, M.S. Chen, D. Porte Jr.
Glycosylated haemoglobin and fasting plasma glucose in the assessment of outpatient glycemic control in NIDDM.
Diabetes Care, 5 (1982), pp. 592-599
[19.]
E. Bonora.
Posprandial peaks as a risk factor for cardiovascular disease: epidemiological perspectives.
Int J Clin Pract, 129 (2002), pp. 5-11
[21.]
C.L. Rohlfing, H.M. Wiedmeyer, R.R. Little, J.D. England, A. Tennill, D.E. Goldstein.
Defining the relationship between plasma glucose and HBA1C: analysis of glucose profiles and HbA1C in the Diabetes Control and Complications Trial.
Diabetes Care, 25 (2002), pp. 275-278
[22.]
F.J. Cañizo, M.N. Moreira-Andrés.
La glucemia posprandial como predictora de los valores de HbA1C.
Endocrinol Nutr, 50 (2003), pp. 84-85
[23.]
Monnier L, Lapinski H, Colette C. Contributions of fasting and posprandial plasma glucose increments to the overall diurnal hyperglycaemia of type 2 diabetic patients. Diabetes Care. 3003;26:881-5.
[24.]
F.J. Del Cañizo-Gómez, M.N. Moreira-Andrés.
Cardiovascular risk factors in patients with type 2 diabetes. Do we follow the guidelines?.
Diabetes Res Clin Pract, 65 (2004), pp. 125-133
[25.]
S. Soonthornpun, C. Rattarasarn, R. Leelawattana, N. Setasuban.
Posprandial plasma glucose: a good index of glycemic control in type 2 diabetic patients having near-normal fasting glucose levels.
Diabetes Res Clin Pract, 46 (1999), pp. 23-27
[26.]
Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus.
Diabetes Care, 22 (1998), pp. S5-S19
[27.]
European Diabetes Policy Group.
A desktop guide to type 2 diabetes mellitus.
Diabet Med, 16 (1999), pp. 716-730
[28.]
American College of Endocrinology.
ACE guidelines for glycemic control.
Endocr Pract, 8 (2002), pp. S6-S11
[29.]
American Association of Clinical Endocrinologists.
The American Association of Clinical Endocrinologists Medical Guidelines for the Management of Diabetes Mellitus: the AACE system of intensive diabetes self-management-2000 update.
Endocr Pract, 6 (2000), pp. 43-84
[30.]
American Diabetes Association Standards of medical care in diabetes.
Diabetes Care, 28 (2005), pp. S4-S36
[31.]
R.J. Heine, B. Balkau, A. Ceriello, S. Del Prato, E.S. Horton, M.R. Taskinen.
What does posprandial hyperglycaemia mean?.
Diabet Med, 21 (2004), pp. 208-213
[32.]
K. Pyörälä, E. Savolainen, E. Lehtovirta, S. Punsar, P. Siltanen.
Glucose tolerance and coronary heart disease. Helsinki Policeman Study.
J Chronic Dis, 32 (1979), pp. 729-745
[33.]
R.P. Donahue, R.D. Abbot, D.M. Reed, K. Yano.
Post challenge glucose concentration and coronary heart disease in men of Japanese ancestry: Honolulu Heart Program.
Diabetes, 36 (1987), pp. 689-692
[34.]
C.A. Jackson, J.S. Yudkin, R.D. Forrest.
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, 17 (1992), pp. 111-123
[35.]
L.P. Lowe, K. Liu, P. Greenland, B.E. Metzger, A.R. Dyer, J. Stamler.
Diabetes asymptomatic hyperglycaemia, and 22-year mortality in black and white men: the Chicago Heart Association Detection Project in Industry Study.
Diabetes Care, 20 (1997), pp. 163-169
[36.]
E. Barrett-Connor, A. Ferrara.
Isolated post challenge hyperglycaemia and the risk of total cardiovascular disease in older women and men: the Rancho Bernardo Study.
Diabetes Care, 21 (1998), pp. 1236-1239
[37.]
J.E. Shaw, A.M. Hodge, M. de Courten, P. Chitson, P.Z. Zimmet.
Isolated post-challenge hyperglycaemia confirmed as a risk factor for mortality.
Diabetologia, 42 (1999), pp. 1050-1054
[38.]
F. De Vegt, M. Dekker, H.G. Ruhè, C.D.A. Stehouwer, G.B.L.M. Nijpels, R.J. Heine.
Hyperglycaemia is associated with all-cause and cardiovascular mortality in the Hoorn population: the Hoorn Study.
Diabetologia, 42 (1999), pp. 926-931
[39.]
J.B. Meigs, D.M. Nathan, R.B. D’Agostino Sr, P.W. Wilson.
Fasting and post-challenge glycaemia and cardiovascular disease risk: the Framingham Offspring Study.
Diabetes Care, 25 (2002), pp. 1845-1850
[40.]
The DECODE Study Group, the European Diabetes Epidemiology Group.
Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria.
Lancet, 354 (1999), pp. 617-621
[41.]
M. Coutinho, H.C. Gerstein, Y. Wang, S. Yusuf.
The relationship between glucose and incident cardiovascular events: a metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12 years.
Diabetes Care, 22 (1999), pp. 233-240
[42.]
B. Balkau, M. Shipley, R.J. Jarret, M. Pyörälä, H. Forhan, E. Eschwège.
High blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men: 20 year followup in the Whitehall Study, the Paris Prospective Study and the Helsinki Policemen Study.
Diabetes Care, 21 (1998), pp. 360-367
[43.]
J.J. O'Sullivan, R.M. Conroy, K. Robinson, N. Hickey, R. Mulcahy.
In hospital prognosis of patients with fasting hyperglycaemia after first myocardial infarction.
Diabetes Care, 14 (1991), pp. 758-760
[44.]
G. Bellodi, V. Manicardi, V. Malavasi, L. Veneri, G. Bernini, P. Bossini, et al.
Hyperglycaemia and prognosis of acute myocardial infarction in patients without diabetes mellitus.
Am J Cardiol, 64 (1989), pp. 885-895
[45.]
K. Malmberg, A. Norhammar, H. Wedel, L. Ryden.
Glycometabolic state at admission: important risk marker of mortality in conventionally treated patients with diabetes mellitus and acute myocardial infarction: long-term results from the diabetes and insulin-glucose infusion in acute myocardial infarction (DIGAMI Study).
Circulation, 99 (1999), pp. 2626-2632
[46.]
P. Pignoli, E. Tremoli, A. Poli, P. Oreste, R. Paoletti.
Intima plus media thickness of the arterial wall: a direct measurement with ultrasound imaging.
Circulation, 74 (1986), pp. 1399-1406
[47.]
M.L. Bots, P.G. Mulder, A. Hofman, G.A. Van Es, D.E. Grobber.
Reproducibility of carotid vessel wall thickness measurements: the Rotterdam Study.
J Clin Epidemiol, 47 (1994), pp. 921-930
[48.]
J. Persson, J. Formgren, B. Israelsson, G. Berglund.
Ultrasounddetermined intima-media thickness and atherosclerosis: direct and indirect validation.
Arterioescler Thromb, 14 (1994), pp. 261-264
[49.]
J.T. Salonen, R. Salonen.
Ultrasonographically assessed carotid morphology and the risk of coronary heart disease.
Arterioescler Thromb, 11 (1991), pp. 1245-1249
[50.]
D.H. O’Leary, J.F. Polak, R.A. Kronmal, T.A. Manolio, G.L. Burke, S.K. Wolfson Jr.
For the Cardiovascular Health Study Collaborative Research Group: carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults.
N Engl J Med, 340 (1999), pp. 14-22
[51.]
T.S. Temelkova-Kurktschiev, C. Koehler, E. Henkel, W. Leonhardt, K. Fuecker, M. Hanefeld.
Post challenge plasma glucose and glycemic spikes are more strongly associated with atherosclerosis than fasting glucose or HbA1C level.
Diabetes Care, 23 (2000), pp. 1830-1834
[52.]
M. Hanefeld.
Posprandial hyperglycaemia: noxious effects on the vessel wall.
Int J Clin Pract Suppl, 129 (2002), pp. 45-50
[53.]
M. Hanefeld, S. Fischer, U. Julius, J. Schulze, U. Schwanebeek, H. Schmechel, et al.
Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11-year follow-up.
Diabetologia, 39 (1996), pp. 1577-1583
[54.]
J.L. Chiasson, R.G. Josse, R. Gomis, M. Hanefeld, A. Karasik, M. Laakso, The STOP-NIDDM Trial Research Group.
Acarbose for prevention of type 2 diabetes mellitus: the STOPNIDDM randomised trial.
Lancet, 359 (2002), pp. 2072-2077
[55.]
J.L. Chiasson, R.G. Josse, R. Gomis, M. Hanefeld, A. Karasik, M. Laakso, The STOP-NIDDM Trial Research Group.
Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM trial.
JAMA, 290 (2003), pp. 486-494
[56.]
M. Hanefeld, J.L. Chiasson, C. Koehler, E. Henkel, F. Schaper, T. Temelkova-Kurktschiev.
Acarbose slows progression of intima- media thickness of the carotid arteries in subjects with impaired glucose tolerance.
Stroke, 35 (2004), pp. 1073-1078
[57.]
K. Esposito, D. Giugliano, F. Nappo, R. Marfella, Campanian Posprandial Hyperglycaemia Study Group.
Regression of carotid atherosclerosis by control of posprandial hyperglycaemia in type 2 diabetes mellitus.
Circulation, 110 (2004), pp. 214-219
[58.]
D. Manzella, R. Grella, A.M. Abbatecola, G. Paolisso.
Repaglinide administration improves brachial reactivity in type 2 diabetic patients.
Diabetes Care, 28 (2005), pp. 366-371
[59.]
A.M. Fontbonne, E.M. Eschwège.
Insulin and cardiovascular disease. Paris Prospective Study.
Diabetes Care, 14 (1991), pp. 461-469
[60.]
A.R. Sharrett, L.E. Chambless, G. Heiss, C.C. Paton, W. Patsch, 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.
Arterioescler Thromb Vasc Biol, 15 (1995), pp. 2122-2129
[61.]
M. Axelsen, U. Smith, J.W. Eriksson, M. Taskinen, A. Jansson P-.
Posprandial hypertriglyceridemia and insulin resistance in normoglycemic first-degree relatives of patients with type 2 diabetes.
Ann Int Med, 131 (1999), pp. 27-31
[62.]
M. Evans, R.A. Anderson, J. Graham, G.R. Ellis, K. Morris, S. Davies, et al.
Ciprofibrate therapy improves endothelial function and reduces posprandial lipemia and oxidation stress in type 2 diabetes mellitus.
Circulation, 101 (2000), pp. 1773-1779
[63.]
C. Rodríguez-Villar, J.M. Manzanares, E. Casals, A. Pérez-Heras, D. Zambón, R. Gomis, et al.
High-monounsaturated fat, oli- ve oil-rich diet has effects similar to high-carbohydrate diet on fasting and posprandial state and metabolic profiles of patients with type 2 diabetes.
Metabolism, 49 (2000), pp. 1511-1517
[64.]
R. Heine, J.M. Dekker.
Beyond posprandial hyperglycaemia: metabolic factors associated with cardiovascular disease.
Diabetologia, 45 (2002), pp. 461-475
[65.]
I.K. Lee, H.S. Kim, J.H. Bae.
Endothelial dysfunction: its relationship with acute hyperglycaemia and hyperlipidemia.
Int J Clin Pract Suppl, 129 (2002), pp. 59-64
[66.]
A. Ceriello, G. Taboga, L. Tonutti, L. Quagliaro, L. Piconi, B. Bais, et al.
Evidence for an independent and cumulative effect of posprandial hypertriglyceridemia and hyperglycaemia on endothelial dysfunction and oxidative stress generation: effects of short and long-term simvastatin treatment.
Circulation, 106 (2002), pp. 1211-1218
[67.]
M. Massi-Benedetti, M.O. Federici.
Cardiovascular risk factors in type 2 diabetes: the role of hyperglycaemia.
Exp Clin Endocrinol Diabetes, 107 (1999), pp. S120-S123
[68.]
B.H. Wolffenbuttel.
Posprandial glucose peaks in the pathogenesis of cardiovascular disease in diabetes mellitus.
Ned Tijdschr Geneeskd, 146 (2002), pp. 654-658
[69.]
W.C. Duckworth.
Hyperglycaemia and cardiovascular disease.
Curr Atheroscler Rep, 3 (2001), pp. 383-391
[70.]
M.H. Shishehbor, R.J. Avilés, M.L. Brennan, X. Fu, M. Goormastic, G.L. Pearce, et al.
Association of nitrotyrosine levels with cardiovascular disease and modulation by statin therapy.
JAMA, 289 (2003), pp. 1675-1680
[71.]
A. Ceriello, L. Quagliaro, B. Catone, R. Pascon, M. Piazzola, B. Bais, et al.
Role of hyperglycaemic in nitro-tyrosine posprandial generation.
Diabetes Care, 25 (2002), pp. 1439-1443
[72.]
R. Marfella, L. Quagliaro, F. Nappo, A. Ceriello, D. Giugliano.
Acute hyperglycaemia induces an oxidative stress in healthy subjects (letter).
J Clin Invest, 108 (2001), pp. 635-636
[73.]
A. Ceriello, L. Quagliaro, M. D’Amico, C. Di Filippo, R. Marfella, F. Nappo, et al.
Acute hyperglycaemia induces nitrotyrosine formation and apoptosis in perfused heart from rat.
Diabetes, 51 (2002), pp. 1076-1082
[74.]
M.J. Mihm, L. Jing, J.A. Baver.
Nitrotyrosine causes selective vascular endothelial dysfunction and DNA damage.
J Cardiovasc Pharmacol, 36 (2000), pp. 182-187
[75.]
R.L. Jones, C.M. Peterson.
Reduced fibrinogen survival in diabetes mellitus: a reversible phenomenon.
J Clin Invest, 63 (1979), pp. 485-493
[76.]
A. Ceriello, D. Giugliano, A. Quatraro, P. Dello Russo, E. Marchi, R. Torella.
Hyperglycaemia may determine fibrinopeptid A plasma level increase in humans.
Metabolism, 38 (1989), pp. 1162-1163
[77.]
A. Ceriello, R. Giacomello, G. Stel, E. Motz, C. Taboga, L. Tonutti, et al.
Hyperglycaemic-induced thrombin formation in diabetes: the possible role of the oxidative stress.
Diabetes, 44 (1995), pp. 924-928
[78.]
A. Ceriello, D. Giugliano, A. Quatraro, P. Dello Russo, R. Torella.
Blood glucose may condition factor VII levels in diabetic and normal subjects.
Diabetologia, 31 (1988), pp. 889-891
[79.]
T. Sakamoto, H. Ogawa, H. Kawano, N. Hirai, S. Miyamoto, K. Takazoe, et al.
Rapid change of platelet aggregability in acute hyperglycaemia detection by a novel laser-light scattering method.
Thromb Haemost, 83 (2000), pp. 475-479
[80.]
A. Ceriello, A. Quatraro, E. Marchi, M. Barbanti, D. Giugliano.
Impaired fibrinolytic response to increased thrombin activation in type 1 diabetes mellitus: effects of the glycosaminoglycan sulodexide.
Diabete Metab, 19 (1993), pp. 225-229
[81.]
A. Ceriello, C. Taboga, L. Tonutti, R. Giacomello, G. Stel, E. Motz, et al.
Post-meal coagulation activation in diabetes mellitus: the effect of acarbose.
Diabetologia, 39 (1996), pp. 469-473
[82.]
E. Ruosladti.
Integrins.
J Clin Invest, 187 (1991), pp. 1-5
[83.]
M.F. Lopes-Virella, G. Virella.
Immune mechanism of atherosclerosis in diabetes mellitus.
Diabetes, 41 (1992), pp. 86-91
[84.]
R. Marfella, K. Esposito, R. Giunta, G. Coppola, L. De Angelis, B. Farzati, et al.
Circulating adhesion molecules in humans: role of hyperglycaemia and hyperinsulinemia.
Circulation, 101 (2000), pp. 2247-2251
[85.]
K. Esposito, F. Nappo, R. Marfella, G. Giugliano, F. Giugliano, M. Ciotola, et al.
Inflammatory cytokine concentrations are acutely increased by hyperglycaemia in humans: role of oxidative stress.
Circulation, 106 (2002), pp. 2069-2072
[86.]
F. Nappo, K. Esposito, M. Cioffi, G. Giugliano, A.M. Molinari, G. Paolisso, et al.
Posprandial endothelial activation in healthy subjects and in type 2 diabetic patients: role of fat and carbohydrate meals.
J Am Coll Cardiol, 39 (2002), pp. 1145-1150
[87.]
A. Festa, R. D’Agostino Jr, R.P. Tracy, S.M. Haffner.
C-reactive protein in more strongly related to post-glucose load glucose than to fasting glucose in non-diabetic subjects: the Insulin Resistance Atherosclerosis Study.
Diabet Med, 19 (2002), pp. 939-943
[88.]
P.H. Groot, W.A. Van Stiphout, X.H. Krauss, H. Jansen, A. Van Tol, E. Van Ramshorst, et al.
Posprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease.
Arterioscler Thromb, 11 (1991), pp. 653-662
[89.]
J.A. Beckman, A.B. Goldfine, M.B. Gordon, M.A. Creager.
Ascorbate restores endothelium-dependent vasodilatation impaired by acute hyperglycaemic in humans.
Circulation, 103 (2001), pp. 1618-1623
[90.]
M.P. Habib, F.D. Dickerson, A.D. Mooradian.
Effects of diabetes, insulin and glucose load on lipid peroxidation in the rat.
Metabolism, 43 (1994), pp. 1442-1445
[91.]
J.C. Brand-Miller.
Glycemic index in relation to coronary disease.
Asia Pac J Clin Nutr, 13 (2004), pp. S3
[92.]
D. Ludwig.
The glycemic index: physiological mechanisms relating to obesity, diabetes and cardiovascular disease.
JAMA, 287 (2002), pp. 2414-2423
[93.]
S. Dickinson, J. Brand-Miller.
Glycemic index, posprandial glycaemia and cardiovascular disease.
Curr Opin Lipidol, 16 (2005), pp. 69-75
[94.]
T. Kunt.
Current strategies for controlling posprandial hyperglycaemia.
Int J Clin Pract, 123 (2001), pp. 19-23
[97.]
P. Home, L. Barrioncanal, A. Lindholm.
Comparative pharmacokinetics and pharmacodynamics of the novel rapid-acting insulin analogue insulin aspart in healthy volunteers.
Eur J Clin Pharmacol, 55 (1999), pp. 199-203
[98.]
S. Heller, S. Amiel, P. Mansell.
Effect of the fast-acting insulin analogue lispro on the risk of nocturnal hypoglycaemia during intensified insulin therapy: UK Lispro Study Group.
Diabetes Care, 22 (1999), pp. 1607-1611
[99.]
C. Hedman, T. Lindstrom, H. Arnqvist.
Direct comparison of insulin lispro and aspart shows small differences in plasma insulin profiles after subcutaneous injection in type 1 diabetes.
Diabetes Care, 24 (2001), pp. 1120-1121
[100.]
G. Bolli, R. Marchi, G. Park, S. Pramming, V. Koivisto.
Insulin analogues and their potential in the management of diabetes mellitus.
Diabetologia, 42 (1999), pp. 1151-1167
[101.]
Z. Vajo, J. Fancett, W. Duckworth.
Recombinant DNA technology in the treatment of diabetes: insulin analogues.
Endocr Rev, 22 (2001), pp. 706-717
[102.]
E.J. Bastyr 3rd, C.A. Stuart, R.G. Brodows, S. Schwartz, C.J. Graf, A. Zagar, For the IOEZ Study Group, et al.
Therapy focused on lowering posprandial glucose, not fasting glucose, may be superior for lowering HbA1C.
Diabetes Care, 23 (2000), pp. 1236-1241
[103.]
P.D. Home, A. Lindholm, B. Hylleberg, P. Round, For the UK Insulin Aspart Study Group.
Improved glycemic control with insulin aspart: a multicenter randomised double-blind crossover trial in type 1 diabetic patients.
Diabetes Care, 21 (1998), pp. 1904-1909
[104.]
A. Ceriello, A. Cavarape, L. Martinelli, R. Da Ros, G. Marra, L. Quagliaro, et al.
The posprandial state in type 2 diabetes and endothelial dysfunction: effects of insulin aspart.
Diabet Med, 21 (2004), pp. 171-175
[105.]
Z. Milicevic, I. Raz, K. Strojek, J. Skrha, M.H. Tan, J.W. Wyatt, et al.
Hyperglycaemia and its effect after acute myocardial infarction on cardiovascular outcomes in patients with type 2 diabetes mellitus (HEART2D) Study design.
J Diabetes Complications, 19 (2005), pp. 80-87
[106.]
E.T. Shapiro, E. Van Cauter, H. Tillil, B.D. Given, L. Hirsch, C. Beebe, et al.
Glyburide enhances the responsiveness of the beta-cell to glucose but does not correct the abnormal patterns of insulin secretion in noninsulin-dependent diabetes mellitus.
J Clin Endocrinol Metab, 69 (1989), pp. 571-576
[107.]
A.D. Mooradian, J.E. Thurman.
Drug therapy of posprandial hyperglycaemia.
Drugs, 57 (1999), pp. 19-29
[108.]
H. Lebovitz.
Insulin segretagogues: old and new.
Diabet Rev, 7 (1999), pp. 139-153
[109.]
A. Dornhorst.
Insulinotropic meglitinide analogues.
Lancet, 358 (2001), pp. 1709-1716
[110.]
L.S. Phillips, B.E. Dunnig.
Nateglinide (Starlix): update on a new antidiabetic agent.
Int J Clin Pract, 57 (2003), pp. 535-541
[111.]
D.R. Owens, S.D. Luzio, I. Ismail, T. Bayer.
Increased prandial insulin secretion after administration of a single preprandial oral dose of repaglinide in patients with type 2 diabetes.
Diabetes Care, 23 (2000), pp. 518-523
[112.]
R. Landgraf, H.J.G. Bilo, P.G. Müller.
A comparison of repaglinide and glibenclamide in the treatment of type 2 diabetic patients previously treated with sulphonylureas.
Eur J Clin Pharmacol, 55 (1999), pp. 165-171
[113.]
B.H.R. Wolffenbuttel, R. Landgraf.
A 1-year multicenter randomized double-blind comparison of repaglinide and glyburide for the treatment of type 2 diabetes: Dutch and German Repaglinide Study Group.
Diabetes Care, 22 (1999), pp. 463-467
[114.]
T. Marbury, C. Huang W-, P. Strange, H. Lebovitz.
Repaglinide versus glyburide: a one-year comparison trial.
Diabetes Res Clin Pract, 43 (1999), pp. 155-166
[115.]
J. Guijo Linares, M. Parramón Ponz, En nombre del Grupo de Estudio de Repaglinida.
Empleo de la repaglinida en diabéticos tipo 2 mal controlados con sulfonilureas: un estudio observacional sobre 327 pacientes.
Endocrinol Nutr, 49 (2002), pp. 217-221
[116.]
R. Moses, R. Slobodniuk, S. Boyages, S. Colagiuri, W. Kidson, J. Carter, et al.
Effect of repaglinide addition to metformin monotherapy on glycemic control in patients with type 2 diabetes.
Diabetes Care, 22 (1999), pp. 119-124
[117.]
J.S. Kristensen, K.B. Frandsen, T. Bayer.
Compared with repaglinide sulphonylurea treatment in type 2 diabetes is associated with a 2.5-fold increase in symptomatic hypoglycaemia with blood glucose levels < 45 mg/dl (abstract).
Diabetes, 49 (2000), pp. A131
[118.]
J.S. Kristensen, K.B. Frandsen, T. Bayer.
Repaglinide treatment is associated with significantly less severe hypoglycaemic events compared to sulphonylurea (abstract).
Diabetologia, 42 (1999), pp. A4
[119.]
H. Schatz.
Preclinical and clinical studies on safety and tolerability of repaglinide.
Exp Clin Endocrinol Diabetes, 107 (1999), pp. S144-S148
[120.]
G. Derosa, A. Mugellini, L. Ciccarelli, G. Crescenzi, R. Fogari.
Comparison of glycemic control and cardiovascular risk profile in patients with type 2 diabetes during treatment with either repaglinide or metformin.
Diabetes Res Clin Pract, 60 (2003), pp. 161-169
[121.]
G. Derosa, A. Mugellini, L. Ciccarelli, G. Crescenzi, R. Fogari.
Comparison between repaglinide and glimepiride in patients with type 2 diabetes mellitus: a one-year, randomised, doubleblind assessment of metabolic parameters and cardiovascular risk factors.
Clin Ther, 25 (2003), pp. 472-484
[122.]
S. Hu, S. Wang, B. Fanelli, P.A. Bell, B.E. Dunning, S. Geisse, et al.
Pancreatic beta-cell K(ATP) channel activity and membrane- binding studies with nateglinide: a comparison with sulfonylureas and repaglinide.
J Pharmacol Exp Ther, 293 (2000), pp. 444-452
[123.]
R.B. Goldberg, D. Einhorn, C. Lucas, M.S. Rendell, P. Damsbo, W.C. Huang, et al.
A randomized placebo-controlled trial of repaglinide in the treatment of type 2 diabetes.
Diabetes Care, 21 (1998), pp. 1897-1903
[124.]
E. Horton, C. Clinkingbeard, M. Gatlin, J. Foley, J. Mallows, S. Shen.
Nateglinide alone and in combination with metformin improves glycemic control by reducing mealtime glucose levels in type 2 diabetes.
Diabetes Care, 23 (2000), pp. 1660-1665
[125.]
J. Kalbag, J. Walter, J. Nedelman, J. McLeod.
Mealtime glucose regulation with nateglinide in healthy volunteers: comparison with repaglinide and placebo.
Diabetes Care, 24 (2001), pp. 73-77
[126.]
M. Saad, P. Hale, N. Khutoryansky.
Efficacy of repaglinide versus nateglinide as monotherapy or metformin combination therapy (abstract).
Diabetes, 51 (2002), pp. A133
[127.]
J.A. Balfour, M.I. Wilde.
Management of type 2 diabetes defining the role of acarbose.
Dis Manage Health Outcomes, 2 (1997), pp. 248-260
[128.]
A.D. Baron.
Posprandial hyperglycaemia and alpha-glucosidase inhibitors.
Diabetes Res Clin Pract, 40 (1998), pp. S51-S55
[129.]
L.J. Scott, C.M. Spencer.
Miglitol: a review of its therapeutic potential in type 2 diabetes mellitus.
Drugs, 59 (2000), pp. 521-549
[130.]
G. Pagano, S. Marena, L. Corgiat-Mansin, F. Cravero, C. Giorda, M. Bozza, et al.
Comparison of miglitol and glibenclamide in diet-treated type 2 diabetic patients.
Diabetes Metab, 21 (1995), pp. 162-167
[131.]
J.L. Chiasson, R.G. Josse, J.A. Hunt, C. Palmason, N.W. Rodger, S.A. Ross, et al.
The efficacy of acarbose in the treatment of patients with non-insulin dependent diabetes mellitus. A multicenter controlled clinical trial.
Ann Intern Med, 121 (1994), pp. 928-935
[132.]
H.E. Lebovitz.
Alpha-glucosidase inhibitors as agents in the treatment of diabetes.
Diabetes Rev, 6 (1998), pp. 132-145
[133.]
M. Hanefeld.
The role of acarbose in the treatment of non-insulin- dependent diabetes mellitus.
J Diabetes Complications, 12 (1998), pp. 226-237
[134.]
R.R. Holman, C.A. Cull, R.C. Turner.
A randomized doubleblind trial of acarbose in type 2 shows improved glycemic control over 3 years (UK Prospective Diabetes Study 44).
Diabetes Care, 22 (1999), pp. 960-964
[135.]
U. Zeymer, A. Schwarzmaier-D’Assie, D. Petzinna, J.L. Chiasson.
STOP-NIDDM Trial Research Group. Effect of acarbose treatment on the risk of silent myocardial infarctions in patients with impaired glucose tolerance: results of the randomised STOP-NIDDM trial electrocardiography substudy.
Eur J Cardiovasc Prev Rehabil, 11 (2004), pp. 412-415
[136.]
S. Franz, L. Calvillo, J. Tillmanns, I. Elbing, C. Dienesch, H. Bischoff, et al.
Repetitive posprandial hyperglycaemia increases cardiac ischemia/reperfusion injury: prevention by the alpha- glucosidase inhibitor acarbose.
FASEB J, 19 (2005), pp. 591-593
[137.]
J. Rosenstock, M. Gatlin, S. Mallows, C. Bush.
Nateglinide improves glycemic control alone and in combination with troglitazone in patients with type 2 diabetes.
Diabetes, (2000), pp. 498
[138.]
P. Raskin, L. Jovanovic, S. Berger, S. Schwartz, V. Woo, R. Ratner.
Repaglinide/troglitazone combination therapy: improved glycemic control in type 2 diabetes.
Diabetes Care, 23 (2000), pp. 979-983
[139.]
P. Raskin, J. Mcgill, P. Hale, N. Khutoryansky, O. Santiago.
Repaglinide/rosiglitazone combination therapy of type 2 diabetes (abstract).
Diabetes, 50 (2002), pp. A128
[140.]
L. Jovanovic, R. Jain, S. Greco, P. Hale, N. Khutoryansky, O. Santiago.
Repaglinide/pioglitazone combination therapy of type 2 diabetes (abstract).
Diabetes, 50 (2002), pp. A439
[141.]
D.A. De Luis, R. Aller, L. Cuéllar, C. Terroba, H. Ovalle, O. Izaola, et al.
Effect of repaglinide addition to NPH insulin monot- herapy on glycemic control in patients with type 2 diabetes.
Diabetes Care, 24 (2001), pp. 1844-1845
[142.]
A. Mitrakou, N. Tountas, A.E. Raptis, R.J. Bauer, H. Schulz, S.A. Raptis.
Long-term effectiveness of a new alpha-glucosidase inhibitor (BAY m1099-miglitol) in insulin-treated type 2 diabetes mellitus.
Diabet Med, 15 (1998), pp. 657-660
[143.]
L.F. Van Gaal, I.H. Leeuw.
Rationale and options for combination therapy in the treatment of type 2 diabetes.
Diabetologia, (2003), pp. M44-50
[144.]
O. Schmitz, B. Nyholm, L. Orskov, C. Gravholt, N. Moller.
Effects of amylin and the amylin agonist pramlintide on glucose metabolism.
Diabet Med, 14 (1997), pp. S19-S23
[145.]
B. Thorens, G. Waeber.
Glucagon-like peptide-I and the control of insulin secretion in the normal state and in NIDDM.
Diabetes, 42 (1993), pp. 1219-1225
[146.]
C.B. Juhl, M. Hollingdal, J. Sturis, G. Jakobsen, H. Agerso, J. Veldhuis, et al.
Bedtime administration of NN2211, a long-acting GLP-1 derivate, substantially reduces fasting and posprandial glycaemia in type 2 diabetes.
Diabetes, 51 (2000), pp. 424-429
[148.]
R. Thomson, A. Gottlieb, K. Organ, J. Koda, J. Kisicki, O. Kolterman.
Pramlintide: a human amylin analogue reduced posprandial plasma glucose, insulin, and C-peptide concentrations in patients with type 2 diabetes.
Diabet Med, 14 (1997), pp. 547-555
[149.]
M. Zander, S. Madsbad, J.L. Madsen, J.J. Holst.
Effect of 6-week course of glucagon-like peptide 1 on glycemic control, insulin sensitivity, and beta-cell function in type 2 diabetes.
Lancet, 359 (2002), pp. 824-830
[150.]
J. Todd, C. Edwards, M. Ghatei, H. Mather, S. Bloom.
Subcutaneous glucagon-like peptide-1 improves posprandial glycemic control over a 3-week period in patients with early type 2 diabetes.
Clin Sci (Lond.), 95 (1998), pp. 325-329
[151.]
J.M. Egan, A. Bulotta, H. Hui, R. Perfetti.
GLP-1 receptor agonists are growth and differentiation factors for pancreatic islet beta cells.
Diabetes Metb Res Rev, 19 (2003), pp. 115-123
[153.]
C. Edwards, S. Stanley, R. Davis, A.E. Brynes, G.S. Frost, L.J. Seal, et al.
Exendin-4 reduces fasting and posprandial glucose and decreases energy intake in healthy volunteers.
Am J Physiol Endocrinol Metab, 281 (2001), pp. E155-E161
[154.]
E.B. Villhauer, J.A. Brinkman, G.B. Naderi, B.F. Burkey, B.E. Dunning, K. Prasad, et al.
1-[[3-Hydroxy-1adamantyl) amino] acetyl]-2-cyano-(S)-pyrrolidine: a potent, selective, and orally bioavailable dipeptidylpeptidase IV inhibitor with antihyperglycemic properties.
J Med Chem, 46 (2003), pp. 2774-2789
[155.]
L. Heinemann, T. Traut, T. Heise.
Time-action profile of inhaled insulin.
Diabet Med, 14 (1997), pp. 63-72
[156.]
T. Heise, K. Rave, S. Bott.
Time-action profile of an inhaled insulin preparation in comparison to insulin lispro and regular insulin (abstract).
Diabetes, 49 (2000), pp. A10
[157.]
W. Cefalu, J. Skyler, I. Kourides, W.H. Landschulz, C.C. Balagtas, S. Cheng, et al.
Inhaled human insulin treatment in patients with type 2 diabetes mellitus.
Ann Intern Med, 134 (2001), pp. 203-207
[158.]
J. Skyler, W. Cefalu, I. Kourides, W.H. Landschulz, C.C. Balagtas, S. Cheng, et al.
Efficacy of inhaled human insulin in type 1 diabetes mellitus: a randomised proof-of-concept study.
Lancet, 357 (2001), pp. 331-335
Copyright © 2005. Sociedad Española de Endocrinología y Nutrición
