Normnahe postprandiale Hyperglykämie - eine essenzielle Komponente guter Diabeteskontrolle und Prävention kardiovaskulärer Erkrankungen

Zusammenfassung

Die postprandiale (pp) Glukosehomöostase ist von zentraler Bedeutung für die Manifestation eines Prädiabetes und die Progression des manifesten Typ-2-Diabetes. Bereits gering erhöhte pp Glukoseanstiege sind mit Störungen der Insulinsekretion, Erhöhung von kardiovaskulären Risikofaktoren, gestörter Gerinnung und Aktivierung der subklinischen Entzündung assoziiert. Störungen der pp Glukoseregulation wirken gleichermaßen diabetogen und atherogen. Dementsprechend zeigen prospektive Studien, dass die pp Hyperglykämie ein eigenständiger kardiovaskulärer Risikofaktor ist. Studien, die auf eine Kontrolle der postprandialen Hyperglykämie ausgerichtet waren, erbrachten eine signifikante Senkung kardiovaskulärer Ereignisse (STOP-NIDDM, MERIA). Im HbA1c-Bereich zwischen 6,5 % und 8 % sind > 60 % der Varianz im HbA1c-Bereich durch die postprandiale Hyperglykämie determiniert. Deshalb sind Monitoring und Behandlung der pp Hyperglykämie ein essenzieller Bestandteil einer guten Diabetestherapie. Ziel ist die normnahe Einstellung mit 2-h-pp-Werten < 140 mg / dl.

Abstract

Postprandial (pp) glucohomeostasis is of central importance for development of impaired glucose tolerance and progression of overt type 2 diabetes. Already minor elevations of pp glucose excursion are associated with impairment of insulin secretion, increase in cardiovascular risk factors, increased coagulation and activation of low grade inflammation resp.. Impaired pp glucoseregulation has harmful effects on progression of diabetes as well as on atherogenesis. In accordance prospective studies reveal that pp hyperglycemia is a cardiovascular risk factor in its own right. Studies directed to control pp hyperglycemia have been shown to achieve a significant reduction in cardiovascular disease (STOP-NIDDM, MERIA). In patients with type 2 diabetes and HbA1c between 6.5 % and 8 % > 60 % of variance in HbA1c is determined by quality of pp glucose control. Therefore monitoring and treatment of pp hyperglycemia is an essential part of good diabetes treatment. Target is a near to normal control with 2 h pp plasma glucose < 140 mg / dl.

Schlüsselwörter

postprandiale Hyperglykämie - Diabeteskontrolle - Risikofaktor - kardiovaskuläre Erkrankungen - Glukotrias

Key words

postprandial hyperglycemia - diabetes control - risk factor - cardiovascular disease - glucotriad

Literatur

• 1 Lawes C M, Parag V, Bennett D A, Suh I, Lam T H, Whitlock G, Barzi F, Woodward M. Asia Pacific Cohort Studies Collaboration . Blood glucose and risk of cardiovascular disease in the Asia Pacific region.  Diabetes Care. 2004;  27 2836-2842
• 2 Hanefeld M, Fischer S, Julius U, Schulze J, Schwanebeck U, Schmechel H, Ziegelasch H J, Lindner J. the DIS Group . Risk factors for myocardial infarction and death in newly detected NIDDM: The Diabetes Intervention Study, 11 years follow-up.  Diabetologia. 1996;  39 1577-1583
• 3 DECODE Study Group, the European Diabetes Epidemiology Group . Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria.  Arch Intern Med. 2001;  161 397-405
• 4 Hanefeld M, Koehler C, Henkel E, Fuecker K, Schaper F, Temelkova-Kurktschiev T. Post-challenge hyperglycaemia relates more strongly than fasting hyperglycaemia with carotid intima-media thickness: the RIAD Study. Risk Factors in Impaired Glucose Tolerance for Atherosclerosis and Diabetes.  Diabet Med. 2000;  17 835-840
• 5 [No authors listed] . The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the diabetes control and complications trial.  Diabetes. 1995;  44 968-983
• 6 Chiasson J L, Josse R G, Gomis R, Hanefeld M, Karasik A, Laakso M. 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. 2003;  290 486-494
• 7 Stettler C, Allemann S, Juni P, Cull C A, Holman R R, Egger M, Krahenbuhl S, Diem P. Glycemic control and macrovascular disease in types 1 and 2 diabetes mellitus: Meta-analysis of randomized trials.  Am Heart J. 2006;  152 27-38
• 8 Gaede P, Vedel P, Parving H H, Pedersen O. Intensified multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: the Steno type 2 randomised study.  Lancet. 1999;  353 617-622
• 9 Stratton I M, Adler A I, Neil H A, Matthews D R, Manley S E, Cull C A, Hadden D, Turner R C, Holman R R. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study.  BMJ. 2000;  321 405-412
• 10 Malmberg K, Norhammar A, Wedel H, Ryden L. 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. 1999;  99 2626-2632
• 11 Hanefeld M, Koehler C, Gallo S, Benke I, Ott P. Impact of the individual components of the metabolic syndrome and their different combinations on the prevalence of atherosclerotic vascular disease in type 2 diabetes: the Diabetes in Germany (DIG) study.  Cardiovasc Diabetol. 2007;  6 13
• 12 Giugliano D, Ceriello A, Paolisso G. Oxidative stress and diabetic vascular complications.  Diabetes Care. 1996;  19 257-267
• 13 Ceriello A, Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited.  Arterioscler Thromb Vasc Biol. 2004;  24 816-823
• 14 Monnier L, Mas E, Ginet C, Michel F, Villon L, Cristol J P, Colette C. Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes.  JAMA. 2006;  295 1681-1687
• 15 Hanefeld 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
• 16 Rudofsky G, Reismann P, Schiekofer S, Petrov D, van Eynatten M, Humpert P M, Müller-Hoff C, Thanh-Phuong T, Lichtenstein S, Bärtsch U, Hamann A, Nawroth P, Bierhaus A. Reduction of postprandial hyperglycemia in patients with type 2 diabetes reduces NF-αB activation in PBMCs.  Horm Met Res. 2004;  36 630-638
• 17 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
• 18 DECODA Study Group; International Diabetes Epidemiology Group . Cardiovascular risk profile assessment in glucose-intolerant Asian individuals - an evaluation of the World Health Organization two-step strategy: the DECODA Study (Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Asia).  Diabet Med. 2002;  19 549-557
• 19 Blake D R, Meigs J B, Muller D C, Najjar S S, Andres R, Nathan D M. Impaired glucose tolerance, but not impaired fasting glucose, is associated with increased levels of coronary heart disease risk factors: results from the Baltimore Longitudinal Study on Aging.  Diabetes. 2004;  53 2095-2100
• 20 Ceriello A. Acute hyperglycaemia: a ‘new’ risk factor during myocardial infarction.  Eur Heart J. 2005;  26 328-331
• 21 Levitan E B, Song Y, Ford E S, Liu S. Is nondiabetic hyperglycemia a risk factor for cardiovascular disease? A meta-analysis of prospective studies.  Arch Intern Med. 2004;  164 2147-2155
• 22 Hanefeld M, Cagatay M, Petrowitsch T, Neuser D, Petzinna D, Rupp M. Acarbose reduces the risk for myocardial infarction in type 2 diabetic patients: meta-analysis of seven long-term studies.  Eur Heart J. 2004;  25 10-16
• 23 Gerstein H C, Yusuf S, Bosch J, Pogue J, Sheridan P, Dinccag N, Hanefeld M, Hoogwerf B, Laakso M, Mohan V, Shaw J, Zinman B, Holman R R. DREAM (Diabetes REduction Assessment with ramipril and rosiglitazone Medication) Trial Investigators . Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trial.  Lancet. 2006;  368 1096-1105
• 24 Knowler W C, Barrett-Connor E, Fowler S E, Hamman R F, Lachin J M, Walker E A, Nathan D M. 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
• 25 Hanefeld M, Chiasson J L, Koehler C, Henkel E, Schaper F, Temelkova-Kurktschiev T. Acarbose slows progression of intima-media thickness of the carotid arteries in subjects with impaired glucose tolerance.  Stroke. 2004;  35 1073-1078
• 26 Esposito K, Giugliano D, Nappo F, Marfella R. Campanian Postprandial Hyperglycemia Study Group . Regression of carotid atherosclerosis by control of postprandial hyperglycemia in type 2 diabetes mellitus.  Circulation. 2004;  110 214-219
• 27 Shichiri M, Kishikawa H, Ohkubo Y, Wake N. Long-term results of the Kumamoto Study on optimal diabetes control in type 2 diabetic patients.  Diabetes Care. 2000;  Suppl 2 B 21-B 29
• 28 Clarke P M, Gray A M, Briggs A, Stevens R J, Matthews D R, Holman R R. UKPDS 72 United Kingdom Prospective Diabetes Study . Cost-utility analyses of intensive blood glucose and tight blood pressure control in type 2 diabetes (UKPDS 72).  Diabetologia. 2005;  48 868-877
• 29 Jönsson T, Ahrén B, Pacini G, Sundler F, Wierup N, Steen S, Sjöberg T, Ugander M, Frostegård J, Göransson L, Lindeberg S A. Paleolithic diet confers higher insulin sensitivity, lower C-reactive protein and lower blood pressure than a cereal-based diet in domestic pigs.  Nutr Metab (Lond). 2006;  3 39
• 30 Mann J, McAuley K. Carbohydrates: is the advice to eat less justified for diabetes and cardiovascular health.  Curr Opin Lipidol. 2007;  18 9-12