Abstract
The high incidence of atherosclerosis and cardiovascular disease is the leading cause of morbidity and mortality among diabetic patients. It is well known that postprandial hyperglycemia is an independent risk factor for diabetic complications and mortality. For better management of diabetic patients, effort must be put forth to not only achieve the HbA1c target, but also to control postprandial hyperglycemia. This article reviews the pathophysiology and clinical aspects of postprandial hyperglycemia to appropriately control blood glucose level.
References
2. Gerich JE. Clinical significance, pathogenesis, and management of postprandial hyperglycemia. Arch Intern Med. 2003. 163:1306–1316.
3. Rohlfing CL, Wiedmeyer HM, Little RR, England JD, Tennill A, Goldstein DE. Defining the relationship between plasma glucose and HbA(1c): analysis of glucose profiles and HbA(1c) in the Diabetes Control and Complications Trial. Diabetes Care. 2002. 25:275–278.
4. Firth RG, Bell PM, Marsh HM, Hansen I, Rizza RA. Postprandial hyperglycemia in patients with noninsulin-dependent diabetes mellitus. Role of hepatic and extrahepatic tissues. J Clin Invest. 1986. 77:1525–1532.
5. 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.
6. Heine RJ, Balkau B, Ceriello A, Del Prato S, Horton ES, Taskinen MR. What does postprandial hyperglycaemia mean? Diabet Med. 2004. 21:208–213.
7. Leiter LA, Ceriello A, Davidson JA, Hanefeld M, Monnier L, Owens DR, Tajima N, Tuomilehto J. International Prandial Glucose Regulation Study Group. Postprandial glucose regulation: new data and new implications. Clin Ther. 2005. 27:Suppl B. S42–S56.