Journal List > J Korean Diabetes > v.17(4) > 1055028

Oh: Postprandial Hyperglycemia

Abstract

Postprandial hyperglycemia is an important factor in the progression of diabetes and related complications. To reduce the burden of the diabetes epidemic in Korea, a better understanding of the pathophysiology of postprandial hyperglycemia is needed as well as optimal treatment modalities based on individual characteristics of the patient. The standard oral glucose tolerance test can be used to identify those at high risk for diabetes and cardiovascular disease. In the treatment of postprandial hyperglycemia, physicians should provide lifestyle modification support as well as appropriate pharmacological treatment, such as incretin-based therapies. Further clinical trials using recently developed anti-diabetic treatments focusing on postprandial hyperglycemia are needed to evaluate the effectiveness of targeting postprandial hyperglycemia in order to prevent diabetes and diabetes complications.

References

1. Ceriello A. Postprandial hyperglycemia and diabetes complications: is it time to treat? Diabetes. 2005; 54:1–7.
2. 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; 26:881–5.
3. Bartoli E, Fra GP, Carnevale Schianca GP. The oral glucose tolerance test (OGTT) revisited. Eur J Intern Med. 2011; 22:8–12.
crossref
4. Abdul-Ghani MA, Williams K, DeFronzo RA, Stern M. What is the best predictor of future type 2 diabetes? Diabetes Care. 2007; 30:1544–8.
crossref
5. Oh TJ, Min SH, Ahn CH, Kim EK, Kwak SH, Jung HS, Park KS, Cho YM. Normal glucose tolerance with a high 1-hour postload plasma glucose level exhibits decreased beta-cell function similar to impaired glucose tolerance. Diabetes Metab J. 2015; 39:147–53.
6. Tschritter O, Fritsche A, Shirkavand F, Machicao F, Häring H, Stumvoll M. Assessing the shape of the glucose curve during an oral glucose tolerance test. Diabetes Care. 2003; 26:1026–33.
crossref
7. Woerle HJ, Szoke E, Meyer C, Dostou JM, Wittlin SD, Gosmanov NR, Welle SL, Gerich JE. Mechanisms for abnormal postprandial glucose metabolism in type 2 diabetes. Am J Physiol Endocrinol Metab. 2006; 290:E67–77.
crossref
8. Avogaro A. Postprandial glucose: marker or risk factor? Diabetes Care. 2011; 34:2333–5.
crossref
9. Raz I, Wilson PW, Strojek K, Kowalska I, Bozikov V, Gitt AK, Jermendy G, Campaigne BN, Kerr L, Milicevic Z, Jacober SJ. Effects of prandial versus fasting glycemia on cardiovascular outcomes in type 2 diabetes: the HEART2D trial. Diabetes Care. 2009; 32:381–6.
crossref
10. NAVIGATOR Study Group. Holman RR, Haffner SM, McMurray JJ, Bethel MA, Holzhauer B, Hua TA, Belenkov Y, Boolell M, Buse JB, Buckley BM, Chacra AR, Chiang FT, Charbonnel B, Chow CC, Davies MJ, Deedwania P, Diem P, Einhorn D, Fonseca V, Fulcher GR, Gaciong Z, Gaztambide S, Giles T, Horton E, Ilkova H, Jenssen T, Kahn SE, Krum H, Laakso M, Leiter LA, Levitt NS, Mareev V, Martinez F, Masson C, Mazzone T, Meaney E, Nesto R, Pan C, Prager R, Raptis SA, Rutten GE, Sandstroem H, Schaper F, Scheen A, Schmitz O, Sinay I, Soska V, Stender S, Tamás G, Tognoni G, Tuomilehto J, Villamil AS, Vozár J, Califf RM. Effect of nateglinide on the incidence of diabetes and cardiovascular events. N Engl J Med. 2010; 362:1463–76.
11. Chiasson JL, Josse RG, 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; 290:486–94.
12. Shiraiwa T, Kaneto H, Miyatsuka T, Kato K, Yamamoto K, Kawashima A, Kanda T, Suzuki M, Imano E, Matsuhisa M, Hori M, Yamasaki Y. Postprandial hyperglycemia is a better predictor of the progression of diabetic retinopathy than HbA1c in Japanese type 2 diabetic patients. Diabetes Care. 2005; 28:2806–7.
crossref
13. Bongaerts BW, Rathmann W, Kowall B, Herder C, Stöckl D, Meisinger C, Ziegler D. Postchallenge hyperglycemia is positively associated with diabetic polyneuropathy: the KORA F4 study. Diabetes Care. 2012; 35:1891–3.
crossref
14. Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA. 2002; 287:2414–23.
15. Malik VS, Popkin BM, Bray GA, Després JP, Hu FB. Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk. Circulation. 2010; 121:1356–64.
crossref
16. Canfora EE, Jocken JW, Blaak EE. Short-chain fatty acids in control of body weight and insulin sensitivity. Nat Rev Endocrinol. 2015; 11:577–91.
crossref
17. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM. 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.
crossref
18. Nauck M. Incretin therapies: highlighting common features and differences in the modes of action of glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors. Diabetes Obes Metab. 2016; 18:203–16.
crossref
TOOLS
Similar articles