OBJECTIVE: To study the features of postprandial glucose state in individuals with normal glucose regulation (NGR) and type 2 diabetes (T2DM) and the relations between hemoglobin A1c (HbA1c) and postprandial glucose in T2DM. METHODS: 41 NGR individuals and 60 newly diagnosed T2DM patients without previous management in Shanghai were measured by continuous glucose monitoring system for 3 days. The postprandial glucose spike (PGS), time to PGS (Deltat), postprandial glucose excursion (PPGE), duration of postprandial glucose (DUR) and incremental area under the curve of postprandial glucose (IAUC) were calculated in each individual. RESULTS: (1) The levels of PGS and Deltat in the T2DM group were significantly higher than those of the NGR group (all P < 0.01). The levels of PPGE, DUR and IAUC of the T2DM group were 5.87 mmol/L +/- 0.19 mmol/L, 14.1 h +/- 0.3 h and 2.04 mmol.L(-1).d +/- 0.09 mmol.L(-1).d respectively, all significantly higher than those of the NGR group (2.10 mmol/L +/- 0.12 mmol/L, 8.3 h +/- 0.4 h and 0.43 mmol.L(-1).d +/- 0.03 mmol.L(-1).d respectively, all P < 0.01). The breakfast had higher PGS and lower Deltat than those of lunch and dinner in the T2DM group (both P < 0.01). The PPGE was arranged from high to low in the order of breakfast, dinner and lunch. The highest IAUC appeared during dinner. (2) There was a significantly correlation between PPGE and IAUC (r = 0.93, P < 0.01) in the T2DM group. After being adjusted by preprandial glucose, the partial correlation of HbA1c and IAUC disappeared (before r = 0.29, P = 0.03, after P = 0.05). (3) The relative contribution of postprandial glucose to overall glucose levels in the T2DM group was significantly higher than that of the NGR group (18.1% +/- 0.8% vs 8.0% +/- 0.7%, P < 0.01), but both were significantly lower than those of preprandial glucose. (4) Relative contribution of postprandial hyperglycemia to overall diurnal hyperglycemia decreased progressively from the lowest to the highest quarter of HbA1c. By contrast, the relative contribution of preprandial hyperglycemia showed a significant increase with increasing levels of HbA1c. Postprandial hyperglycemia played a major role when the HbA1c level below 7.5% (P < 0.05). CONCLUSION: (1) The features of postprandial glucose state in T2DM is representative in the delay of PGS and excessive glucose excursion for a long time after the ingestion of a meal. (2) HbA1c can't reflect postprandial glucose excursions. PPGE can be used as a simple clinic index to evaluate the amplitude of postprandial glucose excursions. (3) Postprandial glucose excursions play a major role in T2DM suffering from mild or moderate hyperglycemia. The present results suggest that postprandial hyperglycemia is an important target for intervention when T2DM patients are approaching the ideal glycemic control.
OBJECTIVE: To study the features of postprandial glucose state in individuals with normal glucose regulation (NGR) and type 2 diabetes (T2DM) and the relations between hemoglobin A1c (HbA1c) and postprandial glucose in T2DM. METHODS: 41 NGR individuals and 60 newly diagnosed T2DM patients without previous management in Shanghai were measured by continuous glucose monitoring system for 3 days. The postprandial glucose spike (PGS), time to PGS (Deltat), postprandial glucose excursion (PPGE), duration of postprandial glucose (DUR) and incremental area under the curve of postprandial glucose (IAUC) were calculated in each individual. RESULTS: (1) The levels of PGS and Deltat in the T2DM group were significantly higher than those of the NGR group (all P < 0.01). The levels of PPGE, DUR and IAUC of the T2DM group were 5.87 mmol/L +/- 0.19 mmol/L, 14.1 h +/- 0.3 h and 2.04 mmol.L(-1).d +/- 0.09 mmol.L(-1).d respectively, all significantly higher than those of the NGR group (2.10 mmol/L +/- 0.12 mmol/L, 8.3 h +/- 0.4 h and 0.43 mmol.L(-1).d +/- 0.03 mmol.L(-1).d respectively, all P < 0.01). The breakfast had higher PGS and lower Deltat than those of lunch and dinner in the T2DM group (both P < 0.01). The PPGE was arranged from high to low in the order of breakfast, dinner and lunch. The highest IAUC appeared during dinner. (2) There was a significantly correlation between PPGE and IAUC (r = 0.93, P < 0.01) in the T2DM group. After being adjusted by preprandial glucose, the partial correlation of HbA1c and IAUC disappeared (before r = 0.29, P = 0.03, after P = 0.05). (3) The relative contribution of postprandial glucose to overall glucose levels in the T2DM group was significantly higher than that of the NGR group (18.1% +/- 0.8% vs 8.0% +/- 0.7%, P < 0.01), but both were significantly lower than those of preprandial glucose. (4) Relative contribution of postprandial hyperglycemia to overall diurnal hyperglycemia decreased progressively from the lowest to the highest quarter of HbA1c. By contrast, the relative contribution of preprandial hyperglycemia showed a significant increase with increasing levels of HbA1c. Postprandial hyperglycemia played a major role when the HbA1c level below 7.5% (P < 0.05). CONCLUSION: (1) The features of postprandial glucose state in T2DM is representative in the delay of PGS and excessive glucose excursion for a long time after the ingestion of a meal. (2) HbA1c can't reflect postprandial glucose excursions. PPGE can be used as a simple clinic index to evaluate the amplitude of postprandial glucose excursions. (3) Postprandial glucose excursions play a major role in T2DM suffering from mild or moderate hyperglycemia. The present results suggest that postprandial hyperglycemia is an important target for intervention when T2DM patients are approaching the ideal glycemic control.