R Peter1, G Dunseath, S D Luzio, D R Owens. 1. Diabetes Research Group, Swansea University, Swansea, United Kingdom. Electronic address: rajpeter@aol.com.
Abstract
AIMS: To re-examine the relative and absolute contributions of fasting/pre-prandial glucose (FPG) and post-prandial glucose (PPG) to 24-h hyperglycaemia and HbA1c respectively in non-insulin treated subjects with type 2 diabetes (T2DM). MATERIALS AND METHODS: A total of 52 T2DM subjects (37 men) had daytime 12h plasma glucose (PG) profiles determined in response to three serial identical test meals commencing at 08 00h with pre-prandial and frequent post-prandial blood samples collected. The overnight PG profile was derived by projecting the 20 00h glucose concentration to the pre-breakfast value at 08 00h. PPG exposure was calculated above fasting/pre-prandial value for each meal. Excess hyperglycaemia was calculated based on a PG>5.5mmol/L with fasting hyperglycaemia being the difference between the two measurements. The subjects were divided into five groups according to the HbA1c (Group 1<7.0%; Group 2: 7.0-<7.5; Group 3: 7.5-<8.0%; Group 4: 8.0-<9.0%; Group 5:≥9.0%). The 24h relative contribution of PPG exposure and fasting hyperglycaemia to excess hyperglycaemia and the absolute contribution of PPG and fasting hyperglycaemia to excess HbA1c (HbA1c - 5.1%) was calculated. RESULTS: With deteriorating glycaemia, the relative contribution of PPG exposure decreased across the groups from 43.5% (HbA1c<7.0%) to 17.8% (HbA1c≥9.0%), whilst the contributions of fasting hyperglycaemia increased from 56.5% to 82.2% (P=0.004), respectively. The absolute contributions of PPG to excess HbA1c was 0.7%, which remained relatively stable across the spectrum of HbA1c, whilst fasting hyperglycaemia increased significantly from groups 1 to 5 (P<0.001). CONCLUSIONS: Fasting hyperglycaemia contributes substantially in all groups, increasing as HbA1c deteriorates. The absolute contribution of PPG to excess HbA1c did not vary across the range of HbA1c, representing a significant relative contribution even in well-controlled subjects with a HbA1c<7.0%.
AIMS: To re-examine the relative and absolute contributions of fasting/pre-prandial glucose (FPG) and post-prandial glucose (PPG) to 24-h hyperglycaemia and HbA1c respectively in non-insulin treated subjects with type 2 diabetes (T2DM). MATERIALS AND METHODS: A total of 52 T2DM subjects (37 men) had daytime 12h plasma glucose (PG) profiles determined in response to three serial identical test meals commencing at 08 00h with pre-prandial and frequent post-prandial blood samples collected. The overnight PG profile was derived by projecting the 20 00h glucose concentration to the pre-breakfast value at 08 00h. PPG exposure was calculated above fasting/pre-prandial value for each meal. Excess hyperglycaemia was calculated based on a PG>5.5mmol/L with fasting hyperglycaemia being the difference between the two measurements. The subjects were divided into five groups according to the HbA1c (Group 1<7.0%; Group 2: 7.0-<7.5; Group 3: 7.5-<8.0%; Group 4: 8.0-<9.0%; Group 5:≥9.0%). The 24h relative contribution of PPG exposure and fasting hyperglycaemia to excess hyperglycaemia and the absolute contribution of PPG and fasting hyperglycaemia to excess HbA1c (HbA1c - 5.1%) was calculated. RESULTS: With deteriorating glycaemia, the relative contribution of PPG exposure decreased across the groups from 43.5% (HbA1c<7.0%) to 17.8% (HbA1c≥9.0%), whilst the contributions of fasting hyperglycaemia increased from 56.5% to 82.2% (P=0.004), respectively. The absolute contributions of PPG to excess HbA1c was 0.7%, which remained relatively stable across the spectrum of HbA1c, whilst fasting hyperglycaemia increased significantly from groups 1 to 5 (P<0.001). CONCLUSIONS:Fasting hyperglycaemia contributes substantially in all groups, increasing as HbA1c deteriorates. The absolute contribution of PPG to excess HbA1c did not vary across the range of HbA1c, representing a significant relative contribution even in well-controlled subjects with a HbA1c<7.0%.