Estimates of the relative and absolute diurnal contributions of fasting and post-prandial plasma glucose over a range of hyperglycaemia in type 2 diabetes

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AimsTo 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 methodsA 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. ResultsWith 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). ConclusionsFasting 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%.