Studies on the relative contributions of fasting and postprandial hyperglycemia (FH and PPH) to HbA in type 2 diabetes (T2D) subjects have yielded inconsistent results. We aimed to assess the relationship by using continuous glucose monitoring (CGM) in a multi-ethnic cohort.,100 T2D adults were assessed with 6-day CGM and HbA . Area under the curve (AUC) ≥5.6 mmol/L was defined as AUC . AUC ≥ each pre-prandial glucose for 4 hours was defined as AUC . The total PPH (AUC ) was the sum of the various AUC The post-prandial contribution to overall hyperglycemia was calculated as (AUC / AUC ) × 100%.,This study comprised of Malays, Indians, and Chinese T2D at 34%, 34%, and 28% respectively. Overall, mean PPH significantly decreased as HbA advanced (MMRM adjusted, Beta-estimate = -3.0, p=0.009). Age (p=0.010) and hypoglycemia (p=0.006) predicted the contribution difference. In oral antidiabetic drug (OAD)-treated subjects (n=58), FH contribution increased from 54% (HbA 6-6.9%) to 67% (HbA ≥10%). FH predominance was significant in poorly-controlled groups (p=0.028 at HbA 9-9.9%; p=0.015 at HbA ≥10%). Among insulin-users (n=42), FH predominated when HbA ≥10% before adjustment for hypoglycemia (p=0.047), whilst PPH was numerically greater when HbA <8%.,FH and PPH contributions were equal in well-controlled Malaysians T2D in real-world practice. FH predominated when HbA was ≥9% and ≥10% in OAD- and insulin-treated subjects respectively. A unique observation was the greater PPH contribution when HbA <8% despite the use of basal and mealtime insulin in this multi-ethnic cohort, which required further validation. This article is protected by copyright. All rights reserved.
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