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Using continuous glucose monitoring to assess contributions of premeal and postmeal glucose levels in diabetic patients treated with metformin alone

Authors :
S.-T. Tu
S.-Y. Wang
S.-D. Lin
S.-R. Hsu
S.-L. Su
Source :
Diabetes & Metabolism. 42:336-341
Publication Year :
2016
Publisher :
Elsevier BV, 2016.

Abstract

Aim This study aimed to determine the contributions of basal excess glycaemia (BEG) and prandial excess glycaemia (PEG) to overall excess glycaemia in type 2 diabetes (T2D) patients treated with metformin alone. Methods Outpatients with T2D treated with metformin alone ( n =46) who underwent continuous glucose monitoring (CGM) were divided into tertiles according to glycated haemoglobin (HbA 1c ) levels. For each CGM trace, the glucose area under the curve (AUC)>5.5mmol/L was expressed as the AUC overall , representing overall excess glycaemia. The sum of glucose AUCs above the premeal glucose level at 4h after breakfast, lunch and dinner was expressed as the AUC peg , representing PEG. The contribution of PEG to overall excess glycaemia was calculated as (AUC peg /AUC overall )×100%. The contribution of BEG was calculated as [(AUC overall −AUC peg )/AUC overall ]×100%. Factors related to PEG contribution were also analysed. Results BEG constituted more than half the overall excess glycaemia in all HbA 1c tertiles. The contribution of PEG was negatively correlated with HbA 1c and mean glucose values before each meal. Prebreakfast and predinner glucose values were the dominant factors affecting PEG contribution and was independent of HbA 1c . Conclusion In patients treated with metformin alone, BEG was the major contributor to excess glycaemia at HbA 1c levels ≥7.7%, while PEG and BEG contributions were similar and stable below this level. For HbA 1c levels ≥7.7%, add-on therapy to metformin should preferentially target control of BEG, whereas targeting both BEG and PEG could be of equivalent importance with lower HbA 1c levels.

Details

ISSN :
12623636
Volume :
42
Database :
OpenAIRE
Journal :
Diabetes & Metabolism
Accession number :
edsair.doi.dedup.....92dc20352dc0fa38d3caebac42381133
Full Text :
https://doi.org/10.1016/j.diabet.2016.03.002