Abstract
Background
The changes in insulin resistance and insulin secretion and their association with
changes in glucose regulation status in Asians with prediabetes remain uncertain.
Materials and Methods
We included Korean adults (aged 20-79 years) with prediabetes who underwent routine
medical check-ups at a mean interval of 5 years. Prediabetes was defined as fasting
plasma glucose (FPG) 5.6-6.9 mmol/l or HbA1c 5.7-6.4% (39-46 mmol/mol). Insulin resistance (HOMA-IR) and beta-cell function (HOMA-%B) indices were
assessed by homeostasis model assessment. Incident diabetes was defined as FPG ≥ 7.0 mmol/l, HbA1c ≥ 6.5% (48 mmol/mol), or initiation of antidiabetic medications.
Results
Among the 7,208 participants with prediabetes, 4,410 (61.2%) remained as prediabetes
(control group), 2,123 (29.5%) reverted to normal glucose regulation (regressors),
and 675 (9.4%) progressed to type 2 diabetes (progressors) after 5 years. Compared
with the control group, the progressors had higher baseline HOMA-IR (2.48 ± 1.45 versus
2.06 ± 1.20, P < 0.001), but similar baseline HOMA-%B (74.6 ± 47.6 versus 73.1 ± 41.4, P=0.68). By contrast, the regressors had lower baseline HOMA-IR (1.98 ± 1.14 versus
2.06 ± 1.20, P = 0.035) but higher baseline HOMA-%B (77.4 ± 43.1 versus 73.1 ± 41.4, P = 0.001). After 5 years, the progressors showed a 31% increase in HOMA-IR (2.48 ±
1.45 versus 3.24 ± 2.10, P < 0.001) and 15% decrease in HOMA-%B (74.6 ± 47.6 versus 63.8 ± 40.4, P < 0.001), whereas the regressors showed 29% decrease in HOMA-IR (1.98 ± 1.14 versus
1.41 ± 0.78, P < 0.001) and 4% increase in HOMA-%B (77.4 ± 43.1 versus 80.2 ± 47.9, P = 0.010).
Conclusions
Although increase in insulin resistance and decrease in beta-cell function both contributed
to the progression to type 2 diabetes from prediabetes, longitudinal change in insulin
resistance was the predominant factor in Koreans.
Key Indexing Terms
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Article info
Publication history
Published online: October 16, 2017
Accepted:
September 25,
2017
Received in revised form:
September 19,
2017
Received:
April 14,
2017
Footnotes
☆This work was presented as a poster in the 52nd European Association for the Study of Diabetes (EASD) Annual Meeting which was held in Munich, Germany on 12-16 September 2016.
☆☆The authors have no financial or other conflicts of interest to disclose.
Identification
Copyright
© 2017 Southern Society for Clinical Investigation. Published by All rights reserved.
