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【转载】10-year trajectory of β-cell function and insulin sensitivity in the development of type 2 diabetes  

2015-11-20 13:40:58|  分类: 医学知识 |  标签: |举报 |字号 订阅

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【转载】10-year trajectory of β-cell function and insulin sensitivity in the development of type 2 diabetes - liusongjifan2 - liusongjifan2的博客
 
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10-year trajectory of β-cell function and insulin sensitivity in the development of type 2 diabetes: a community-based prospective cohort study

,,,
 Soo Lim, MD
,
 Prof Hak Chul Jang, MD
,
 Prof Kyong Soo Park, MD?correspondenceemail
,
 Prof Nam H Cho, PhD?correspondenceemail
*Contributed equally
?Contributed equally
Published Online: 11 November 2015

showArticle Info

Publication History
Published Online:11 November 2015
? 2015 Elsevier Ltd. All rights reserved.
This article can be found in the following collections: Diabetes
Jump to SectionIntroductionMethodsResultsDiscussionSupplementary MaterialReferences

Summary

Background

The relative contributions of β-cell function and insulin sensitivity in the pathogenesis of type 2 diabetes are not fully understood. We investigated the longitudinal change in β-cell function and insulin sensitivity in the development of diabetes and the role of genetic variants in deterioration of glucose tolerance.

Methods

We followed up 4106 participants with normal glucose tolerance (NGT) from the Korean Genome and Epidemiology Study with oral glucose tolerance tests every 2 years for 10 years. We estimated pancreatic β-cell function with the 60 min insulinogenic index (IGI60) and insulin sensitivity with the composite (Matsuda) insulin sensitivity index (ISI). We investigated the association of 66 known type 2 diabetes genetic variants with risk of prediabetes or diabetes and impaired β-cell function and insulin sensitivity.

Findings

During 10 years of follow-up, 1093 (27%) of 4106 participants developed prediabetes and 498 (12%) participants developed diabetes. Compared with participants who remained NGT, those who progressed to diabetes had a lower IGI60 (unadjusted data 5·1 μU/mmol [95% CI 0·5–56·1] vs 7·9 μU/mmol [0·5–113·8]; p<0·0001) and lower ISI (unadjusted data 8·2 [2·6–26·0] vs 10·0 [3·2–31·6]; p<0·0001) at baseline. Participants who had NGT at 10 years showed a decrease in ISI (adjusted data 10·1 [9·9–10·3] vs 7·4 [7·3–7·6]; p<0·0001) but a compensatory increase in IGI60 (adjusted data 6·9 μU/mmol [6·5–7·2] vs 11·7 μU/mmol [11·2–12·1]; p<0·0001) compared with baseline. By contrast, participants who developed diabetes showed a decrease in ISI (adjusted data 8·4 [8·0–8·7] vs 3·0 [2·8–3·2]; p<0·0001) but no significant compensatory increase (p=0·95) in IGI60. A genetic variant near the glucokinase gene (rs4607517) was significantly associated with progression to prediabetes or diabetes (hazard ratio 1·27, 1·16–1·38; p=1·70?×?10?7).

Interpretation

Decreased β-cell function, which might be determined partly by genetic factors, and impaired β-cell compensation for progressive decline in insulin sensitivity are crucial factors in the deterioration of glucose tolerance.

Funding

South Korean Ministry of Health & Welfare.

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