Associations of the HOMA2‐%B and HOMA2‐IR with progression to diabetes and glycaemic deterioration in young and middle‐aged Chinese

医学 内科学 2型糖尿病 队列 胰岛素抵抗 糖尿病 危险系数 优势比 胰岛素 内分泌学 置信区间
作者
Baoqi Fan,Hongjiang Wu,Mai Shi,Aimin Yang,Eric S. H. Lau,Claudia H.T. Tam,Dandan Mao,Cadmon K.P. Lim,Alice P.S. Kong,Ronald C.W.,Elaine Chow,Andrea O. Y. Luk,Juliana C.N. Chan
出处
期刊:Diabetes-metabolism Research and Reviews [Wiley]
卷期号:38 (5) 被引量:14
标识
DOI:10.1002/dmrr.3525
摘要

Abstract Aims Insulin deficiency (ID) and resistance (IR) contribute to progression from normal glucose tolerance to diabetes to insulin requirement although their relative contributions in young‐onset diabetes is unknown. Methods We examined the associations of HOMA2 using fasting plasma glucose and C‐peptide in Chinese aged 20–50 years with (1) progression to type 2 diabetes (T2D) in participants without diabetes in a community‐based cohort (1998–2013) and (2) glycaemic deterioration in patients with T2D in a clinic‐based cohort (1995–2014). We defined ID as HOMA2‐%B below median and insulin IR as HOMA2‐IR above median. Results During 10‐year follow‐up, 62 (17.9%) of 347 community‐dwelling participants progressed to T2D. After 8.6 years, 291 (48.1%) of 609 patients with T2D had glycaemic deterioration. At baseline, progressors for T2D had higher HOMA2‐IR, while in patients with T2D, progressors for glycaemic deterioration had higher HOMA2‐IR and lower HOMA2‐%B than non‐progressors. The non‐ID/IR group and the ID/IR group had an adjusted odds ratios of 2.47 (95% CI: 1.28, 4.94) and 5.36 (2.26, 12.79), respectively, for incident T2D versus the ID/non‐IR group. In patients with T2D, 50% of the ID/IR group required insulin at 6.7 years versus around 11 years in the non‐ID/IR or ID/non‐IR, and more than 15 years in the non‐ID/non‐IR group. Compared with the latter group, the adjusted hazard ratios were 2.74 (1.80, 4.16) in the ID/non‐IR, 2.73 (1.78, 4.19) in the non‐ID/IR and 4.46 (2.87, 6.91) in the ID/IR group ( p ‐interaction = 0.049). Conclusions In young Chinese adults, IR and ID contributed to progression to T2D and glycaemic deterioration.

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