Usually, the increment of 30-minute postchallenge plasma glucose (ΔG30-0) represents the highest glucose spike in the population with normal glucose regulation (NGR). The aim of this study was to explore the differences in ΔG30-0 and urinary albumin excretion, a marker for widespread vascular damage, between premenopausal and postmenopausal women, and the relationship between ΔG30-0 and urinary albumin excretion.
A population-based cross-sectional study, consisting of 5,289 participants aged 20 to 75 years from six different communities, was conducted in Shanghai between 2007 and 2008. We assessed postchallenge blood glucose and insulin at 0-, 30-, and 120-minute urinary albumin and creatinine. ΔG30-0 was calculated as 30-minute postchallenge glucose minus fasting plasma glucose, and the albumin-to-creatinine ratio (ACR) was used to reflect urinary albumin excretion. Among these, the data of 2,240 women with NGR were analyzed.
(1) Postmenopausal women had higher ΔG30-0 and ACR than did premenopausal women (3.55 ± 1.52 mmol/L vs 3.21 ± 1.49 mmol/L and 6.92 [4.91-10.99] mg/g vs 6.18 [4.17-10.07] mg/g, respectively; all P < 0.001). (2) Multivariable logistic regression showed that ΔG30-0 was independently associated with increased ACR in postmenopausal women with NGR (odds ratio, 1.10; P = 0.048) but not in premenopausal women. (3) The main factor associated with ΔG30-0 was the early-phase glucose disposition index drawn from the multivariable linear regression, which explained approximately 19% and 28% of the variation of ΔG30-0 in premenopausal and postmenopausal women, respectively (both P < 0.001).
In the NGR population, postmenopausal women have higher ΔG30-0 and ACR compared with premenopausal women. The relationship between ΔG30-0 and increased urine albumin excretion existed in postmenopausal women.
From the 1Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated to Sixth People’s Hospital; 2Shanghai Diabetes Institute; 3Shanghai Clinical Center of Diabetes; and 4Shanghai Zhabei Center for Disease Control and Prevention, Shanghai, China.
Received February 17, 2011; revised and accepted April 12, 2011.
Funding/support: This work was supported by the Major Program of Shanghai Municipality for Basic Research (08dj1400601), Shanghai Key Laboratory of Diabetes Mellitus (08DZ2230200), Joint program from the National Natural Science Foundation of China and Canadian Institutes of Health Research (30811120437), and the Shanghai United Developing Technology Project of Municipal Hospitals (SHDC12010115).
Financial disclosure/conflicts of interests: None reported.
Drs. Li and Hou contributed equally to the work.
Address correspondence to: Weiping Jia, MD, PhD, Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated to Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China. E-mail: email@example.com