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OBJECTIVE: To examine the relative contributions of [beta]-cell dysfunction and insulin resistance to postpartum diabetes risk among obese and nonobese women with prior gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS: We performed a cross-sectional survey 1-5 years after 1,263 women who had GDM gave birth. Polytomous logistic regression models were used to assess the associations of [beta]-cell dysfunction (the lower quartile of HOMA-%[beta]), insulin resistance (the upper quartile of HOMA-IR), decreased insulin sensitivity (the lower quartile of HOMA-%S), and different categories of BMI with prediabetes and diabetes risk. RESULTS: [beta]-Cell dysfunction, insulin resistance, and decreased insulin sensitivity all were significantly associated with hyperglycemic status across normal weight, overweight, and obese groups, and the patterns of insulin resistance and decreased insulin sensitivity were similar. BMI was inversely associated with [beta]-cell dysfunction and positively associated with insulin resistance across normal glucose, prediabetes, and diabetes categories. Compared with women with normal glucose and weight, obese women with normal glucose had increased [beta]-cell secretory function (odds ratio [OR] 0.09 [95% CI 0.02-0.37]) and insulin resistance (OR 17.4 [95% CI 9.47-31.9]). Normal weight diabetic women displayed the most [beta]-cell dysfunction (OR 13.6 [95% CI 4.06-45.3]), whereas obese diabetic women displayed the highest insulin resistance (OR 45.8 [95% CI 18.5-113]). CONCLUSIONS: For women with prior GDM, [beta]-cell dysfunction had more pronounced contribution to postpartum diabetes among nonobese subjects, whereas insulin resistance contributed more to postpartum hyperglycemia among obese subjects. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the race-specific association between a history of GDM and incidence of type 2 diabetes and evaluate how the risk changed over different years after delivery. We performed two large cohorts - the Coronary Artery Risk Development in Young Adults (CARDIA) cohort with African Americans and whites in the U.S. (188 GDM and 1625 non-GDM women), and the Tianjin GDM Observational Study with Chinese in China (1263 GDM and 705 non-GDM women). The multivariate cox regression model was used to assess the risk of incident diabetes postpartum between women with and without GDM. During a mean follow-up of 13.9 years, 419 women developed type 2 diabetes. After adjustment for multiple confounding factors, Chinese women with GDM had a higher risk of incident diabetes within 5 years postpartum than African Americans with GDM compared with Chinese and African Americans without GDM (Hazard ratio 71.5 in Chinese vs. 11.0 in African Americans). When the risk of incident diabetes was analyzed within 10 years, white women with GDM seemed to have a higher hazard ratio than African American and Chinese women with GDM compared with women without GDM of different race. In comparison to African American women without GDM, different racial women with GDM showed an increased risk of type 2 diabetes within 10 years postpartum, however, white women without GDM had a decreased risk of type 2 diabetes. The largest increased risk of type 2 diabetes over 10 years postpartum appeared in Chinese women with GDM (Hazard ratio 23.9), followed by African American women with GDM (Hazard ratio 4.92), and the smallest was seen in white women with GDM (Hazard ratio 3.57). Chinese women with a history of GDM had the highest risk of incident diabetes postpartum. The different genetic backgrounds and other risk factors among different races might contribute to the racial differences in the incidence of diabetes postpartum among women with GDM. Disclosure: Y. Shen: None. L. Hou: None. H. Liu: None. L. Wang: None. J. Leng: None. W. Li: None. G. Hu: None. Funding: Tianjin Women's and Children's Health Center; Tianjin Public Health Bureau; European Foundation for the Study of Diabetes/Chinese Diabetes Society; Lilly Program for Collaborative Research between China and Europe; National Institute of Diabetes and Digestive and Kidney Diseases (R01DK100790 to G.H.); National Institute of General Medical Sciences (U54GM104940 to G.H.) [ABSTRACT FROM AUTHOR]