Lack of Racial Disparity in Incident Prediabetes and Glycemic Progression Among Black and White Offspring of Parents With Type 2 Diabetes: The Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) Study
Lack of Racial Disparity in Incident Prediabetes and Glycemic Progression Among Black and White Offspring of Parents With Type 2 Diabetes: The Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) Study
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DOI：
10.1210/jc.2014-1077
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发表时间：
2014-06-01
影响因子：
5.8
通讯作者：
Wan, Jim
中科院分区：
文献类型：
--
作者：
Dagogo-Jack, Samuel;Edeoga, Chimaroke;Wan, Jim
背景：虽然2型糖尿病(T2D)在糖尿病前期人群中的发病率是众所周知的(类似于每年10%)，但在血糖正常的人群中，糖尿病前期的发病率尚不清楚。此外，在糖尿病预防计划中，糖尿病发病率存在正常/种族差异，报告的T2D患病率存在明显的种族/民族差异。设计和方法：我们招募了376名(217名黑人，159名白人)患有T2D(平均年龄44.2岁)的父母的非糖尿病子女，并每季度跟踪他们一次，为期5.5年。评估包括人体测量、身体成分、口服葡萄糖耐量试验、生化、能量消耗、胰岛素敏感性和胰岛素分泌。结果：在343名有可评估数据的参与者中，101名(49名白人，52名黑人)发展为糖尿病前期，10名(4名白人，6名黑人)在平均2.62年的随访期内发展为糖尿病。在糖尿病前期(32.7%的白人，30%的黑人)或合并糖尿病/糖尿病(35%的白人，30%的黑人)的累积发病率方面没有明显的种族差异。糖尿病前期的显著预测因素包括年龄、性别、躯干脂肪、2小时负荷后血糖(2hrPG)、胰岛素敏感性和胰岛素分泌。在Cox比例风险模型中，调整年龄和性别后，2hrPG和腹型肥胖是糖尿病前期/糖尿病发病的独立预测因素[相对危险度(95%可信区间[CI])分别为：躯干脂肪质量2.90(95%可信区间1.74-4.82)，P<；0.0001；2hrPG 2.54(95%可信区间1.46-4.40)，P=.0009]。在这两项指标中，躯干脂肪质量和2hrPG位于第90个百分位数的人患糖尿病前期的风险是位于第10个百分位数的人的7倍。结论：父母患有2型糖尿病的黑人和白人子女患糖尿病前期的风险相似，每年约为11%。因此，有必要对亲代糖尿病患者进行密切监测，并及时进行干预，以预防血糖紊乱。
Background: Although the incidence of type 2 diabetes (T2D) among persons with prediabetes is well known (similar to 10%/y), the incidence of prediabetes among normoglycemic persons is unclear. Also, in the Diabetes Prevention Program, noracial/ethnic differences were seen in diabetes incidence, where as marked racial/ethnic disparities are reported in the prevalence of T2D. We aimed to obtain estimates of incident prediabetes and determine whether racial disparities manifest during transition to prediabetes.Design and Methods: We enrolled 376 (217 black, 159 white) nondiabetic offspring of parents with T2D (mean age 44.2 y) and followed them up quarterly for 5.5 years. Assessments included anthropometry, body composition, oral glucose tolerance test, biochemistries, energy expenditure, insulin sensitivity, and insulin secretion. The primary outcome was progression to impaired fasting glucose and/or impaired glucose tolerance (or diabetes).Results: Of 343 participants with evaluable data, 101 subjects (49 white, 52 black) developed prediabetes, and 10 (4 white, 6 black) developed diabetes during a mean follow-up of 2.62 years. There was no significant racial difference in the cumulative incidence of prediabetes (32.7% white, 30% black) or combined prediabetes/diabetes (35% white, 30% black). Significant predictors of prediabetes included age, gender, trunk fat, 2-hour postload glucose (2hrPG), insulin sensitivity, and insulin secretion. In a Cox proportional-hazards model, with adjustment for age and sex, the 2hrPG and abdominal obesity were independent predictors of incident prediabetes/diabetes [relative hazards(95% confidence interval [CI]) for the 90th vs 10th percentile: trunk fat mass 2.90 (95% CI 1.74-4.82), P < .0001; 2hrPG 2.54 (95% CI 1.46-4.40), P = .0009]. Having the trunk fat mass and the 2hrPG at the 90th percentile conferred a 7-fold hazard of prediabetes compared with persons at the 10th percentile for both measures.Conclusion: Black and white offspring of parents with type 2 diabetes develop prediabetes at a similar high rate of approximately 11% per year. Therefore, close surveillance, with prompt intervention to prevent dysglycemia, is warranted in persons with parental diabetes.