Dagogo-Jack Samuel, Edeoga Chimaroke, Ebenibo Sotonte, Nyenwe Ebenezer, Wan Jim
Department of Medicine (S.D.-J., C.E., S.E., E.N.), Division of Endocrinology, Diabetes and Metabolism, General Clinical Research Center (S.D.-J.), and Department of Preventive Medicine (J.W.), University of Tennessee Health Science Center, Memphis, Tennessee 38163.
J Clin Endocrinol Metab. 2014 Jun;99(6):E1078-87. doi: 10.1210/jc.2014-1077. Epub 2014 Mar 14.
Although the incidence of type 2 diabetes (T2D) among persons with prediabetes is well known (∼10%/y), the incidence of prediabetes among normoglycemic persons is unclear. Also, in the Diabetes Prevention Program, no racial/ethnic differences were seen in diabetes incidence, whereas 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.
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).
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.
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.
虽然糖尿病前期人群中2型糖尿病（T2D）的发病率是众所周知的（约10%/年），但血糖正常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，糖尿病发病率未见种族/民族差异，而T2D患病率则报告存在明显的种族/民族差异。我们旨在获得糖尿病前期发病率的估计值，并确定在向糖尿病前期转变过程中种族差异是否会显现。
我们招募了376名（217名黑人，159名白人）父母患有T2D的非糖尿病后代（平均年龄44.2岁），并对他们进行了为期5.5年的季度随访。评估包括人体测量、身体成分、口服葡萄糖耐量试验、生化指标、能量消耗、胰岛素敏感性和胰岛素分泌。主要结局是进展为空腹血糖受损和/或葡萄糖耐量受损（或糖尿病）。
在343名有可评估数据的参与者中，101名受试者（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年的随访期间发展为糖尿病。糖尿病前期的累积发病率（白人32.7%，黑人30%）或糖尿病前期/糖尿病合并发病率（白人35%，黑人30%）没有显著的种族差异。糖尿病前期的显著预测因素包括年龄、性别、躯干脂肪、负荷后2小时血糖（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和腹部肥胖是糖尿病前期/糖尿病发病的独立预测因素[第90百分位数与第10百分位数相比的相对风险（95%置信区间[CI]）：躯干脂肪量2.90（95%CI 1.74 - 4.82），P <.0001；2hrPG 2.54（95%CI 1.46 - 4.40），P =.0009]。与两项指标均处于第10百分位数的人相比，躯干脂肪量和2hrPG处于第90百分位数的人患糖尿病前期的风险高7倍。
父母患有2型糖尿病的黑人和白人后代患糖尿病前期的年发生率相似，约为11%。因此，对于有糖尿病家族史的人，有必要进行密切监测，并及时干预以预防血糖异常。
