Long-term diabetogenic effect of single pregnancy in women with previous gestational diabetes mellitus
Long-term diabetogenic effect of single pregnancy in women with previous gestational diabetes mellitus
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DOI：
10.1016/s0140-6736(96)90405-5
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发表时间：
1996-01-27
期刊：
影响因子：
168.9
通讯作者：
Buchanan, TA
中科院分区：
文献类型：
--
作者：
Peters, RK;Kjos, SL;Buchanan, TA
背景 怀孕与显着的胰岛素抵抗有关，这似乎对一般人群中非胰岛素依赖型糖尿病 (NIDDM) 的长期风险影响很小（如果有的话）。本研究的目的是测试妊娠是否会改变胰腺 β 细胞功能障碍高发女性患 NIDDM 的风险（如妊娠糖尿病史所示）。 方法 该队列由 666 名在高风险计划生育诊所就诊的患有妊娠糖尿病的拉丁裔女性组成。他们被随访了长达 7.5 年，在此期间，他们每年都会被称重并接受口服葡萄糖耐量测试。研究人员检查了额外妊娠以及其他糖尿病危险因素的影响。结果显示，87 名女性 (13%) 完成了额外妊娠。其中 80 名女性在额外妊娠后并未立即患 NIDDM，其随后的 NIDDM 年发病率为 30.9%（95% CI 12.7-49.1），是队列整体 NIDDM 年发病率（11.9%；95% CI 10.0-13.8）的 2.5 倍以上。使用是否存在额外妊娠作为时间相关变量的比例风险回归分析证实，在调整妊娠期间其他潜在糖尿病危险因素（产前口服葡萄糖耐量、最高空腹血糖、诊断时孕龄）后，与没有额外妊娠的女性相比，额外妊娠将 NIDDM 比率提高至 3.34（95% CI 1.80-6.19） 妊娠糖尿病）和随访期间（产后体重指数 [BMI]、葡萄糖耐量、体重变化、母乳喂养和避孕措施使用月数）。体重增加也与 NIDDM 风险增加独立相关；调整额外妊娠和其他潜在危险因素后，随访期间每增加 10 磅（4.5 千克），比率为 1.95（95% CI 1.63-2.33）。 解释 该研究表明，在一组胰腺 β 细胞功能障碍高发的女性中，单次妊娠（与体重增加的众所周知的影响无关）加速了 NIDDM 的发展。这一发现意味着胰岛素抵抗的发作可能会导致β细胞功能下降，从而导致许多高危个体患上NIDDM。
Background Pregnancy is associated with marked insulin resistance that seems to have little, if any, impact on the long-term risk of non-insulin-dependent diabetes mellitus (NIDDM) in the general population. The aim of this study was to test whether pregnancy would alter the risk of NIDDM among women with a high prevalence of pancreatic beta-cell dysfunction, as indicated by a history of gestational diabetes mellitus.Methods The cohort consisted of 666 Latino women with gestational diabetes attending a high-risk family planning clinic. They were followed up for up to 7.5 years, during which lime they were weighed and underwent an oral glucose-tolerance test annually. The effect of an additional pregnancy, and of other risk factors for diabetes, was examined.Findings 87 (13%) of the women completed an additional pregnancy. 80 of those women did not have NIDDM immediately after the additional pregnancy and their subsequent annual incidence rate of NIDDM was 30.9% (95% CI 12.7-49.1), more than 2.5 times the annual incidence rate of NIDDM in the cohort overall (11.9%; 95% CI 10.0-13.8). Proportional hazards regression analysis using the presence or absence of an additional pregnancy as a time-dependent variable confirmed that an additional pregnancy increased the rate ratio of NIDDM to 3.34(95% CI 1.80-6.19), compared with women without an additional pregnancy after adjustment for other potential diabetes risk factors during the index pregnancy (antepartum oral glucose tolerance, highest fasting glucose, gestational age at diagnosis of gestational diabetes) and during follow-up (postpartum body mass index [BMI], and glucose tolerance, weight change, breast feeding, and months of contraceptive use). Weight gain also was independently associated with an increased risk of NIDDM; the rate ratio was 1.95 (95% CI 1.63-2.33) for each 10 lb (4.5 kg) gained during follow-up after adjustment for the additional pregnancy and the other potential risk factors.Interpretation The study showed that a single pregnancy, independent of the well-known effect of weight gain, accelerated the development of NIDDM in a group of women with a high prevalence of pancreatic beta-cell dysfunction. This finding implies that episodes of insulin resistance may contribute to the decline in beta-cell function that leads to NIDDM in many high-risk individuals.