Tanayott Thaweethai, Zainab Soetan, Kaitlyn James, Jose C Florez, Camille E Powe
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We derived the pregnancy insulin physiology (PIP) index to quantify β-cell compensation for insulin resistance.</p><p><strong>Results: </strong>Among 166 participants, 21 had early GDM and 24 developed classic GDM. Insulin sensitivity was reduced slightly in early pregnancy (β = -0.20, P < 0.001) and substantially in mid-late pregnancy (β = -0.47, P < 0.001) compared with postpartum. Insulin secretory response (adjusted for insulin sensitivity) was augmented in early pregnancy (β = 0.16, P < 0.001) and mid-late pregnancy (β = 0.16, P = 0.001) compared with postpartum. Compared with postpartum, the PIP index was augmented in early pregnancy (β = 215, P = 0.04) but not mid-late pregnancy (β = 55, P = 0.64). Early GDM was distinguished by a substantial reduction in early pregnancy insulin sensitivity (β = -0.59, P < 0.001) compared with postpartum. Both early and classic GDM lacked evidence of early pregnancy augmentation of insulin secretory response (adjusted for insulin sensitivity) and the PIP index (P > 0.1 vs. postpartum). Early pregnancy PIP index predicted GDM independent of participant characteristics (area under the curve without PIP index 0.70 [95% CI 0.61-0.79], area under the curve with PIP index 0.87 [95% CI 0.80-0.93]).</p><p><strong>Conclusions: </strong>β-Cell function is enhanced in early pregnancy. 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We evaluated longitudinal changes in insulin secretory response (log Stumvoll first-phase estimate) and insulin sensitivity (log Matsuda index) using linear mixed models. We then evaluated participants who met GDM criteria in early pregnancy (early GDM) and mid-late pregnancy (classic GDM) separately from those without GDM. We derived the pregnancy insulin physiology (PIP) index to quantify β-cell compensation for insulin resistance.</p><p><strong>Results: </strong>Among 166 participants, 21 had early GDM and 24 developed classic GDM. Insulin sensitivity was reduced slightly in early pregnancy (β = -0.20, P < 0.001) and substantially in mid-late pregnancy (β = -0.47, P < 0.001) compared with postpartum. Insulin secretory response (adjusted for insulin sensitivity) was augmented in early pregnancy (β = 0.16, P < 0.001) and mid-late pregnancy (β = 0.16, P = 0.001) compared with postpartum. Compared with postpartum, the PIP index was augmented in early pregnancy (β = 215, P = 0.04) but not mid-late pregnancy (β = 55, P = 0.64). Early GDM was distinguished by a substantial reduction in early pregnancy insulin sensitivity (β = -0.59, P < 0.001) compared with postpartum. Both early and classic GDM lacked evidence of early pregnancy augmentation of insulin secretory response (adjusted for insulin sensitivity) and the PIP index (P > 0.1 vs. postpartum). Early pregnancy PIP index predicted GDM independent of participant characteristics (area under the curve without PIP index 0.70 [95% CI 0.61-0.79], area under the curve with PIP index 0.87 [95% CI 0.80-0.93]).</p><p><strong>Conclusions: </strong>β-Cell function is enhanced in early pregnancy. 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引用次数: 1
摘要
目的:探讨血糖正常妊娠和妊娠期糖尿病(GDM)的胰岛素生理变化。研究设计和方法:受试者在妊娠≤15周(妊娠早期)、妊娠24-32周(妊娠中后期)和产后6-24周进行口服糖耐量试验。我们使用线性混合模型评估胰岛素分泌反应(log Stumvoll第一阶段估计)和胰岛素敏感性(log Matsuda指数)的纵向变化。然后，我们将妊娠早期(早期GDM)和妊娠中后期(典型GDM)符合GDM标准的参与者与非GDM的参与者分开评估。我们推导出妊娠胰岛素生理(PIP)指数来量化β细胞对胰岛素抵抗的补偿。结果:166例受试者中，早期GDM 21例，经典GDM 24例。与产后相比，胰岛素敏感性在妊娠早期略有降低(β = -0.20, P < 0.001)，在妊娠中后期显著降低(β = -0.47, P < 0.001)。与产后相比，妊娠早期(β = 0.16, P < 0.001)和妊娠中后期(β = 0.16, P = 0.001)的胰岛素分泌反应(经胰岛素敏感性调整)增强。与产后比较，妊娠早期PIP指数增高(β = 215, P = 0.04)，而妊娠中后期无增高(β = 55, P = 0.64)。与产后相比，早期GDM的特点是妊娠早期胰岛素敏感性显著降低(β = -0.59, P < 0.001)。早期和经典GDM均缺乏妊娠早期胰岛素分泌反应(经胰岛素敏感性调整)和PIP指数增强的证据(与产后相比P > 0.1)。妊娠早期PIP指数预测GDM与受试者特征无关(无PIP指数曲线下面积0.70 [95% CI 0.61-0.79]，有PIP指数曲线下面积0.87 [95% CI 0.80-0.93])。结论:妊娠早期β-细胞功能增强。妊娠早期β细胞功能缺陷预示GDM。
Distinct Insulin Physiology Trajectories in Euglycemic Pregnancy and Gestational Diabetes Mellitus.
Objective: To evaluate changes in insulin physiology in euglycemic pregnancy and gestational diabetes mellitus (GDM).
Research design and methods: Participants underwent oral glucose tolerance tests at ≤15 weeks' gestation (early pregnancy), 24-32 weeks' gestation (mid-late pregnancy), and 6-24 weeks postpartum. We evaluated longitudinal changes in insulin secretory response (log Stumvoll first-phase estimate) and insulin sensitivity (log Matsuda index) using linear mixed models. We then evaluated participants who met GDM criteria in early pregnancy (early GDM) and mid-late pregnancy (classic GDM) separately from those without GDM. We derived the pregnancy insulin physiology (PIP) index to quantify β-cell compensation for insulin resistance.
Results: Among 166 participants, 21 had early GDM and 24 developed classic GDM. Insulin sensitivity was reduced slightly in early pregnancy (β = -0.20, P < 0.001) and substantially in mid-late pregnancy (β = -0.47, P < 0.001) compared with postpartum. Insulin secretory response (adjusted for insulin sensitivity) was augmented in early pregnancy (β = 0.16, P < 0.001) and mid-late pregnancy (β = 0.16, P = 0.001) compared with postpartum. Compared with postpartum, the PIP index was augmented in early pregnancy (β = 215, P = 0.04) but not mid-late pregnancy (β = 55, P = 0.64). Early GDM was distinguished by a substantial reduction in early pregnancy insulin sensitivity (β = -0.59, P < 0.001) compared with postpartum. Both early and classic GDM lacked evidence of early pregnancy augmentation of insulin secretory response (adjusted for insulin sensitivity) and the PIP index (P > 0.1 vs. postpartum). Early pregnancy PIP index predicted GDM independent of participant characteristics (area under the curve without PIP index 0.70 [95% CI 0.61-0.79], area under the curve with PIP index 0.87 [95% CI 0.80-0.93]).
Conclusions: β-Cell function is enhanced in early pregnancy. Deficient first-trimester β-cell function predicts GDM.
期刊介绍：
The journal's overarching mission can be captured by the simple word "Care," reflecting its commitment to enhancing patient well-being. Diabetes Care aims to support better patient care by addressing the comprehensive needs of healthcare professionals dedicated to managing diabetes.
Diabetes Care serves as a valuable resource for healthcare practitioners, aiming to advance knowledge, foster research, and improve diabetes management. The journal publishes original research across various categories, including Clinical Care, Education, Nutrition, Psychosocial Research, Epidemiology, Health Services Research, Emerging Treatments and Technologies, Pathophysiology, Complications, and Cardiovascular and Metabolic Risk. Additionally, Diabetes Care features ADA statements, consensus reports, review articles, letters to the editor, and health/medical news, appealing to a diverse audience of physicians, researchers, psychologists, educators, and other healthcare professionals.
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