1217-P: Insulin Sensitivity and Insulin Secretion Differentially Affect Birthweight and Postpartum Glucose

IF 6.2 1区医学 Q1 ENDOCRINOLOGY & METABOLISM

Diabetes Pub Date : 2024-07-19 DOI:10.2337/db24-1217-p

EMILY A. ROSENBERG, KAITLYN JAMES, DEEPTI PANT, SARAH HSU, ROBIN L. AZEVEDO, CHLOE MICHALOPOULOS, TANAYOTT THAWEETHAI, CAMILLE E. POWE, ARANTXA MEDINA BAEZ

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引用次数: 0

Abstract

Background: Insulin deficiency and insulin resistance are two fundamental mechanisms that lead to hyperglycemia. Despite variation in the underlying physiology, individuals with hyperglycemia in pregnancy are treated similarly. Methods: Pregnant women with diabetes risk factors completed a 2-hr 75-gram oral glucose tolerance test (OGTT) at 10-15 weeks’ gestation, 24-32 weeks’ gestation, and postpartum. We tested for associations between insulin sensitivity (opposite of insulin resistance, Matsuda index) or insulin secretory response (Stumvoll estimate) in the 1st trimester with birthweight percentile (for gestational age and sex) or 2-hr post-OGTT glucose postpartum. We used linear regression, adjusting for age, race/ethnicity, education, gestational age, BMI, GDM treatment (birthweight analyses), weeks postpartum (glucose analyses) and insulin sensitivity (insulin secretory response analyses). Results: We studied N=151 pregnant women at a median [IQR] =12 [11-13] weeks’ gestation. N=107 had data at median [IQR] 9 [7-13] weeks postpartum. A 1-unit increase in 1st trimester insulin sensitivity (log Matsuda) was associated with a decrease of 6.9 in birthweight percentile (95% CI [-13.7, -0.05] P=0.045). 1st trimester insulin secretory response (log Stumvoll) was not associated with birthweight (β=-12.7 95% CI [-28.3, 2.9] P=0.11). 1st trimester insulin sensitivity was not associated with postpartum 2-hr OGTT glucose (β=-0.80 95% CI [-9.6, 8.0] mg/dL P=0.86), while a 1 unit increase in 1st trimester insulin secretory response was associated with a 36 mg/dL decrease in 2-hr OGTT glucose (95% CI [-53.7, -18.8] P=<0.001). Conclusion: Early pregnancy insulin sensitivity is more strongly associated with birthweight, while insulin secretory response has a stronger relationship with postpartum glycemia. Insulin resistance may confer more risk for perinatal complications, while insulin deficiency may confer more risk for postpartum hyperglycemia. Disclosure E.A. Rosenberg: None. K. James: None. D. Pant: None. S. Hsu: None. R.L. Azevedo: None. C. Michalopoulos: None. T. Thaweethai: None. C.E. Powe: Consultant; Mediflix. Other Relationship; Wolters Kluwer Health. A. Medina Baez: None.

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1217-P：胰岛素敏感性和胰岛素分泌对出生体重和产后血糖的影响不同

背景：胰岛素缺乏和胰岛素抵抗是导致高血糖的两种基本机制。尽管潜在的生理机制存在差异，但对妊娠期高血糖患者的治疗方法却大同小异。方法：具有糖尿病风险因素的孕妇分别在妊娠 10-15 周、24-32 周和产后完成 2 小时 75 克口服葡萄糖耐量试验（OGTT）。我们检测了妊娠头三个月胰岛素敏感性（胰岛素抵抗的相反值，松田指数）或胰岛素分泌反应（Stumvoll 估计值）与出生体重百分位数（胎龄和性别）或产后 2 小时口服葡萄糖耐量试验后血糖之间的关系。我们采用线性回归法，对年龄、种族/民族、教育程度、胎龄、体重指数、GDM 治疗（出生体重分析）、产后周数（葡萄糖分析）和胰岛素敏感性（胰岛素分泌反应分析）进行了调整。研究结果我们对妊娠中位数[IQR] =12 [11-13]周的 151 名孕妇进行了研究。107名孕妇在产后9[7-13]周获得了中位数[IQR]数据。孕期前三个月胰岛素敏感性（松田对数）每增加 1 个单位，出生体重百分位数就会减少 6.9（95% CI [-13.7, -0.05] P=0.045）。怀孕头三个月的胰岛素分泌反应（log Stumvoll）与出生体重无关（β=-12.7 95% CI [-28.3, 2.9] P=0.11）。孕期前三个月的胰岛素敏感性与产后 2 小时 OGTT 血糖无关（β=-0.80 95% CI [-9.6, 8.0] mg/dL P=0.86），而孕期前三个月胰岛素分泌反应每增加 1 个单位，产后 2 小时 OGTT 血糖就会下降 36 mg/dL (95% CI [-53.7, -18.8] P=<0.001)。结论孕早期胰岛素敏感性与出生体重的关系更密切，而胰岛素分泌反应与产后血糖的关系更密切。胰岛素抵抗可能会增加围产期并发症的风险，而胰岛素缺乏可能会增加产后高血糖的风险。披露 E.A. Rosenberg：无。K. James：无。D. Pant：无：无。S. Hsu：无。R.L. Azevedo: None.C. Michalopoulos：无。T. Thaweethai：无：无。C.E. Powe：顾问；Mediflix.其他关系；Wolters Kluwer Health。A. Medina Baez：无。

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来源期刊

Diabetes 医学-内分泌学与代谢

CiteScore

12.50

自引率

2.60%

发文量

1968

审稿时长

1 months

期刊介绍： Diabetes is a scientific journal that publishes original research exploring the physiological and pathophysiological aspects of diabetes mellitus. We encourage submissions of manuscripts pertaining to laboratory, animal, or human research, covering a wide range of topics. Our primary focus is on investigative reports investigating various aspects such as the development and progression of diabetes, along with its associated complications. We also welcome studies delving into normal and pathological pancreatic islet function and intermediary metabolism, as well as exploring the mechanisms of drug and hormone action from a pharmacological perspective. Additionally, we encourage submissions that delve into the biochemical and molecular aspects of both normal and abnormal biological processes. However, it is important to note that we do not publish studies relating to diabetes education or the application of accepted therapeutic and diagnostic approaches to patients with diabetes mellitus. Our aim is to provide a platform for research that contributes to advancing our understanding of the underlying mechanisms and processes of diabetes.