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"Youngsun Hong"

Original Article
[English]
Decreased Insulin Secretion in Women with Previous Gestational Diabetes Mellitus
Yoon Pyo Lee, Soo Kyung Lim, Ji young Chang, Eun kyo Jung, Youn-i Choi, Jee-Young Oh, Youngsun Hong, Yeon-Ah Sung, Hyejin Lee
Ewha Med J 2015;38(1):30-35.   Published online March 26, 2015
DOI: https://doi.org/10.12771/emj.2015.38.1.30
Objectives

Gestational diabetes mellitus (GDM) affects 2%-4% of the all pregnant women, and it is a major risk factor for development of type 2 DM. We performed this cross-sectional study to determine whether there were defects in insulin secretory capacity or insulin sensitivity in women with previous GDM.

Methods

On 6-8 weeks after delivery, 75 g oral glucose tolerance test was performed in 36 women with previous GDM and 19 non-pregnant control women matched with age and weight. Intravenous glucose tolerance test was performed on 10-14 weeks after delivery. Insulin secretory capacity measured as the acute insulin response to glucose (AIRg) and insulin sensitivity as minimal model derived sensitivity index (SI) were obtained. AIRg×SI (β-cell disposition index) was used as an index of β-cell function.

Results

Women with previous GDM were classified into normal glucose tolerance (postpartum-NGT, n=19) and impaired glucose tolerance (postpartum-IGT, n=17). Postpartum fasting glucose levels were significantly higher in postpartum-IGT compared to postpartum-NGT and control (P<0.05). AIRg×SI was significantly lower in postpartum-IGT compared to control (P<0.05). SI was lower in postpartum-NGT and postpartum-IGT compared to control, but the difference did not have the statistical significance. Frequency of parental history of type 2 diabetes was significantly greater in postpartum-IGT compared to postpartum-NGT (P<0.05).

Conclusion

Women with previous GDM showed impaired insulin secretion although their glucose tolerance states were restored to normal. It suggests impaired early insulin secretion may be a major pathophysiologic factor for development of type 2 DM, and this defect may be genetically determined.

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