Diabetes & Metabolism Journal

Original Articles

Lifestyle and Behavioral Interventions
The Preventive Effect of Physical Activity on Gestational Diabetes Mellitus: A Korean Longitudinal Prospective Cohort Study: Ji Hyae Lim, Min Hyoung Kim, Hye-Ji Han, Su Ji Yang, Myung-Gwan Kim, Hyun Jung Lee, You Jung Han, Jin Hoon Chung, Dong Wook Kwak, Seongwoo Yang, Moon Young Kim, Hyun Mee Ryu; Received May 30, 2024 Accepted December 3, 2024 Published online April 23, 2025; DOI: https://doi.org/10.4093/dmj.2024.0280 [Epub ahead of print]

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Abstract PDF Supplementary Material PubReader ePub: Background
To assess longitudinally physical activity patterns and intensity from pre-pregnancy to postpartum and evaluate the association between timing and type of physical activity and the development of gestational diabetes mellitus (GDM).
Methods
The Korean Pregnancy Outcome Study (KPOS) is a prospective cohort study conducted from 2013 to 2017. Our study included 3,457 participants with singleton pregnancies in KPOS, classified according to the pregnancy outcome: GDM (n=231) and normal (n=3,226). Physical activity data were collected at five time points using the short form of the International Physical Activity Questionnaire: before pregnancy, at 12, 24, and 36 gestational weeks (GW), and 6–8 weeks postpartum. Pre-pregnancy physical activity was collected through recall at 12 GW.
Results
Maternal age, pre-pregnancy body mass index, educational status, smoking, mini dietary assessment index, first-degree family history of diabetes, hypertension, parity, pre-existing GDM, and previous macrosomia showed significant differences between the GDM group and the normal group (P<0.05 for all). Pre-pregnancy muscle-strengthening activity was significantly associated with a lower risk of GDM (adjusted odds ratio, 0.46; 95% confidence interval, 0.25 to 0.85).
Conclusion
These findings suggest that physical activity, such as muscle-strengthening activities before pregnancy, could be a preventive strategy to reduce GDM risk. Although the study does not provide evidence that physical activity during pregnancy and postpartum reduces GDM risk, it offers significant insights into the importance of maintaining a healthy level of physical activity from pre-pregnancy to prevent GDM.

Autoimmune Hypoglycemia in a Patient with Characterization of Insulin Receptor Autoantibodies: Suk Chon, Moon Chan Choi, Yun Jung Lee, You Cheol Hwang, In-Kyung Jeong, Seungjoon Oh, Kyu Jeung Ahn, Ho Yeon Chung, Jeong-Taek Woo, Sung-Woon Kim, Jin-Woo Kim, Young Seol Kim; Diabetes Metab J. 2011;35(1):80-85. Published online February 28, 2011; DOI: https://doi.org/10.4093/dmj.2011.35.1.80

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Background

Type B insulin resistance syndrome is a manifestation of autoantibodies to the insulin receptor that results in severe hyperglycemia and acanthosis nigricans. However, the mechanisms by which these autoantibodies induce hypoglycemia are largely unknown. In this paper, we report the case of patient with type B insulin resistance syndrome who presented with frequent severe fasting hypoglycemia and acanthosis nigricans.

Methods

To evaluate the mechanism of hypoglycemia, we measured the inhibition of insulin binding to erythrocytes and IM9 lymphocytes in a sample of the patient's dialyzed serum before and after immunosuppressive therapy.

Results

In the patient's pre-treatment serum IgG, the binding of ¹²⁵I-insulin to erythrocytes was markedly inhibited in a dose-dependent manner until the cold insulin level reached 10^-9 mol/L. We also observed dose-dependent inhibition of insulin binding to IM9 lymphocytes, which reached approximately 82% inhibition and persisted even when diluted 1:20. After treatment with glucocorticoids, insulin-erythrocyte binding activity returned to between 70% and 80% of normal, while the inhibition of insulin-lymphocyte binding was reduced by 17%.

Conclusion

We treated a patient with type B insulin resistance syndrome showing recurrent fasting hypoglycemia with steroids and azathioprine. We characterized the patient's insulin receptor antibodies by measuring the inhibition of insulin binding.

Citations

Citations to this article as recorded by

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