Abstract
Aim. The aim of this study is to investigate the relationship between the common C49620T polymorphism in the sulfonylurea receptor (SUR1) gene and glucose metabolism, β-cell secretory function and insulin resistance in women with a history of gestational diabetes (GDM). Material and Methods. Study group included 199 women, diagnosed GDM within the last 5–12 years and control group of comparable 50 women in whom GDM was excluded during pregnancy. Blood glucose and insulin levels were measured during oral glucose tolerance test. Indices of insulin resistance (HOMA-IR) and β-cell function (HOMA %B) were calculated. In all patients, the C49620T polymorphism in intron 15 of the SUR1 gene was determined. Results. The distribution of the studied polymorphism in the two groups did not differ from each other (χ 2 = 0.34, P = 0.8425). No association between the distribution of polymorphisms and coexisting glucose metabolism disorders (χ 2 = 7,13, P = 0, 3043) was found. No association was also observed between the polymorphism and HOMA %B or HOMA-IR. Conclusions. The polymorphism C49620T in the SUR1 gene is not associated with insulin resistance and/or insulin secretion in women with a history of GDM and does not affect the development of GDM, or the development of glucose intolerance in the studied population.
Highlights
Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy [1]
The study group consisted of 199 women, mean age 38.4 ± 6.6 years, who gave birth 5–12 years before the present study and in whom GDM was diagnosed during pregnancy with use of an oral glucose tolerance test (OGTT)
With regard to insulin sensitivity, homeostasis model assessment (HOMA)-IR and HOMA %S parameters were similar in both groups, whereas HOMA %B was found to be significantly lower in the study group
Summary
Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy [1]. Key predisposing factors to DM2 in such women include (1) obesity before and after pregnancy, (2) number of pregnancies, (3) age, (4) need for insulin therapy due to GDM, (5) obstetric failure, and (6) a positive family history of DM2 [2, 6,7,8] Both insulin resistance and inadequate insulin secretion are considered as Experimental Diabetes Research possible causes of the increased risk of DM2 [9,10,11,12]. It is not clear, what is their role in the development of DM2 in women with a history of GDM
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