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Need for insulin to control gestational diabetes is reflected in the ambulatory arterial stiffness index

DOI: 10.1186/1471-2393-13-9

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Abstract:

Plasma glucose, lipids, HOMA –IR (homeostasis model assessment of insulin resistance) and AASI, as obtained from 24-hour ambulatory blood pressure monitoring in third trimester pregnancy and at three months postpartum, were measured in three groups of women: controls (N = 32), women with GDM on diet (N = 42) and women with GDM requiring insulin treatment (N = 10).Women with GDM had poorer glycemic control and higher HOMA-IR during and after pregnancy and their total and LDL (low density lipoprotein) cholesterol levels were significantly higher after pregnancy than in the controls. After delivery, there was an improvement in AASI from 0.26 ± 0.10 to 0.17 ± 0.09 (P = 0.002) in women with GDM on diet, but not in women with GDM receiving insulin whose AASI tended to worsen after delivery from 0.30 ± 0.23 to 0.33 ± 0.09 (NS), then being significantly higher than in the other groups (P = 0.001-0.047).Women with GDM had more unfavorable lipid profile and higher blood glucose values at three months after delivery, the metabolic profile being worst in women requiring insulin. Interestingly, the metabolic disturbances at three months postpartum were accompanied by a tendency towards arterial stiffness to increase in women requiring insulin.Gestational diabetes mellitus (GDM) is defined as glucose intolerance with its onset or first recognition during pregnancy and it occurs in 3–6% of all pregnancies [1]. In Finland, the frequency is even higher, up to 8% [2]. Individuals with GDM exhibit a tendency to develop diabetes in later life [3,4], and it also exhibits an association with pregnancy-induced hypertension [5]. The metabolic syndrome with dyslipidemia as one of its components is more common in women with previous GDM [6,7]. During a GDM pregnancy, the maternal lipids are strong predictors for fetal lipids and abnormal growth [8], with high maternal triglyceride levels leading to fetal macrosomia. When dietary therapy is not successful in maintaining appropriate glucose va

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