Abstract

PurposeTo evaluate the effect of gestational diabetes on omentin-1 in maternal and cord plasma. As a potent mediator of insulin resistance, Omentin-1, an adipokine derived from human adipose and placental tissue, may be an important player in the pathophysiology of gestational diabetes.MethodsThis was a prospective case–control study. The study included 96 women with gestational diabetes and 96 pregnant women without. Omentin-1 was measured at the time of the oral glucose tolerance test, at 32 weeks in maternal plasma and right after delivery in umbilical cord blood by ELISA assay.ResultsOver a period of 2 years, 200 patients were enrolled. Omentin-1 levels did not significantly differ between both groups throughout the pregnancy: omentin-1 levels were 157 ± 83 ng/ml in women with gestational diabetes and 158 ± 93 ng/ml in women without gestational diabetes (p = 0.94) at time of the oral glucose tolerance test and 118 ± 77 ng/ml in women with diabetes and 150 ± 89 ng/ml in women without (p = 0.12) at 32 weeks, respectively. Both groups showed a decrease in omentin-1 levels throughout pregnancy, with a more pronounced decrease in diabetic women (13 ± 53 versus 4 ± 48 ng/ml; p = 0.5). Neonatal omentin-1 levels were significantly lower in offspring of diabetic mothers: 106 ± 61 versus 134 ± 45 ng/ml (p = 0.03).ConclusionsThere was no significant difference in omentin-1 levels between healthy and diabetic mothers throughout the pregnancy. However, we found significantly lower omentin-1 levels in offspring of diabetic mothers. This may indicate a risk for the development of insulin resistance in later life.

Highlights

  • In each pregnancy, a physiological insulin resistance syndrome occurs to ensure that the fetus is sufficiently supplied with glucose

  • The study was adequately powered, maternal lipids and omentin-1 levels did not differ between women with and without GDM

  • Omentin-1 levels decreased throughout pregnancy

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Summary

Introduction

A physiological insulin resistance syndrome occurs to ensure that the fetus is sufficiently supplied with glucose Despite this physiological insulin resistance, most women stay normoglycemic throughout the pregnancy because of adequate β-cell function. If this physiological compensation fails, gestational diabetes occurs. Gestational diabetes is one of the most common pregnancy-associated diseases with a prevalence of 5–10% of all pregnancies and its prevalence is increasing [1, 2] It includes facets of type 2 diabetes (DM2) like insulin. Adipokines influence metabolic processes through various pathways like appetite control, inflammation, regulation of adipogenesis, and alter insulin sensitivity and secretion [9].

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