Abstract

Th (T helper) cells are differentiated into either Th1 or Th2 phenotype. It is generally considered that Th1 phenotype is proinflammatory, whereas Th2 phenotype exerts anti-inflammatory or protective effects. Gestational diabetes mellitus (GDM) has been associated with a decreased Th1 phenotype, whereas macrosomia is marked with high expression of Th1 cytokines. Besides, these two pathological situations are marked with high concentrations of inflammatory mediators like tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), known to play a pivotal role in insulin resistance. Dietary n-3 polyunsaturated fatty acids (n-3 PUFAs) may exert a beneficial effect by shifting Th1/Th2 balance to a Th2 phenotype and increasing insulin sensitivity. In this paper, we shed light on the role of T-cell malfunction that leads to an inflammatory and pathophysiological state, related to insulin resistance in GDM and macrosomia. We will also discuss the nutritional management of these pathologies by dietary n-3 polyunsaturated fatty acids (PUFAs).

Highlights

  • Called gestational diabetes mellitus (GDM), is an important risk factor for foetal overgrowth, termed macrosomia, which is influenced by maternal hyperglycemia and endocrine status through placental circulation [1]

  • Both in 100% and in 0% calcium media, TG-induced increases in [Ca2+]i in T-cells are higher in GDM dames and macrosomic rats than those in control animals [27], demonstrating that T-cell calcium signaling is altered in these two pathological situations

  • We have reported that tumor necrosis factorα (TNF-α) and IL-6 are increased in GDM women [39]

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Summary

Introduction

Called gestational diabetes mellitus (GDM), is an important risk factor for foetal overgrowth, termed macrosomia, which is influenced by maternal hyperglycemia and endocrine status through placental circulation [1]. Macrosomia has generally been defined as a birth weight greater than or equal to the 90th percentile birth weight for gestational age, that is, infants who weigh >4000 g at delivery, regardless of gestational age or sex [2,3,4]. Infants born to diabetic mothers are at an increased risk for hypoglycaemia, respiratory distress syndrome, hyperbilirubinemia, and hypertrophic cardiomyopathy [3]. There exists a correlationship between maternal and foetal plasma cholesterol levels in 5-6-month-old human foetuses [5, 6]. It is noteworthy that several alterations in the metabolism of carbohydrates and lipids, observed in newborn babies of diabetic mothers, persist postnatally [7,8,9]

In Utero Programming Is Responsible for Alterations Observed in Adulthood
Cell-Mediated Immunity in Diabetic
Proinflammatory Adipokines and Cytokines in GDM and Macrosomia
Findings
Conclusion
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