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RESEARCH PRODUCT

Role of T-Cell Polarization and Inflammation and Their Modulation by n-3 Fatty Acids in Gestational Diabetes and Macrosomia.

Chahid BenammarOussama GrissaAziz HichamiInes MrizakNaim Akhtar Khan

subject

0301 basic medicinemedicine.medical_specialty[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionEndocrinology Diabetes and MetabolismAcyl-chainLymphocyte SubpopulationsInflammationReview ArticleBiologyProinflammatory cytokinePeripheral-Blood03 medical and health sciencesInsulin resistanceInternal medicinemedicineMultiple-sclerosislcsh:RC620-627chemistry.chemical_classificationMonocyte recruitmentNutrition and DieteticsPlasma leptinUnique populationInsulin-resistancemedicine.diseasePhenotypePathophysiologyGestational diabetesDocosahexaenoic acidlcsh:Nutritional diseases. Deficiency diseasesC-Reactive Protein030104 developmental biologyEndocrinologychemistryTumor necrosis factor alphamedicine.symptomFood SciencePolyunsaturated fatty acid

description

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).

10.1155/2016/3124960https://pubmed.ncbi.nlm.nih.gov/27313878