BSPED2013 Poster Presentations (1) (89 abstracts)
Immune cell dysregulation – contributing to the risk of development of metabolic disease in childhood obesity
Eirin Carolan 1 , Andrew Hogan 1 , Michelle Corrigan 1 , Jean O’Connell 1 , Niamh Foley 4 , Luke O’Neill 4 , Declan Cody 2 & Donal O’Shea 3
1Obesity Immunology Group, Education Research Centre, St Vincent’s University Hospital, Dublin 4, Ireland; 2Department of Diabetes and Endocrinology, Our Lady’s Children’s Hospital, Crumlin, Dublin 12, Ireland; 3Department of Endocrinology, St Columcille’s Hospital, Loughlinstown, Dublin, Ireland; 4Trinity Biomedical Sciences Institute, School of Biochemistry and Immunology, Trinity College Dublin, Dublin, Ireland.
Background: Although the association between obesity, chronic low-grade inflammation and immune dysregulation is well described in adults, there is a paucity of literature regarding this in children. We hypothesized that childhood obesity is associated with significant immune dysregulation.
Methods: Expression of cytokines and microRNAs (miR) involved in the pathogenesis of metabolic disease were assessed in 49 participants aged 6–18 years. Invariant NKT cells, NK cells, T cells and B cells were enumerated by staining with relevant antibodies and flow cytometry.
Results: The age and BMI Z-score of the obese participants were 12.9±3.1 years and 3.4±0.4 respectively and the non-obese participants were 12.2±3.2 years and 0.2±1.1. None had type 2 diabetes.
CD163 is a macrophage surface receptor that is shed into the circulation and is measured in its soluble form in serum. Serum concentrations of sCD163 were associated with an increased risk of development of T2DM in a prospective adult study.
INKT cells regulate the innate and adaptive immune system and are dysfunctional in obesity.
MicroRNAs (miRs) are post transcriptional regulators of gene expression. MiR-33a and MiR-33b play an important role in cholesterol homeostasis and insulin signalling, with expression of both greater than three-fold higher in the obese children (P<0.05 for both).
| Parameter | Obese (n=29) | Non-obese (n=20) | P value |
| Fasting insulin (pmol/l) | 149±104 | 27.6±20.2 | <0.001 |
| Invariant natural killer T cell (%CD3+T cells) iNKT | 0.32±0.03 | 0.54±0.02 | <0.001 |
| Soluble CD163 (ng/ml) | 135.7±9.32 | 109.1±7.55 | 0.03 |
| IL1β (pg/ml) | |||
| Post TLR4 stimulation of PBMCs | 2108±708.2 | 1518±479.6 | 0.01 |
| Data expressed as mean±S.D. P values calculated using independent-samples t-test. | |||
Conclusion: Immune cell distribution, tissue inflammation and metabolic gene expression are abnormal in obese children. This demonstrates the imperative to tackle obesity from an early age.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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