ESPE Abstracts (2015) 84 FC8.2

Apoptosis Inhibitor of Macrophages: an Anti-Inflammatory Adipocyte Factor in Mild Adolescent Obesity?

Alexia Karvelaa, Aikaterini Avgeria, Eleni D Vlotinoub, George Georgiouc, Dionysios Papaxristoub, Toru Miyazakid & Bessie E Spiliotisa

aResearch Laboratory of the Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University of Patras School of Medicine, Patras, Greece; bDepartment of Anatomy, Histology, Embryology, Faculty of Medicine, University of Patras, Patras, Greece; cDepartment of Pediatric Surgery, Karamandaneio Childrens Hospital, Patras, Greece; dLaboratory of Molecular Biomedicine for Pathogenesis, Faculty of Medicine, Center for Disease Biology and Integrative Medicine, University of Tokyo, Tokyo, Japan

Background: Adipose tissue (AT) in obesity is characterized by low grade inflammation. The apoptosis inhibitor of macrophages (AIM; also called CD5L) is incorporated into adipocytes leading to increased lipolysis. Excess AIM-dependent lipolysis induces adipose tissue macrophage recruitment. M1 (proinflammatory) macrophage infiltration, with surface marker CD40, correlates with metabolic complications.

Objective and hypotheses: To study serum levels and AT expression of AIM in lean and obese children correlated with CD40 expression.

Method: Paraffin embedded abdominal AT microarrays from 33 lean and 29 obese prepubertal children and adolescents were used. Intensity and distribution of AIM and CD40 were studied with immunohistochemistry, size and total adipocyte numbers by image analysis (adiposoft) and serum AIM by ELISA.

Results: AIM serum levels were lower in males vs females (3.92±1.38 vs 5.58±1.51, P=0.0005) irrespective of BMI and pubertal status. Also, males with adipocyte size <33 μM had lower serum AIM levels compared to those with ≥33 μM (3.23±1.27 vs 4.27±1.31, P=0.028). Most obese males had higher AIM tissue distribution in the adipocytes (64.7%, P=0.021) and macrophages (88.2%, P=0.024) vs lean males. Particularly, most male obese adolescents (76.9%, P=0.031) had a large (≥33 μM) adipocyte size, small (<80) adipocyte number (83.3%, P=0.023), and lower intensity of macrophage CD40 (P=0.043) with high intensity of adipocyte AIM vs male lean adolescents.

Conclusion: Our study shows the presence of AIM in the adipocytes of children even from an early age. Males showed lower AIM serum levels than the females that were further decreased when the adipocyte size decreased. Obesity in the males was associated with higher tissue AIM distribution in both adipocytes and macrophages. Obese adolescent males particularly showed an association of low CD40 (M1 macrophage marker) intensity with high AIM adipocyte intensity suggesting an anti-inflammatory role of AIM in the adipocytes in male adolescents with mild obesity possibly reflecting a protective mechanism against metabolic complications in this age group.

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