ESPE2014 Poster Category 2 Fat Metabolism & Obesity (12 abstracts)
aResearch Laboratory of the Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University of Patras School of Medicine, Patras, Greece; bDepartment of AnatomyHistologyEmbryology, Faculty of Medicine, University of Patras, Patras, Greece; cDepartment of Pediatric Surgery, Karamandaneio Childrens Hospital, Patras, Greece
Background: Morbid childhood obesity predisposes to metabolic disorders such as diabetes type 2. In mice, heat-producing brown-like (beige) adipocytes can suppress weight gain and metabolic disease through the action of uncoupling protein 1 (UCP1) localized in the mitochondria.
Objective and hypotheses: To study the expression of UCP1 in the adipose tissue of lean&obese children and adolescents.
Method: Paraffin embedded subcutaneous abdominal adipose tissue microarrays were developed from surgical biopsies of 33 lean (BMI <85%) and 29 obese (BMI ≥95%) prepubertal children (groups A: 2 months7 years and B: 812 years) and adolescents (1015 years of age). Staining intensity and distribution of UCP1 were studied with immunohistochemistry and mean adipocyte size and total number were estimated by image analysis (adiposoft).
Results: UCP1 was expressed in the mitochondria of morphologically white adipocytes in all groups without typical beige multilocular lipid droplet morphology. The lean and obese prepubertal children expressed UCP1 with a higher distribution (>50% of tissue) compared to the lean and obese adolescents (P=0.01). UCP1 intensity was high in: i) 100% of group A lean and 50% of group A obese, ii) 100% of group B lean and obese, and iii) 67% of lean and 54% of obese adolescents, (P=0.022). Adipocyte size and number did not differ between lean and obese of each group, although size tended to increase with age. The children with high UCP1 intensity though, exhibited a higher adipocyte number (107.33±35.02 vs 83.0±17.93, P=0.011).
Conclusion: The expression of UCP1 in typical white adipocytes in the children and adolescents may reflect a transitional stage of browning recently observed in young sheep studies. UCP1 expression during childhood may contribute towards increased metabolic rate and decreased adipocyte size in an attempt to protect against the development of metabolic disorders. The decreased distribution of UCP1 positive adipocytes in the adolescents may reflect the loss of browning with age and puberty that may impair further the metabolism of obese adolescents.