1 Department of Health, Kinesiology, and Applied Physiology, Concordia University, Montreal, QC, Canada.
2 Metabolism, Obesity, and Nutrition Laboratory, School of Health, Concordia University, Montreal, QC, Canada.
3 Centre de recherche - Axe maladies chroniques, Centre intégré universitaire de santé et de services sociaux du Nord-de-l'Ile-de-Montréal, Hôpital du Sacré-Coeur de Montréal, Montreal, QC, Canada.
4 Division of Geriatric Medicine, Department of Medicine, McGill University, McGill University Health Centre (MUHC)-Montreal General Hospital, Montreal, QC, Canada.
5 Division of Endocrinology, Department of Medicine, McGill University, Royal Victoria Hospital, MUHC Glen site, Montreal, QC, Canada.
6 Division of Experimental Medicine, Department of Medicine, McGill University, MUHC Glen site, Montreal, QC, Canada.
7 Cardiovascular Health Across the Lifespan (CHAL) Program, Research Institute of the MUHC, Montreal, QC, Canada.
8 Division of Internal Medicine, Department of Medicine, McGill University, Royal Victoria Hospital, MUHC Glen site, Montreal, QC, Canada.

Introduction: Adipose tissue inflammation, driven in part by immune cells, may contribute to the elevated type 2 diabetes risk in adults with childhood-onset obesity (CO) compared to those with adult-onset obesity (AO). Weight loss can modify adipose tissue immune cell composition, but whether these changes differ by obesity onset remains unknown.

Methods: We compared abdominal and femoral subcutaneous adipose tissue (SAT) immune cell percentages between people with CO and AO before and after moderate (~10%) weight loss. We collected abdominal and femoral SAT from females with CO or AO before (CO: n=14; AO: n=13) and after (CO: n=8; AO: n=6) diet- and exercise-induced weight loss. We used flow cytometry to quantify the percentages of macrophages and T cells in the stromovascular fraction of both SAT regions.

Results: Abdominal CD68⁺CD206^{- '}pro-inflammatory' macrophages were slightly higher in AO than CO at baseline but declined in AO only, equalizing between groups after weight loss. Femoral CD68⁺CD206^- macrophages, as well as abdominal and femoral CD68⁺CD206⁺ 'anti-inflammatory' macrophages and CD3⁺CD8⁺ T cells, did not differ between groups at baseline or change after weight loss. Abdominal and femoral CD3⁺CD4⁺ T cells-potentially pro- or anti-inflammatory-increased after weight loss in AO but remained unchanged in CO.

Discussion: Our findings, though preliminary, do not support the hypothesis that SAT immune cell profiles account for the elevated type 2 diabetes risk in CO. Weight loss appears to alter some immune cell populations in AO but not in CO. The long-term metabolic consequences of these changes-or lack thereof-remain to be determined.