Murphy Jessica, Morais José A, Tsoukas Michael A, Cooke Alexandra B, Daskalopoulou Stella S, Santosa Sylvia
Department of Health, Kinesiology, and Applied Physiology, Concordia University, Montreal, QC, Canada.
Metabolism, Obesity, and Nutrition Laboratory, School of Health, Concordia University, Montreal, QC, Canada.
Front Immunol. 2025 Aug 4;16:1601847. doi: 10.3389/fimmu.2025.1601847. eCollection 2025.
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.
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: =14; AO: =13) and after (CO: =8; AO: =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.
Abdominal CD68CD206pro-inflammatory' macrophages were slightly higher in AO than CO at baseline but declined in AO only, equalizing between groups after weight loss. Femoral CD68CD206 macrophages, as well as abdominal and femoral CD68CD206 'anti-inflammatory' macrophages and CD3CD8 T cells, did not differ between groups at baseline or change after weight loss. Abdominal and femoral CD3CD4 T cells-potentially pro- or anti-inflammatory-increased after weight loss in AO but remained unchanged in CO.
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.
部分由免疫细胞驱动的脂肪组织炎症，可能导致儿童期起病肥胖（CO）的成年人相较于成年期起病肥胖（AO）的成年人患2型糖尿病的风险升高。体重减轻可改变脂肪组织免疫细胞组成，但这些变化是否因肥胖起病类型而异仍不清楚。
我们比较了CO和AO人群在适度（约10%）体重减轻前后腹部和股部皮下脂肪组织（SAT）中免疫细胞的百分比。我们收集了CO或AO女性在饮食和运动诱导体重减轻前（CO：n = 14；AO：n = 13）和后（CO：n = 8；AO：n = 6）的腹部和股部SAT。我们使用流式细胞术量化两个SAT区域血管基质部分中巨噬细胞和T细胞的百分比。
基线时，AO腹部CD68⁺CD206⁻“促炎”巨噬细胞略高于CO，但仅在AO中下降，体重减轻后两组间趋于相等。股部CD68⁺CD206⁺巨噬细胞，以及腹部和股部CD68⁺CD206⁺“抗炎”巨噬细胞和CD3⁺CD8⁺ T细胞，在基线时两组间无差异，体重减轻后也未改变。腹部和股部CD3⁺CD4⁺ T细胞（可能促炎或抗炎）在AO体重减轻后增加，但在CO中保持不变。
我们的发现虽然是初步的，但不支持SAT免疫细胞谱导致CO中2型糖尿病风险升高的假设。体重减轻似乎改变了AO中的一些免疫细胞群体，但在CO中没有。这些变化（或没有变化）的长期代谢后果仍有待确定。
