Endocrine Research Unit, Mayo Clinic, Rochester, MN.
Facultad de Medicina, Universidad de Panamá, Panama City, Republic of Panama.
Diabetes. 2022 Mar 1;71(3):381-393. doi: 10.2337/db21-0609.
The role of adipose tissue (AT) inflammation in AT function in humans is unclear. We tested whether AT macrophage (ATM) content, cytokine gene expression, and senescent cell burden (markers of AT inflammation) predict AT insulin resistance measured as the insulin concentration that suppresses lipolysis by 50% (IC50). We studied 86 volunteers with normal weight or obesity at baseline and a subgroup of 25 volunteers with obesity before and after weight loss. There was a strong positive relationship between IC50 and abdominal subcutaneous and femoral fat cell size (FCS). The positive, univariate relationships between IC50 and abdominal AT inflammatory markers CD68, CD14, CD206 ATM/100 adipocytes, senescent cells, IL-6, and TNF-α mRNA were not significant after adjustment for FCS. A 10% weight loss significantly reduced IC50; however, there was no reduction in adipose ATM content, senescent cells, or cytokine gene expression. Our study suggests that commonly used markers of AT inflammation are not causally linked to AT insulin resistance, whereas FCS is a strong predictor of AT insulin resistance with respect to lipolysis.
脂肪组织（AT）炎症在人类 AT 功能中的作用尚不清楚。我们测试了脂肪组织巨噬细胞（ATM）含量、细胞因子基因表达和衰老细胞负担（AT 炎症的标志物）是否可以预测作为抑制脂肪分解 50%的胰岛素浓度的胰岛素抵抗（IC50）。我们研究了 86 名基线时体重正常或肥胖的志愿者和 25 名肥胖志愿者的亚组，他们在减肥前后都进行了研究。IC50 与腹部皮下和股骨脂肪细胞大小（FCS）之间存在很强的正相关关系。在调整 FCS 后，IC50 与腹部 AT 炎症标志物 CD68、CD14、CD206、ATM/100 脂肪细胞、衰老细胞、IL-6 和 TNF-α mRNA 之间的正相关、单变量关系不再显著。体重减轻 10%显著降低了 IC50；然而，脂肪组织 ATM 含量、衰老细胞或细胞因子基因表达并没有减少。我们的研究表明，常用的 AT 炎症标志物与 AT 胰岛素抵抗没有因果关系，而 FCS 是脂肪分解的 AT 胰岛素抵抗的一个强有力的预测因子。
