J Clin Invest:脂肪组织氧合度降低与肥胖症患者的胰岛素抵抗有关

2021-05-08 MedSci原创 MedSci原创

动物模型研究数据显示,脂肪组织(AT)氧合的减少参与了肥胖引起的胰岛素抵抗的发病机制。近日,研究人员评估了AT氧合对人的AT生物学和胰岛素敏感性的潜在影响,研究结果已发表于J Clin Invest。

动物模型研究数据显示,脂肪组织(AT)氧合的减少参与了肥胖引起的胰岛素抵抗的发病机制。近日,研究人员评估了AT氧合对人的AT生物学和胰岛素敏感性的潜在影响,研究结果已发表于J Clin Invest。

按脂肪和胰岛素敏感性,研究人员对参与者进行了严格的分层:代谢健康的瘦体质参与者(MHL;n = 11)、代谢健康的肥胖参与者(MHO;n = 15)和代谢不健康的肥胖参与者(MUO;n = 20),评估皮下AT氧分压(pO2),肝脏和全身的胰岛素敏感性,参与炎症、纤维化和支链氨基酸(BCAA)分解的基因和途径的AT表达,炎症的系统标志物,以及血浆BCAA浓度。

 

结果显示,pO2从MHL到MHO再到MUO组逐渐下降,并与肝脏和全身的胰岛素敏感性呈正相关。AT pO2与参与BCAA分解的基因的表达呈正相关,同时AT pO2与血浆BCAA浓度之间呈负相关。AT pO2与炎症和纤维化标志物的AT基因表达呈负相关。血浆PAI-1从MHL组到MHO组再到MUO组都有所增加,并与AT pO2呈负相关,而其他细胞因子和趋化因子的血浆浓度在MHL组和MUO组之间没有差别。

综上所述,该研究结果支持这样的观点,即肥胖者的AT氧合减少通过增加血浆PAI-1浓度和减少AT BCAA分解,从而增加血浆BCAA浓度来促进胰岛素抵抗。

 

原始出处:

 

Vincenza Cifarelli, et al., Decreased adipose tissue oxygenation associates with insulin resistance in individuals with obesity. J Clin Invest. 2020 Dec 1;130(12):6688-6699. doi: 10.1172/JCI141828.

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    2021-12-16 baoya
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