SBP2 deficiency in adipose tissue macrophages drives insulin resistance in obesity

Ning Wang, Hor Yue Tan, Sha Li, Di Wang, Yu Xu, Cheng Zhang, Wen Xia, Chi Ming Che, Yibin Feng*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

17 Citations (Scopus)


Proinflammatory activation and accumulation of adipose tissue macrophages (ATMs) are associated with increased risk of insulin resistance in obesity. Here, we described the previously unidentified role of selenocysteine insertion sequence-binding protein 2 (SBP2) in maintaining insulin sensitivity in obesity. SBP2 was suppressed in ATMs of diet-induced obese mice and was correlated with adipose tissue inflammation. Loss of SBP2 initiated metabolic activation of ATMs, inducing intracellular reactive oxygen species content and inflammasome, which subsequently promoted IL-1-associated local proliferation and infiltration of proinflammatory macrophages. ATM-specific knockdown of SBP2 in obese mice promoted insulin resistance by increasing fat tissue inflammation and expansion. Reexpression of SBP2 improved insulin sensitivity. Last, an herbal formula that specifically induced SBP2 expression in ATMs can experimentally improve insulin sensitivity. Clinical observation revealed that it improved hyperglycemia in patients with diabetes. This study identified SBP2 in ATMs as a potential target in rescuing insulin resistance in obesity.

Original languageEnglish
Article numbereaav0198
Number of pages11
JournalScience advances
Issue number8
Publication statusPublished - Aug 2019

Scopus Subject Areas

  • General


Dive into the research topics of 'SBP2 deficiency in adipose tissue macrophages drives insulin resistance in obesity'. Together they form a unique fingerprint.

Cite this