MiR-150 regulates obesity-Associated insulin resistance by controlling B cell functions

Wei Ying, Alexander Tseng, Richard Cheng An Chang, Haiqing Wang, Yu Lieh Lin, Srikanth Kanameni, Tyler Brehm, Andrew Morin, Benjamin Jones, Taylor Splawn, Michael Criscitiello, Michael C. Golding, Fuller W. Bazer, Stephen Safe, Beiyan Zhou

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


Adipose tissue resident B cells account for more than 20% of stromal cells within visceral adipose tissues; however, their functions in the adipose tissue niche are poorly elucidated. Here we report that miR-150 modulates adipose tissue function by controlling activation of B cells and their interactions with other immune cells. miR-150KO mice displayed exacerbated obesity-Associated tissue inflammation and systemic insulin resistance, which is recapitulated by adoptive transfer of B cells, but not purified immunoglobulin, into obese B null mice. Using purified cell populations, we found that enhanced proinflammatory activation of adipose tissue T cells and macrophages was due to miR-150KO B cells action but not cell-Autologous mechanisms. miR-150KO B cells displayed significantly enhanced antigen presentation upon stimulation, ultimately leading to elevated inflammation and insulin resistance, compared to wild type B cells. Knockdown of identified miR-150 target genes, Elk1, Etf1 or Myb attenuated B cell action by altering B cell receptor pathways and MHCII cell surface presentation. Our results demonstrate a critical role for miR-150 in regulating B cell functions in adipose tissue which ultimately regulate both metabolic and immunologic homeostasis in the adipose tissue niche.

Original languageEnglish (US)
Article number20176
JournalScientific Reports
StatePublished - Feb 1 2016

ASJC Scopus subject areas

  • General


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