HDAC11 suppresses the thermogenic program of adipose tissue via BRD2

Rushita A. Bagchi, Bradley S. Ferguson, Matthew S. Stratton, Tianjing Hu, Maria A. Cavasin, Lei Sun, Ying Hsi Lin, Dianxin Liu, Pilar Londono, Kunhua Song, Maria F. Pino, Lauren M. Sparks, Steven R. Smith, Philipp E. Scherer, Sheila Collins, Edward Seto, Timothy A. McKinsey

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


Little is known about the biological function of histone deacetylase 11 (HDAC11), which is the lone class IV HDAC. Here, we demonstrate that deletion of HDAC11 in mice stimulates brown adipose tissue (BAT) formation and beiging of white adipose tissue (WAT). Consequently, HDAC11-deficient mice exhibit enhanced thermogenic potential and, in response to high-fat feeding, attenuated obesity, improved insulin sensitivity, and reduced hepatic steatosis. Ex vivo and cell-based assays revealed that HDAC11 catalytic activity suppresses the BAT transcriptional program, in both the basal state and in response to β-adrenergic receptor signaling, through a mechanism that is dependent on physical association with BRD2, a bromodomain and extraterminal (BET) acetyl-histone-binding protein. These findings define an epigenetic pathway for the regulation of energy homeostasis and suggest the potential for HDAC11-selective inhibitors for the treatment of obesity and diabetes.

Original languageEnglish (US)
JournalJCI Insight
Issue number15
StatePublished - Aug 9 2018


  • Adipose tissue
  • Metabolism
  • Transcription

ASJC Scopus subject areas

  • Medicine(all)


Dive into the research topics of 'HDAC11 suppresses the thermogenic program of adipose tissue via BRD2'. Together they form a unique fingerprint.

Cite this