Distinct cellular and molecular mechanisms for β3 adrenergic receptor-induced beige adipocyte formation

Yuwei Jiang, Daniel C. Berry, Jonathan M. Graff

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Beige/brite adipocytes are induced within white adipose tissues (WAT) and, when activated, consume glucose and fatty acids to produce heat. Classically, two stimuli have been used to trigger a beiging response: cold temperatures and β3-adrenergic receptor (Adrb3) agonists. These two beiging triggers have been used interchangeably but whether these two stimuli may induce beiging differently at cellular and molecular levels remains unclear. Here, we found that cold-induced beige adipocyte formation requires Adrb1, not Adrb3, activation. Adrb1 activation stimulates WAT resident perivascular (Acta2+) cells to form cold-induced beige adipocytes. In contrast, Adrb3 activation stimulates mature white adipocytes to convert into beige adipocytes. Necessity tests, using mature adipocyte-specific Prdm16 deletion strategies, demonstrated that adipocytes are required and are predominant source to generate Adrb3-induced, but not coldinduced, beige adipocytes. Collectively, we identify that cold temperatures and Adrb3 agonists activate distinct cellular populations that express different β-adrenergic receptors to induce beige adipogenesis.

Original languageEnglish (US)
Article numbere30329
JournaleLife
Volume6
DOIs
StatePublished - Oct 11 2017

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Adrenergic Receptors
Chemical activation
White Adipose Tissue
Tissue
Adrenergic Agonists
Adipocytes
White Adipocytes
Fatty Acids
Adipogenesis
Glucose
Temperature
Hot Temperature
Beige Adipocytes
Population

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

Cite this

Distinct cellular and molecular mechanisms for β3 adrenergic receptor-induced beige adipocyte formation. / Jiang, Yuwei; Berry, Daniel C.; Graff, Jonathan M.

In: eLife, Vol. 6, e30329, 11.10.2017.

Research output: Contribution to journalArticle

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