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Transcriptional attributes of constitutively active brown adipose tissue in nonhuman primates
Author(s) -
Ha Jung-Heun,
Gourineni Vishnupriya,
Lee Mee Ae,
Temel Ryan,
Chung Soonkyu
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.819.31
Subject(s) - prdm16 , biology , myogenesis , brown adipose tissue , adipogenesis , adipose tissue , microbiology and biotechnology , endocrinology , downregulation and upregulation , thermogenesis , lineage (genetic) , medicine , gene , myocyte , genetics
Brown adipose tissue plays a key role in adaptive thermogenesis. There is a substantial amount of inducible‐BAT in cold acclimated adult humans. However, the presence of constitutively active BAT (cBAT) and its origin are uncertain. They are unrevealed due to the limited accessibility of human BAT. In this study, we collected cBAT from the nonhuman primates housed at room temp and investigated morphological characteristics of cBAT and developmental lineage of cBAT by examining the transcriptional attributes. cBAT was recognizable at the supraclavicular region. IHC analysis showed that cBAT abundantly expressed UCP1 and displayed a unique lipid droplet morphology rather than the classical BAT morphology. There was a predominant increase of brown adipogenic marker genes including PRDM16, PGC1a and ADRB3 in cBAT compared to WAT. In addition, expression of adipokines and proinflammatory genes was decreased in cBAT indicating reduced endocrine function. Intriguingly, miR193b‐365 which represses myogenesis and maintains BAT differentiation was markedly upregulated suggesting cBAT is likely originated from myocyte‐lineage stem cells. Collectively, our work demonstrates that metabolically active BAT exists constitutively in supraclavicular region of nonhuman primates without any adrenoceptor stimuli, and this cBAT depot may diverge from myocyte precursor rather than transdifferentiate from the WAT. Grant Funding Source : NIH NCRR