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AMPKα1 deficiency suppresses brown adipogenesis in favor of fibrogenesis during brown adipose tissue development

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=28668388

Biochem Biophys Res Commun. 2017 Sep 16;491(2):508-514. doi: 10.1016/j.bbrc.2017.06.149. Epub 2017 Jun 28.

AMPKα1 deficiency suppresses brown adipogenesis in favor of fibrogenesis during brown adipose tissue development.

Zhao J1Yang Q2Zhang L3Liang X2Sun X4Wang B2Chen Y2Zhu M4Du M5.

Author information

Abstract

Brown adipose tissue (BAT) dissipates energy for thermogenesis which reduces or prevents obesity and metabolic dysfunction. AMP-activated protein kinase (AMPK) is a master regulator of energy metabolism and its activity is inhibited in the developing BAT due to obesity. We previously found that AMPK is required for brown fat development and thermogenic function, but the non-brown adipogenic differentiation of progenitor cells due to AMPKα1 deficiency has not been defined. We found that, in vivo, the thermogenic capacity and morphology of BAT were compromised due to AMPK deficiency, which was correlated with decreased progenitor density in BAT. In addition, the expression of fibrogenic markers was higher in AMPK deficient compared to wild-type mice. Furthermore, we transplanted AMPKα1 wild-type (WT) and floxed BAT into the same recipient mice; following tamoxifen induced AMPKα1 knockout in floxed BAT, the fibrogenesis was enhanced compared to WT mice. Taken together, our data demonstrated that AMPKα1 deficiency suppressed brown adipogenesis in favor of fibrogenesis during BAT development.

KEYWORDS: 

AMPKα1; Brown adipose tissue; Fibrogenesis; Progenitor cells; Thermogenesis

PMID: 28668388 PMCID: PMC5737707 DOI: 10.1016/j.bbrc.2017.06.149

[Indexed for MEDLINE] Free PMC Article


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