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Depletion of white adipocyte progenitors suppresses obesity development (LB763)
Author(s) -
Daquinag Alexes,
Tseng Chieh,
Salameh Ahmad,
Zhang Yan,
Kolonin Mikhail
Publication year - 2014
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.28.1_supplement.lb763
Subject(s) - adipocyte , white adipose tissue , progenitor cell , endocrinology , medicine , adipose tissue , biology , population , microbiology and biotechnology , stem cell , environmental health
The study objective is to test a new approach to obesity prevention. Overgrowth of white adipose tissue (WAT) in obesity occurs as a result of adipocyte hypertrophy and hyperplasia. Expansion and renewal of adipocytes relies on proliferation and differentiation of white adipocyte progenitors (WAP), however, the requirement of WAP for obesity development has not been proven. Here, we investigate whether depletion of WAP can be used to prevent WAT expansion. We test this approach by using a hunter‐killer peptide designed to induce apoptosis selectively in WAP. We show that targeted WAP cytoablation results in a long‐term WAT growth suppression despite increased caloric intake in a mouse diet‐induced obesity model. Our data indicate that WAP depletion results in a compensatory beige adipocyte differentiation from an alternative progenitor cell population. Consistent with reported thermogenic capacity of beige adipose tissue, WAP‐depleted mice display increased energy expenditure. We conclude that targeting of adipocyte progenitors could be developed as a strategy to modulate WAT metabolic activity. Grant Funding Source : American Heart Association and Cancer Prevention and Research Institute of Texas