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Effects of orexin A on proliferation, survival, apoptosis and differentiation of 3T3‐L1 preadipocytes into mature adipocytes
Author(s) -
Skrzypski M.,
Kaczmarek P.,
Le T.T.,
Wojciechowicz T.,
Pruszyńska-Oszmalek E.,
Szczepankiewicz D.,
Sassek M.,
Arafat A.,
Wiedenmann B.,
Nowak K.W.,
Strowski M.Z.
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.10.013
Subject(s) - 3t3 l1 , medicine , endocrinology , apoptosis , protein kinase b , microbiology and biotechnology , adipogenesis , pi3k/akt/mtor pathway , chemistry , adipocyte , phosphorylation , biology , signal transduction , adipose tissue , biochemistry
Metabolic activities of orexin A (OXA) in mature adipocytes are mediated via PI3K/PKB and PPARγ. However, the effects of OXA on preadipocytes are largely unknown. We report here that OXA stimulates the proliferation and viability of 3T3‐L1 preadipocytes and protects them from apoptosis via ERK1/2, but not through PKB. OXA reduces proapoptotic activity of caspase‐3 via ERK1/2. Inhibition of ERK1/2 prevents the differentiation of preadipocytes into adipocytes. Unlike insulin, neither short‐term nor prolonged exposure of 3T3‐L1 preadipocytes to OXA induces preadipocyte differentiation to adipocytes, despite increased ERK1/2 phosphorylation. Unlike insulin, OXA fails to activate PKB, which explains its inability to induce the differentiation of preadipocytes.