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BCAT2 regulates BCAA metabolic fate during adipogenesis
Author(s) -
Noriega Lilia G,
Estrada Isabela,
Tenorio Miriam R,
Torres Nimbe,
Tovar Armando R.
Publication year - 2013
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.27.1_supplement.113.6
Subject(s) - adipogenesis , catabolism , branched chain amino acid , valine , leucine , endocrinology , biology , medicine , adipocyte , gene , chemistry , biochemistry , microbiology and biotechnology , amino acid , metabolism , adipose tissue
Adipogenesis is a controlled differentiation process regulated by a network of transcription factors that include C/EBPβ and PPARγ. PPARγ binds to the vicinity of >;5000 genes through the different stages of differentiation (Nielsen et al, Genes Dev 2008(22):2953–2967). An analysis of these genes revealed that one of them is the mitochondrial branched‐chain aminotransferase (BCAT2) gene. BCAT2 catalyze the first enzymatic step of the branched chain amino acids (BCAA) catabolism. However, the role of BCTA2 during adipogenesis is barely known. Thus, we have evaluated BCAT2 expression and the oxidation, incorporation to lipids or proteins of the three BCAA, leucine, isoleucine and valine, during adipogenesis. Undifferentiated 3T3‐L1 did not express BCAT2 but both its mRNA and protein levels were gradually increased after induction of differentiation, reaching their maximum level at day 12. Regarding BCAA metabolic fate, BCAA were incorporated into protein when BCAT2 was not present, and were mainly oxidized and incorporated into lipids as BCAT2 increased during the differentiation process. Interestingly, leucine was mainly oxidized in adipocytes from lean mice and this was decreased in adipocytes from obese mice. These data demonstrate that BCAT2 regulates the metabolic fate of BCAA during adipogenesis and establish a process that is altered during obesity. Supported by CONACYT‐155949 to LGN.