Premium
Profiling metabolic remodeling in PP2Acα deficiency and chronic pressure overload mouse hearts
Author(s) -
Dong Dachuan,
Li Liangyuan,
Gu Pengyu,
Jin Tao,
Wen Mingda,
Yuan Caihua,
Gao Xiang,
Liu Chang,
Zhang Zhao
Publication year - 2015
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.2015.10.016
Subject(s) - transporter , enzyme , pressure overload , beta oxidation , biology , metabolism , messenger rna , gene , fatty acid metabolism , fatty acid , biochemistry , medicine , chemistry , endocrinology , microbiology and biotechnology , muscle hypertrophy , cardiac hypertrophy
Our understanding of how metabolic switches occur in the failing heart is still limited. Here, we report the emblematic pattern of metabolic alternations in two different mouse models. PP2Acα deficient hearts exhibited a dramatic decrease in the levels of mRNA encoding for transporters and enzymes involved in glucose utilization, which compensated by higher expression levels of genes controlling fatty acid utilization. These features were partly reproduced in cultured PP2Acα KD cardiomyocytes. Equivalently, a decrease in the expression of most of the transporters and enzymes controlling both glucose and fatty acid metabolism were observed in TAC model.