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Short term consumption of a Western diet induces pathological hypertrophy in young mouse hearts
Author(s) -
Medford Heidi M,
Marsh Susan A
Publication year - 2012
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.26.1_supplement.1134.11
Subject(s) - medicine , endocrinology , muscle hypertrophy , pathological , atrial natriuretic peptide , myocardial infarction , biology , pressure overload , heart disease , cardiac hypertrophy
Diets high in sugar and saturated fat (“Western” diet, WES) contribute to the incidence of metabolic syndrome and cardiovascular disease. A hallmark of severe cardiovascular or heart disease is growth of the heart in response to cellular pathology, pressure overload, or tissue damage from myocardial infarction; this is termed pathological cardiac hypertrophy. The development of pathological cardiac hypertrophy in adult hearts is regulated by interactions between repressor element 1‐silencing transcription factor (REST), mSin3A and histone deacetylases (HDAC), and downstream activation of mediators of the fetal gene program, such as atrial natriuretic peptide (ANP) and α‐actin; the fetal gene program is not activated during physiological hypertrophy such as that induced by exercise. To investigate the effects of WES on regulation of cardiac hypertrophy we fed 5 week old C57BL/6 mice either a WES (n=8) or control diet (n=8) for two weeks. WES mice exhibited significantly higher fasting blood glucose and heart wet weight versus control (P<0.05). REST and ANP were higher in WES while α‐actin was lower compared to mice that consumed the control diet. There were no differences in mSin3A or HDACs 1–5. Taken together, these data suggest that even short durations of WES consumption promote pathological rather than physiological hypertrophy and that this may be mediated, at least in part, by the REST complex.