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Low carbohydrate diet modifies cardiac oxidative metabolism under normoxia and ischemia/reperfusion conditions
Author(s) -
Wang Peipei,
Douglas Sam,
Lloyd Steven
Publication year - 2010
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.24.1_supplement.787.10
Subject(s) - perfusion , ischemia , medicine , metabolism , carbohydrate metabolism , chemistry , endocrinology , oxidative phosphorylation , reperfusion injury , cardiac function curve , insulin , cardiology , biochemistry , heart failure
The effects of Low carbohydrate diets (LCD) on the heart have not been well investigated. We showed that LCD increases ischemic myocardial injury. Here we investigated the effect of LCD on cardiac metabolism, a contributor to cardiac function, during normoxia (NOR) and ischemia/reperfusion (I/R) in the isolated rat heart. Adult rats were fed LCD (60% kcal fat/30% protein/10% CHO) or control diet (CONT; 16%/19%/65%) for 2 weeks. Hearts were isolated and subject to NOR or I/R (60 min global low flow ischemia, 0.3ml/min, followed by 60 min reperfusion) with insulin (15 or 30 ƒÝU/ml) and 3‐hydroxybutyrate (3‐HB, 0.6 or 1.2 mM; N=18 to 19 at each level). After perfusion with 13C‐labeled substrates, TCA cycle entry was measured by 13C‐NMR. Analysis was conducted using a general linear model examining effect of diet, perfusion condition (NOR or I/R), and perfusion buffer (with 4 levels of insulin and 3‐HB). The model demonstrated a strong effect of diet (P<0.01) and perfusion condition (P<0.001) on substrate oxidation, with palmitate oxidation higher with LCD and I/R. There was no effect of perfusion buffer within the ranges studied. Functional recovery in I/R was lower in LCD (P < 0.05), consistent with earlier findings. These results suggest that the LCD‐induced increase of myocardial injury following ischemia‐reperfusion described in previous reports might be due to alteration of cardiac metabolism.