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Metabolic and Cardiac Dysfunction are Unaffected by High Sugar Intake in a Hamster Model of Heart Failure
Author(s) -
Hecker Peter Ammon,
Galvao Tatiana F,
O'Shea Karen M,
Brown Bethany H,
Henderson Reney,
Riggle Heather,
Gupte Sachin A,
Stanley William C
Publication year - 2011
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.25.1_supplement.825.11
Americans consume high amounts of sugar which may increase the risk of heart disease and diabetes. A high sugar diet accelerates the progression of heart failure in hypertensive rats and mice. We used the cardiomyopathic TO‐2 hamsters, a non‐hypertensive model of heart failure, to determine if a long‐term high sugar diet (57% of energy from a 1:1 mix of sucrose:fructose) is detrimental compared to standard high starch chow in this model. After 24 weeks, TO‐2 hamsters fed the high starch chow had systolic dysfunction compared to normal healthy F1B hamsters (36% decrease in ejection fraction), and systemic metabolic abnormalities including higher circulating glucose (108% increase), triglycerides (216% increase) and free fatty acids (64% increase), and lower insulin (39% decrease). Surprisingly, none of these parameters were affected by high sugar intake. Left ventricular activities of the mitochondrial oxidative enzymes citrate synthase, MCAD, and ICDH were decreased in TO‐2 hamsters, indicative of decreased oxidative capacity, and were unaffected by diet. Finally, no differences were observed in [NADPH], but lipid peroxidation products (MDA+4HA) were increased by 20% in TO‐2 hamsters and unaffected by diet. The results indicate that although cardiomyopathic hamsters are metabolically dysfunctional, this was unaffected by high sugar intake. NIH grants HL074237 & HL072751.