Cardiovascular Research Advance Access first published online on March 14, 2008
This version [Corrected Proof] published online on April 10, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn074
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Role of diet and fuel overabundance in the development and progression of heart failure
1 Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
2 Division of Cardiology, Department of Medicine, University of Maryland, 20 Penn St, HSF-II, Room S022, Baltimore, MD 21201, USA
* Corresponding author. Tel: +1 410 706 3585; fax: +1 410 706 3583. E-mail address: wstanley{at}medicine.umaryland.edu
Under physiological conditions, the human heart derives energy from glucose, fatty acids, and/or lactate depending upon substrate availability, circulating hormone levels, and nutritional status. Circulating free fatty acid and glucose levels often exceed the normal range, as observed with type 2 diabetes, obesity, or physical inactivity. Chronic exposure of the heart to high plasma levels of free fatty acids may cause accumulation of toxic lipid intermediates within cardiomyocytes. Furthermore, suppression of glucose oxidation by increased fatty acid uptake shunts glucose into the oxidative pentose phosphate and hexosamine biosynthetic pathways, both of which yield potentially harmful products. Noxious derivatives of aberrant glucose and fatty acid oxidation can activate signalling cascades leading to myocyte dysfunction or death, processes termed ‘glucotoxicity’ and ‘lipotoxicity’. This review discusses the effects of dietary extremes (e.g. high fat and high carbohydrate consumption) and substrate overabundance in the context of heart failure (HF) development and progression. Emerging data suggest that substrate excess leads to cardiac dysfunction and HF, which may be prevented or slowed by maintaining low body fat and high insulin sensitivity and consuming a diet of low glycaemic load that is high in mono- and polyunsaturated fatty acids.
KEYWORDS Diabetes; Diet; Glucotoxicity; Heart; Lipotoxicity
Time for primary review: 24 days
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  W. C. Stanley, K. B. Shah, and M. F. Essop Does Junk Food Lead to Heart Failure?: Importance of Dietary Macronutrient Composition in Hypertension Hypertension, December 1, 2009; 54(6): 1209 - 1210. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Suzuki, M. Ueno, M. Uno, Y. Hirose, Y. Zenimaru, S. Takahashi, J.-i. Osuga, S. Ishibashi, M. Takahashi, M. Hirose, et al. Effects of hormone-sensitive lipase disruption on cardiac energy metabolism in response to fasting and refeeding Am J Physiol Endocrinol Metab, November 1, 2009; 297(5): E1115 - E1124. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. Chess, R. J. Khairallah, K. M. O'Shea, W. Xu, and W. C. Stanley A high-fat diet increases adiposity but maintains mitochondrial oxidative enzymes without affecting development of heart failure with pressure overload Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1585 - H1593. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. H. Opie and J. Knuuti The adrenergic-Fatty Acid load in heart failure. J. Am. Coll. Cardiol., October 27, 2009; 54(18): 1637 - 1646. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Serpillon, B. C. Floyd, R. S. Gupte, S. George, M. Kozicky, V. Neito, F. Recchia, W. Stanley, M. S. Wolin, and S. A. Gupte Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH Am J Physiol Heart Circ Physiol, July 1, 2009; 297(1): H153 - H162. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. B. Levitan, A. Wolk, and M. A. Mittleman Consistency With the DASH Diet and Incidence of Heart Failure Arch Intern Med, May 11, 2009; 169(9): 851 - 857. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Albert Heart Failure in the Urban African Enclave of Soweto: A Case Study of Contemporary Epidemiological Transition in the Developing World Circulation, December 2, 2008; 118(23): 2323 - 2325. [Full Text] [PDF]
|
|
|
|
|
|
D. J. Chess, W. Xu, R. Khairallah, K. M. O'Shea, W. J. Kop, A. M. Azimzadeh, and W. C. Stanley The antioxidant tempol attenuates pressure overload-induced cardiac hypertrophy and contractile dysfunction in mice fed a high-fructose diet Am J Physiol Heart Circ Physiol, December 1, 2008; 295(6): H2223 - H2230. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Chicco, G. C. Sparagna, S. A. McCune, C. A. Johnson, R. C. Murphy, D. A. Bolden, M. L. Rees, R. T. Gardner, and R. L. Moore Linoleate-Rich High-Fat Diet Decreases Mortality in Hypertensive Heart Failure Rats Compared With Lard and Low-Fat Diets Hypertension, September 1, 2008; 52(3): 549 - 555. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. D. Lopaschuk and D. P. Kelly Signalling in cardiac metabolism Cardiovasc Res, July 15, 2008; 79(2): 205 - 207. [Full Text] [PDF]
|
|