Mechanism for obesity-induced increase in myocardial lipid peroxidation

Vincent, H. K.; Powers, S. K.; Dirks, AJ; Scarpace, P. J.

doi:10.1038/sj.ijo.0801536

Cited by 125 publications

(109 citation statements)

References 36 publications

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“…Increased fatty acid uptake and oxidation by the heart can also increase MV O 2 , because more oxygen is required to generate ATP from fatty acid than by glucose metabolism, and increased oxygen may be consumed by fatty acid esterification and reactive oxygen species production. 8,10,27 Our finding that increasing BMI was an independent predictor of decreased efficiency extends the findings of previous ex vivo studies to obese humans. These previous studies demonstrated that increased MV O 2 , MFAUp, and MFAO were associated with decreased efficiency.…”

Section: Discussionsupporting

confidence: 79%

“…6,7 Other data from studies conducted in animals demonstrate that increased fatty acid availability and myocardial lipid content predispose the myocardium to increased oxidative stress and myocardial injury. 10,11 It is not known whether the changes in myocardial fatty acid metabolism and efficiency observed in animal models of obesity and insulin resistance also occur in humans. Therefore, the purpose of the present study was to determine the effect of obesity and insulin resistance in women on myocardial fatty acid metabolism, oxygen consumption, and efficiency.…”

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confidence: 99%

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Effect of Obesity and Insulin Resistance on Myocardial Substrate Metabolism and Efficiency in Young Women

et al. 2004

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Background-Obesity is a risk factor for impaired cardiac performance, particularly in women. Animal studies suggest that alterations in myocardial fatty acid metabolism and efficiency in obesity can cause decreased cardiac performance.In the present study, we tested the hypothesis that myocardial fatty acid metabolism and efficiency are abnormal in obese women. (rϭ0.58, PϽ0.005). A multivariate, stepwise regression analysis showed that BMI was the only independent predictor of MV O 2 and efficiency (Pϭ0.0005 and PϽ0.05, respectively). Glucose AUC was the only independent predictor of MFAUp, MFAU, and MFAO (PϽ0.05, Ͻ0.005, and Ͻ0.005, respectively). Conclusions-In young women, obesity is a significant predictor of increased MV O 2 and decreased efficiency, and insulin resistance is a robust predictor of MFAUp, MFAU, and MFAO. This increase in fatty acid metabolism and decrease in efficiency is concordant with observations made in experimental models of obesity. These metabolic changes may play a role in the pathogenesis of decreased cardiac performance in obese women.

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

Effect of Obesity and Insulin Resistance on Myocardial Substrate Metabolism and Efficiency in Young Women

et al. 2004

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“…Finally, myocardial lipid content is also increased in lean Zucker rats fed a high-fat diet and is associated with myocardial oxidative injury. 24 As for obese humans, lipid excess in the myocardium, as assessed by magnetic resonance spectroscopy, has been demonstrated and correlates with left ventricular mass and systolic dysfunction. 25 In summary, genetic rodent models of obesity and dietinduced obesity in rodents and humans show cardiac lipid accumulation within myocytes.…”

Section: Ectopic Fat Storage In the Heartmentioning

confidence: 99%

Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases

et al. 2004

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In humans and most animal models, the development of obesity leads not only to increased fat depots in classical adipose tissue locations but also to significant lipid deposits within and around other tissues and organs, a phenomenon known as ectopic fat storage. The purpose of this review is to explore the possible locations of ectopic fat in key target-organs of cardiovascular control (heart, blood vessels and kidneys) and to propose how ectopic fat storage can play a role in the pathogenesis of cardiovascular diseases associated with obesity. In animals fed a high-fat diet, cardiac fat depots within and around the heart impair both systolic and diastolic functions, and may in the long-term promote heart failure. Accumulation of fat around blood vessels (perivascular fat) may affect vascular function in a paracrine manner, as perivascular fat cells secrete vascular relaxing factors, proatherogenic cytokines and smooth muscle cell growth factors. Furthermore, high amounts of perivascular fat could mechanically contribute to the increased vascular stiffness seen in obesity. Finally, accumulation of fat in the renal sinus may limit the outflow of blood and lymph from the kidney, which would alter intrarenal physical forces and promote sodium reabsorption and arterial hypertension. Taken together, ectopic fat storage in key target-organs of cardiovascular control may impair their functions, contributing to the increased prevalence of cardiovascular diseases in obese subjects.

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“…53 It has been proposed that in the early stages of obesity there may be an initial elevation in antioxidant enzymes to counteract oxidative stress, whereas chronic obesity continually depletes the sources of antioxidant enzymes. 23,54 The degree of adiposity also affects enzyme activities. In a cross-sectional study, Olusi 23 found that erythrocyte CuZn-SOD activity was lower in the very obese (853 vs 1464 U/g Hb), and GPX activity was lower in the obese (76 vs 98.4 U/g Hb) than in the nonobese controls.…”

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confidence: 99%

Biomarkers and potential mechanisms of obesity-induced oxidant stress in humans

2005

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Objective: Oxidative stress may be the unifying mechanism underlying the development of comorbidities in obesity. Evidence suggests that a clustering of sources of oxidative stress exists in obesity: hyperglycemia, hyperleptinemia, increased tissue lipid levels, inadequate antioxidant defenses, increased rates of free radical formation, enzymatic sources within the endothelium, and chronic inflammation. Method: This review provides a summary of the available evidence on systemic oxidative stress in humans and specific metabolic pathways by which obesity may elevate systemic oxidant stress. The authors suggest possible methods of reducing oxidative stress such as antioxidant supplementation, caloric restriction and/or physical activity and surgical intervention to combat free radicals and reduce adipose tissue. Results: Obesity is associated with oxidative stress and can be reduced with weight loss (regardless of exercise or surgery induced weight loss), caloric restriction or antioxidant rich diets. Conclusion: Oxidative stress levels are elevated in human obesity, and these levels are modifiable with various lifestyle modifications and surgical interventions.

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Mechanism for obesity-induced increase in myocardial lipid peroxidation

Cited by 125 publications

References 36 publications

Effect of Obesity and Insulin Resistance on Myocardial Substrate Metabolism and Efficiency in Young Women

Effect of Obesity and Insulin Resistance on Myocardial Substrate Metabolism and Efficiency in Young Women

Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases

Biomarkers and potential mechanisms of obesity-induced oxidant stress in humans

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