Dietary fatty acids and myocardial function

Lamers, Jos M. J.; Hartog, J. M.; Verdouw, P. D.; Hülsmann, W.C.

doi:10.1007/978-3-662-08390-1_25

Cited by 30 publications

(23 citation statements)

References 69 publications

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“…A potential mechanism for increased lipid damage in obesity is that increased lipid substrate within the myocardium can serve as a larger target for oxidation by free radicals. 2,16 Increasing the number of lipid molecules within the cardiovascular system (within the cardiac cells and embedded within the coronary vasculature intimal layers) may amplify lipid peroxidation injury. 11 In the high-fat feeding model, it seems possible that the elevated lipid content is due to fat storage within the myocytes 39 and fat deposition onto the coronary endothelium.…”

Section: Elevated Total Lipid Contentmentioning

confidence: 99%

“…At least four general potential mechanisms could contribute to the obesity-related myocardial lipid peroxidation: (a) increased myocardial work and subsequent radical production via mitochondrial respiration; 4 (b) decreased myocardial antioxidant defense; 12 ± 14 (c) increased fat deposition within myocardial tissue; 15,16 andaor (d) increased rates of radical formation such as superoxide (O 2 À ) or the hydroxyl radical. 17 Theoretically, it is possible that all of these mechanisms are present and participate in the increase in myocardial lipid peroxidation in obesity.…”

Section: Introductionmentioning

confidence: 99%

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Mechanism for obesity-induced increase in myocardial lipid peroxidation

et al. 2001

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OBJECTIVE:To determine the mechanisms underlying the obesity-induced increase in myocardial lipid peroxidation in the faafa rat. We hypothesized that elevated heart work (ie rate-pressure product), an increased rate of superoxide (O 2 À ) production, total myocardial lipid content, andaor insuf®cient antioxidant defenses are potential contributors to myocardial lipid peroxidation in obesity. DESIGN: Comparative, experimental study of myocardial tissue in 16-week-old lean control (Faa?, normal diet), obese high-fat fed (Faa?, 45% dietary fat), and obese fatty (faafa, normal diet) Zucker rats. MEASUREMENTS: Myocardial work (heart rate Â systolic blood pressure), myocardial lipid content, oxidative and antioxidant enzyme activities (citrate synthase (CS), catalase (CAT), glutathione peroxidase (GPX), superoxide dismutase (SOD)), the rate of papillary muscle superoxide radical production in vitro, thiol content, basal and post-oxidative challenge myocardial lipid peroxidation levels using thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides (PEROX) as indices of lipid peroxidation. RESULTS: Compared to lean controls, the high-fat fed and fatty animals had similar elevations (P`0.05) in myocardial TBARS and PEROX (23%, 25% and 29% 45%, respectively; P`0.05), and elevated susceptibilities to oxidative stress in vitro following exposure to oxidizing agents (P`0.05). Resting heart work was slightly higher (P`0.05) in both the high-fat fed and fatty animals compared to controls. Myocardial lipid content, SOD activities and non-protein thiol (glutathione) levels were elevated (P`0.05) in high-fat fed and fatty animals compared to controls. The rate of superoxide formation by isolated papillary muscles in vitro did not differ among groups (P`0.05). Regression analysis revealed that the myocardial lipid content contributed most to myocardial lipid peroxidation (R 2 0.76, P`0.05). CONCLUSIONS: Myocardial oxidative injury is closely associated with myocardial lipid content, but is not closely correlated with heart work, insuf®cient antioxidant defenses or a greater rate of superoxide production.

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Section: Elevated Total Lipid Contentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mechanism for obesity-induced increase in myocardial lipid peroxidation

et al. 2001

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“…While SFA rich foods are atherogenic and reduce coronary reserve 1,3,4 , UFAs have an anti-atherogenic effect 1,5 and protect the heart against the adverse effects of acute phase myocardial infarction 5,6 . Studies on UFA have shown beneficial results in the cardiovascular system 1,5,6 , experiments have shown that diets rich in UFA and SFA cause structural and metabolic damage in the myocardium [6][7][8][9][10] . While both diets cause disorganized sarcolemma, lipid deposits 9,10 , and myocardial oxidative stress 6,10 , the UFA rich diet also promotes necrosis 7 and abnormal muscle striation 8 .…”

Section: Introductionmentioning

confidence: 99%

“…Studies on UFA have shown beneficial results in the cardiovascular system 1,5,6 , experiments have shown that diets rich in UFA and SFA cause structural and metabolic damage in the myocardium [6][7][8][9][10] . While both diets cause disorganized sarcolemma, lipid deposits 9,10 , and myocardial oxidative stress 6,10 , the UFA rich diet also promotes necrosis 7 and abnormal muscle striation 8 .…”

Section: Introductionmentioning

confidence: 99%

“…Although literature shows that UFA rich diets cause morphometabolic alterations [6][7][8][9][10] , information is contradictory with respect to their effects on myocardium mechanical function 7,9,[11][12][13][14][15] . Although previous studies have shown that diet caused depressed cardiac function depression in isolated rabbit 12 and rat 13 papillary muscle, recent data from our laboratory 15 have shown that, in agreement with other authors 7,9,11,14 , UFA diet does not alter functional performance.…”

Section: Introductionmentioning

confidence: 99%

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Influências de dietas ricas em ácidos graxos saturados e insaturados sobre o miocárdio de ratos

Pinotti¹,

Dal-Pai-Silva²,

Sugizaki³

et al. 2007

Arq. Bras. Cardiol.

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SummaryObjectives: To study the influence of saturated (SFA) and unsaturated fatty acid (UFA) rich diets on mechanical function, morphology and oxidative stress in rat myocardium.Methods: Male, 60-day-old Wistar rats were fed a control (n=8), a SFA (n=8), or a UFA-rich diet (n=8) for sixty days. Mechanical function was studied in isolated left ventricle papillary muscle under isometric and isotonic contractions, in basal conditions (1.25mM calcium chloride) and after 5.2mM calcium chloride and beta-adrenergic stimuli with 1.0µM isoproterenol. Left ventricle fragments were used to study oxidative stress and morphology under light and electron microscopy.Results: SFA and UFA-rich diets did not change myocardium mechanical function. Both diets caused oxidative stress, with high lipid hydroperoxide and low superoxide-dismutase concentrations. UFA rich diet decreased catalase expression and SFA rich diet decreased the amount of myocardial glutathione-peroxidase. Both diets promoted light ultrastructural injuries such as lipid deposits and cell membrane injuries.Conclusion: Results suggest that SFA and UFA rich diets do not alter isolated muscle mechanical function, but promote light myocardial morphological injuries and oxidative stress.

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