High carbohydrate and high fat diets protect the heart against ischaemia/reperfusion injury

Salie, Ruduwaan; Huisamen, Barbara; Lochner, Amanda

doi:10.1186/s12933-014-0109-8

Cited by 44 publications

(50 citation statements)

References 50 publications

(82 reference statements)

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“…In addition, the insulin levels were even lower in HFLCD that in control group. diet and HFD) in Wistar rats resulted in cardioprotection against acute ischemia/reperfusion damage and in the activation of the RISK pathway in an ex vivo model, thus supporting the findings of the present study [41]. The term insulin resistance implies an inadequate effect of insulin on glucose metabolism, but does not address other aspects of insulin action.…”

Section: Discussionsupporting

confidence: 88%

Obesity induced by high fat diet attenuates postinfarct myocardial remodeling and dysfunction in adult B6D2F1 mice

Poncelas

Inserte

Vilardosa

et al. 2015

Journal of Molecular and Cellular Cardiology

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Section: Discussionsupporting

confidence: 88%

Obesity induced by high fat diet attenuates postinfarct myocardial remodeling and dysfunction in adult B6D2F1 mice

Poncelas

Inserte

Vilardosa

et al. 2015

Journal of Molecular and Cellular Cardiology

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“…The paradox has also been described in type 2 diabetic patients with cardiovascular co-morbidity, in whom overweight and obesity may enhance survival in a setting of insulin-resistant diabetes [32]. Animal studies have confirmed the increased resistance to ischemic heart injury in obese, as well as lean, type 2 diabetic rats and rabbits [33–35], as well as in rats [11] and mice fed a HFD [36, 37]. Despite these findings, the existence and relevance of obesity-dependent cardioprotection remains controversial.…”

Section: Discussionmentioning

confidence: 99%

“…Recent data imply that an obesogenic high fat diet enhance myocardial tolerance against ischemic-reperfusion induced injury (IR), but this cardioprotection was not associated with activation of ERK p44/p42 or PKB/Akt dependent RISK signaling (reperfusion injury salvage kinase pathway) [11], a pathway widely accepted to mediate protection against reperfusion injury [12, 13]. Furthermore, a recent study by Salie et al suggests that hearts protected by obesogenic diets are unresponsive to additional cardioprotective conditioning maneuvers, such as ischemic preconditioning (IPC) or β-adrenergic preconditioning (β-PC), indicating that the hearts were maximally protected by the diets [11].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, a recent study by Salie et al suggests that hearts protected by obesogenic diets are unresponsive to additional cardioprotective conditioning maneuvers, such as ischemic preconditioning (IPC) or β-adrenergic preconditioning (β-PC), indicating that the hearts were maximally protected by the diets [11]. Both IPC and β-PC may elicit protection against IR induced injury via the β-adrenergic cAMP - PKA signal transduction pathway [14–16].…”

Section: Introductionmentioning

confidence: 99%

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Long-term consumption of an obesogenic high fat diet prior to ischemia-reperfusion mediates cardioprotection via Epac1-dependent signaling

et al. 2016

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BackgroundObesity is still considered a risk factor for cardiovascular disease, although more recent knowledge also suggests obesity to be associated with reduced morbidity and mortality - the “obesity paradox”. This study explores if long-term feeding of an obesogenic high fat diet renders the myocardium less susceptible to ischemic-reperfusion induced injury via Epac-dependent signaling.MethodsWild type (wt), Epac1 (Epac1−/−) and Epac2 (Epac2−/−) deficient mice were fed a high fat (HFD) or normal chow diet (ND) for 33 ± 1 weeks. Six experimental groups were included: (1) control wt ND (wt ND), (2) control wt HFD (wt HFD), (3) Epac1−/− mice on ND (Epac1−/− ND), (4) Epac1−/− mice on HFD (Epac1−/− HFD), (5) Epac2−/− mice on ND (Epac2−/− ND), and (6) Epac2−/− mice on HFD (Epac2−/− HFD). Isolated ex vivo mice hearts were perfused in a constant pressure Langendorff mode, and exposed to 30min of global ischemia (GI) and 60min of reperfusion. Endpoints were infarct size and functional recovery.ResultsAll groups fed a HFD presented with significantly enhanced body weight, visceral fat content and reduced glucose clearance compared to corresponding ND groups. Although the HFD cohorts presented with an overall comparable systemic capability to clear glucose, the Epac1−/− HFD group presented with glucose levels slightly above the human diabetes criteria at the end of the intraperitoneal glucose tolerance test (ipGTT). Moreover, the HFD significantly reduced infarct size in both wild type (wt HFD 41.3 ± 5.5% vs. wt ND 58.0 ± 9.8%, p < 0.05) and Epac2−/− cohorts (Epac2−/− HFD 34.4 ± 7.2% vs. Epac2−/− ND 56.5 ± 3.8%, p < 0.05). Interestingly, however, the HFD did not reduce infarct size in Epac1−/− deficient mice hearts (Epac1−/− HFD 65.1 ± 5.1% vs. Epac1−/− ND 56.1 ± 3.5%, ns.).ConclusionEpac1-dependent signaling is involved in mediating the cardioprotection afforded by long-term feeding of an obesogenic high fat diet in mice hearts.

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“…In accordance with this, ex vivo hearts from high fat-fed mice subjected to ischemia-reperfusion showed increased infarct size. Although the literature supports that long-term HFD feeding is associated with increased infarct size (29,49), there are also studies reporting reduced infarct size following obesogenic diets (13,41). Factors such as differences in age, diet composition, and feeding period, as well as ex vivo perfusion conditions (i.e., energy substrate composition), may contribute to some of these discrepancies.…”

Section: Discussionmentioning

confidence: 99%

Exercise training promotes cardioprotection through oxygen-sparing action in high fat-fed mice

Lund

Hafstad

Boardman

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Lund J, Hafstad AD, Boardman NT, Rossvoll L, Rolim NP, Ahmed MS, Florholmen G, Attramadal H, Wisløff U, Larsen TS, Aasum E. Exercise training promotes cardioprotection through oxygen-sparing action in high fat-fed mice. Am J Physiol Heart Circ Physiol 308: H823-H829, 2015. First published January 30, 2015; doi:10.1152/ajpheart.00734.2014.-Although exercise training has been demonstrated to have beneficial cardiovascular effects in diabetes, the effect of exercise training on hearts from obese/diabetic models is unclear. In the present study, mice were fed a high-fat diet, which led to obesity, reduced aerobic capacity, development of mild diastolic dysfunction, and impaired glucose tolerance. Following 8 wk on high-fat diet, mice were assigned to 5 weekly high-intensity interval training (HIT) sessions (10 ϫ 4 min at 85-90% of maximum oxygen uptake) or remained sedentary for the next 10 constitutive weeks. HIT increased maximum oxygen uptake by 13%, reduced body weight by 16%, and improved systemic glucose homeostasis. Exercise training was found to normalize diastolic function, attenuate diet-induced changes in myocardial substrate utilization, and dampen cardiac reactive oxygen species content and fibrosis. These changes were accompanied by normalization of obesity-related impairment of mechanical efficiency due to a decrease in work-independent myocardial oxygen consumption. Finally, we found HIT to reduce infarct size by 47% in ex vivo hearts subjected to ischemia-reperfusion. This study therefore demonstrated for the first time that exercise training mediates cardioprotection following ischemia in diet-induced obese mice and that this was associated with oxygen-sparing effects. These findings highlight the importance of optimal myocardial energetics during ischemic stress. cardiac efficiency; myocardial oxygen consumption; mechanoenergetics; high-intensity exercise; diet-induced obesity THERE HAS BEEN a dramatic transition from physical activity to sedentary lifestyle during the last century. This has resulted in an epidemic increase in the prevalence of metabolic syndrome, obesity, and diabetes, all of which increase the risk of developing cardiovascular and metabolic disorders (15, 42). Cardiovascular diseases are the major causes of morbidity and mortality in type 2 diabetic patients (25) who are at higher risk of developing heart failure, angina, acute myocardial infarction, and dying from an acute myocardial infarction (2).Diabetes-related cardiac complications are due to increased coronary artery disease as well as the development of a specific diabetic cardiomyopathy characterized by ventricular dysfunction in the absence of coronary artery disease or hypertension (24). Although the pathogenesis of diabetes/obesity-related cardiomyopathy is multifactorial and complex, decreased cardiac efficiency seems to play an essential role and is an early hallmark of the diabetic heart (5, 9, 22, 36).Physical training is a well-documented measure to reduce the development of obesity/diabetes, as well as an effec...

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High carbohydrate and high fat diets protect the heart against ischaemia/reperfusion injury

Cited by 44 publications

References 50 publications

Obesity induced by high fat diet attenuates postinfarct myocardial remodeling and dysfunction in adult B6D2F1 mice

Obesity induced by high fat diet attenuates postinfarct myocardial remodeling and dysfunction in adult B6D2F1 mice

Long-term consumption of an obesogenic high fat diet prior to ischemia-reperfusion mediates cardioprotection via Epac1-dependent signaling

Exercise training promotes cardioprotection through oxygen-sparing action in high fat-fed mice

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