Myocardial dysfunction induced by food restriction is related to calcium cycling and beta-adrenergic system changes

Gut, Ana Lúcia; Okoshi, Marina Politi; Padovani, Carlos Roberto; Aragon, Flávio Ferrari; Cicogna, Antônio Carlos

doi:10.1016/s0271-5317(03)00071-x

Cited by 21 publications

(30 citation statements)

References 27 publications

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“…Myocardial performance was evaluated by studying the isolated papillary muscle from the left ventricle (LV) as described previously 21,22 . Briefly, rats were anesthetized with sodium pentobarbital (50 mg/kg intraperitoneal) and euthanized.…”

Section: Isolated Muscle Performancementioning

confidence: 99%

Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos

Lima-Leopoldo¹,

Leopoldo²,

Sugizaki³

et al. 2011

Arq. Bras. Cardiol.

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Section: Isolated Muscle Performancementioning

confidence: 99%

Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos

Lima-Leopoldo¹,

Leopoldo²,

Sugizaki³

et al. 2011

Arq. Bras. Cardiol.

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“…It has been suggested that malnutrition may alter the adrenergic response due to attenuation of the phosphorylation of proteins related to the control of intracellular Ca 2+ , impairing the mechanical cardiac performance in murine models [7,19]. Moreover, there is evidence that these changes may be associated with a decreased number of β-adrenergic receptors or alterations of intracellular signal transduction pathways dependent on the adrenergic activation of G protein [8]. However, the modulatory effect of protein restriction on β-adrenergic receptors expression and/or function still poorly understood, and needs to be established in further studies.…”

Section: Discussionmentioning

confidence: 99%

“…Even more scarce is information regarding the cardiac molecular and cellular adaptations that are induced by protein restriction, which can potentially modify the biomechanical contractile pattern of cardiomyocytes [5]. Previous studies indicated that a 50% food restriction is able to induce cardiac dysfunction that manifests as pathological changes in contraction and relaxation of the whole heart [7], which are possibly associated with a decreased sensitivity to calcium [8]. However, the current evidence does not allow determining how much each of the individual diet components contributed to or was a determinant of cardiac dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Basal and �-Adrenergic Cardiomyocytes Contractility Dysfunction Induced by Dietary Protein Restriction is Associated with Downregulation of SERCA2a Expression and Disturbance of Endoplasmic Reticulum Ca²⁺Regulation in Rats

Penitente

Novaes

Silva

et al. 2014

Cell Physiol Biochem

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Background: The mechanisms responsible for the cardiac dysfunction associated with dietary protein restriction (PR) are poorly understood. Thus, this study was designed to evaluate the effects of PR on calcium kinetics, basal and β-adrenergic contractility in murine ventricular cardiomyocytes. Methods: After breastfeeding male Fisher rats were distributed into a control group (CG, n = 20) and a protein-restricted group (PRG, n = 20), receiving isocaloric diets for 35 days containing 15% and 6% protein, respectively. Biometric and hemodynamic variables were measured. After euthanasia left ventricles (LV) were collected for histopathological evaluation, SERCA2a expression, cardiomyocytes contractility and Ca²⁺sparks analysis. Results: PRG animals showed reduced general growth, increased heart rate and arterial pressure. These animals presented extracellular matrix expansion and disorganization, cardiomyocytes hypotrophy, reduced amplitudes of shortening and maximum velocity of contraction and relaxation at baseline and after β-adrenergic stimulation. Reduced SERCA2a expression as well as higher frequency and lower amplitude of Ca²⁺sparks were observed in PRG cardiomyocytes. Conclusion: The observations reveal that protein restriction induces marked myocardial morphofunctional damage. The pathological changes of cardiomyocyte mechanics suggest the potential involvement of the β-adrenergic system, which is possibly associated with changes in SERCA2a expression and disturbances in Ca²⁺ intracellular kinetics.

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“…In normotensive animals, morphological, ultrastructural, and functional myocardial changes were slight. [77][78][79][80][81][82] However, in the hypertrophied heart of hypertensive rats, structural changes were more severe and were combined with ventricular and myocardial systolic dysfunction. [83][84][85][86] Therefore, severe food restriction induces mild morphological and functional changes in normal hearts, which are exacerbated in hemodynamic overloaded hearts.…”

Section: Clinical Consequences Of Cachexiamentioning

confidence: 99%

Cardiac cachexia and muscle wasting: definition, physiopathology, and clinical consequences

Okoshi¹,

Romeiro²,

Martínez³

et al. 2014

RRCC

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Cachexia and muscle wasting are frequently observed in heart failure patients. Cachexia is a predictor of reduced survival, independent of important parameters such as age, heart failure functional class, and functional capacity. Muscle and fat wasting can also predict adverse outcome during cardiac failure. Only more recently were these conditions defined in International Consensus. Considering that heart failure is an inflammatory disease, cardiac cachexia has been diagnosed by finding a body weight loss .5%, in the absence of other diseases and independent of other criteria. Muscle wasting has been defined as lean appendicular mass corrected for height squared of 2 standard deviations or more below the mean for healthy individuals between 20 years and 30 years old from the same ethnic group. The etiology of heart failure-associated cachexia and muscle wasting is multifactorial, and the underlying physiopathological mechanisms are not completely understood. The most important factors are reduced food intake, gastrointestinal alterations, immunological activation, neurohormonal abnormalities, and an imbalance between anabolic and catabolic processes. Cachexia and muscle wasting have clinical consequences in several organs and systems including the gastrointestinal and erythropoietic systems, and the heart, previously affected by the primary disease. We hope that a better understanding of the mechanisms involved in their physiopathology will allow the development of pharmacological and nonpharmacological therapies to effectively prevent and treat heart failure-induced cachexia and muscle wasting before significant body weight and muscle wasting occurs.

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Myocardial dysfunction induced by food restriction is related to calcium cycling and beta-adrenergic system changes

Cited by 21 publications

References 27 publications

Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos

Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos

Basal and �-Adrenergic Cardiomyocytes Contractility Dysfunction Induced by Dietary Protein Restriction is Associated with Downregulation of SERCA2a Expression and Disturbance of Endoplasmic Reticulum Ca²⁺Regulation in Rats

Cardiac cachexia and muscle wasting: definition, physiopathology, and clinical consequences

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Myocardial dysfunction induced by food restriction is related to calcium cycling and beta-adrenergic system changes

Cited by 21 publications

References 27 publications

Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos

Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos

Basal and �-Adrenergic Cardiomyocytes Contractility Dysfunction Induced by Dietary Protein Restriction is Associated with Downregulation of SERCA2a Expression and Disturbance of Endoplasmic Reticulum Ca2+Regulation in Rats

Cardiac cachexia and muscle wasting: definition, physiopathology, and clinical consequences

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Product

Resources

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Basal and �-Adrenergic Cardiomyocytes Contractility Dysfunction Induced by Dietary Protein Restriction is Associated with Downregulation of SERCA2a Expression and Disturbance of Endoplasmic Reticulum Ca²⁺Regulation in Rats