Ghrelin improves disturbed myocardial energy metabolism in rats with heart failure induced by isoproterenol

Xu, Jianping; Wang, Hongxia; Wang, Wen; Zhang, Like; Tang, Chaoshu

doi:10.1002/psc.1253

Cited by 14 publications

(13 citation statements)

References 55 publications

(68 reference statements)

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“…The results demonstrated that ghrelin can improve cardiac function in CHF rats, as indicated by increases in LVSP and LV dp/dt max and by decreases in LVEDP, left ventricular mass to body weight (LVM/BW), and the number of apoptotic cardiomyocytes. These results are consistent with previous findings that ghrelin prevents early left ventricular remodeling in rats with MI [26], [27]. We further clarified that increased serum ghrelin levels are a protective response in HF, which can improve cardiac function and improve the HF prognosis.…”

Section: Discussionsupporting

confidence: 93%

Mechanisms of Ghrelin Anti-Heart Failure: Inhibition of Ang II-Induced Cardiomyocyte Apoptosis by Down-Regulating AT1R Expression

Yang

Liu

et al. 2014

PLoS ONE

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BackgroundGhrelin is a novel growth hormone–releasing peptide administered to treat chronic heart failure (CHF). However, the underlying mechanism of its protective effects against heart failure (HF) remains unclear.Methods and ResultsA total of 68 patients with CHF and 20 healthy individuals were included. The serum levels of Angiotensin II (Ang II) and ghrelin were measured using ELISA. The results showed that Ang II and ghrelin were both significantly increased in CHF patients and that the ghrelin levels were significantly positively correlated with Ang II. The left anterior descending coronary artery was ligated to establish a rat model of CHF, and cultured cardiomyocytes from neonatal rats were stimulated with Ang II to explore the role of ghrelin in CHF. The results showed that ghrelin inhibited cardiomyocyte apoptosis both in vivo and in vitro. Furthermore, caspase-3 expression was examined, and the results revealed that Ang II induces cardiomyocyte apoptosis through the caspase-3 pathway, whereas ghrelin inhibits this action. Lastly, to further elucidate the mechanism by which ghrelin inhibits Ang II action, the expression of the AT1 and AT2 receptors was evaluated; the results showed that Ang II up-regulates the AT1 and AT2 receptors in cardiomyocytes, whereas ghrelin inhibits AT1 receptor up-regulation but does not affect AT2 receptor expression.ConclusionsThese data suggest that the serum levels of ghrelin are significantly positively correlated with Ang II in CHF patients and that ghrelin can inhibit Ang II-induced cardiomyocyte apoptosis by down-regulating AT1R, thereby playing a role in preventing HF.

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Section: Discussionsupporting

confidence: 93%

Mechanisms of Ghrelin Anti-Heart Failure: Inhibition of Ang II-Induced Cardiomyocyte Apoptosis by Down-Regulating AT1R Expression

Yang

Liu

et al. 2014

PLoS ONE

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“…Since the AMPK has a prominent role in energy sensing and metabolism (25, 26), the present findings provide important evidence of interaction between ghrelin and metabolism regulation in hypoxic conditions, probably through AMPK. As reported by Xu et al, it is also remarkable that exogenous administration of ghrelin could be a new therapeutic approach to the treatment of severe CHF because it can attenuate the myocardial metabolic disorders (27). Another fact is that chronic peripheral ghrelin administration to lean rats up-regulates AKT activation in the muscle (28).…”

Section: Discussionmentioning

confidence: 99%

Effect of Ghrelin on Aldolase Gene Expression in the Heart of Chronic Hypoxic Rat

Aliparasti

Alipour

Almasi

et al. 2012

Int J Endocrinol Metab

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BackgroundChronic hypoxia causes apoptosis of cardiac myocytes, however, energy production by anaerobic glycolysis protects myocardium against hypoxia injuries. Aldolase A is a well-characterised key enzyme of the glycolysis pathway. Ghrelin, a 28-amino-acid peptide, synthesizes in the stomach and has protective roles in cardiovascular systems and also affects metabolic pathways.ObjectivesTherefore, the aim of this study was to evaluate the effect of ghrelin on aldolase A gene expression after chronic hypoxia in the rat hearts.Materials and MethodsTwenty four adult male wistar rats were randomly divided into three groups. Hypoxic rats with saline or ghrelin treatment were placed in a normobaric hypoxic chamber (O2 11 %), for two weeks. Controls remained in room air. Aldolase A gene expression was measured by Real-Time RT-PCR.Resultsthe transcriptiom rate of Aldolase A in hypoxic animals did not change significantly compared to negative control ones. During chronic hypoxia, ghrelin treatment increased the amount of heart Aldolase A gene expression compared to negative controls (P = 0.029). Hypoxic animals that were treated with ghrelin were significantly more polycythemic than the controls and even hypoxic with saline treated rats (P < 0.001).ConclusionsIt seems that ghrelin interferes in the cardiac metabolism through upregulation of glycolytic enzymes. In other words, it may protect heart from possible hypoxia induced damages.

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“…Body weights were measured weekly. After 15 weeks, the ghrelin (Tocris Co., Bristol, UK) was administered subcutaneously 100 μ g/kg twice daily for 10 days [15, 16]. …”

Section: Methodsmentioning

confidence: 99%

Systemic Ghrelin Administration Alters Serum Biomarkers of Angiogenesis in Diet-Induced Obese Mice

Khazaei

Tahergorabi

2013

International Journal of Peptides

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Introduction. Ghrelin is a gastrointestinal endocrine peptide that was initially identified as the endogenous ligand of growth hormone secretagogue receptor; however, recently, the cardiovascular effect of this peptide has been indicated. In this study, we investigated the effect of ghrelin administration on serum biomarkers of angiogenesis including leptin, nitric oxide (NO), vascular endothelial growth factor (VEGF), and its soluble receptor (VEGF receptor 1 or sFlt-1) in control- and diet-induced obese mice. Methods. Male C57BL/6 mice were randomly divided into four groups, normal diet (ND) or control, ND + ghrelin, high-fat-diet (HFD) or obese and HFD + ghrelin (n = 6/group). Obese and control groups received either HFD or ND for 15 weeks. Then, the ghrelin was injected subcutaneously 100 µg/kg twice daily for 10 days. At the end of experiment, blood samples were collected for blood glucose, serum insulin, VEGF, sFlt-1, NO, and leptin measurements. Results. The obese animals had higher serum NO and leptin concentrations without changes in serum VEGF and sFlt-1 levels compared to control. Administration of ghrelin significantly increased serum VEGF and decreased serum leptin and NO concentrations in HFD group. Conclusion. Since ghrelin changes serum biomarkers of angiogenesis, it seems that it gets involved during states with abnormal angiogenesis.

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Ghrelin improves disturbed myocardial energy metabolism in rats with heart failure induced by isoproterenol

Cited by 14 publications

References 55 publications

Mechanisms of Ghrelin Anti-Heart Failure: Inhibition of Ang II-Induced Cardiomyocyte Apoptosis by Down-Regulating AT1R Expression

Mechanisms of Ghrelin Anti-Heart Failure: Inhibition of Ang II-Induced Cardiomyocyte Apoptosis by Down-Regulating AT1R Expression

Effect of Ghrelin on Aldolase Gene Expression in the Heart of Chronic Hypoxic Rat

Systemic Ghrelin Administration Alters Serum Biomarkers of Angiogenesis in Diet-Induced Obese Mice

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