Abstract

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.

Highlights

  • Ghrelin is a gastrointestinal endocrine peptide that was initially identified as the endogenous ligand of growth hormone secretagogue receptor; recently, the cardiovascular effect of this peptide has been indicated

  • The results indicated no significant differences in serum vascular endothelial growth factor (VEGF) and sFlt-1 between obese and control animals

  • The main finding of this study is that the obese mice had higher serum insulin, nitric oxide (NO), and leptin concentrations compared to control without changes in serum VEGF and sFlt-1 levels

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Summary

Introduction

Ghrelin is a gastrointestinal endocrine peptide that was initially identified as the endogenous ligand of growth hormone secretagogue receptor; recently, the cardiovascular effect of this peptide has been indicated. The impact of ghrelin on cardiovascular system has been reported [10] including a decrease of peripheral vascular resistance in consequence an increase in cardiac index and stroke volume [11], improvement of ventricular remodeling [12], protection of myocytes from apoptosis [13], decrease of cardiac injury induced by ischemia/reperfusion (I/R) injury [14], and reduction of the infarct size (L). It improves endothelial dysfunction, reduces vasoconstrictor effect of endothelin-1, and decreases blood pressure [10]

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