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

authors:

avatar Mohammad Reza Aliparasti 2 , avatar Mohammad Reza Alipour 3 , avatar Shohreh Almasi 2 , avatar Hadi Feizi 4 , *

Department of Immunology, Tabriz University of Medical Sciences, IR Iran
Tuberculosis and Lung Research Center, Tabriz University of Medical Sciences, IR Iran
Department of Physiology, Hormozgan University of Medical Sciences, hfeizyk@gmail.com, IR Iran

how to cite: Aliparasti M R, Alipour M R, Almasi S, Feizi H. Effect of Ghrelin on Aldolase Gene Expression in the Heart of Chronic Hypoxic Rat. Int J Endocrinol Metab. 2012;10(3): 553-557. https://doi.org/10.5812/ijem.3914.

Abstract

Background:

Chronic 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.

Objectives:

Therefore, 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 Methods:

Twenty 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.

Results:

the 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).

Conclusions:

It seems that ghrelin interferes in the cardiac metabolism through up-regulation of glycolytic enzymes. In other words, it may protect heart from possible hypoxia induced damages.

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