Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA043

Poster Communications

Diabetes mellitus is associated with increased ghrelin level in the rat heart

E. A. Adeghate1, M. Lotfy3, C. D'Souza1, S. Tariq1, F. C. Howarth4, J. Singh2

1. Department of Anatomy, United Arab Emirates University, Al Ain, United Arab Emirates. 2. School of Forensic Sciences, University of Central Lancashire, Preston, United Kingdom. 3. Department of Biology, United Arab Emirates University, Al Ain, Abu Dhabi, United Arab Emirates. 4. Department of Physiology, United Arab Emirates University, Al Ain, Abu Dhabi, United Arab Emirates.


Diabetes mellitus (DM) is associated with increased risk of cardiovascular diseases leading to premature death. The structure and function of cardiac muscle are grossly impaired after the onset of DM. The functions of atrial and ventricular cardiomyocytes are controlled by a variety of neurotransmitters from both the sympathetic and parasympathetic pathways. In addition to neurotransmitters, peptides such as ghrelin have been shown to affect the function of the heart. The pattern of distribution of ghrelin in the diabetic rat heart is poorly understood. The cellular localization and distribution of ghrelin in the heart of a rodent model of DM was examined using immunohistochemistry. DM was induced by intraperitoneal injection of streptozotocin (60 mg kg-1). Wistar rats with blood glucose level equal or greated than 300 mg dl-1 were considered diabetic. Four weeks after the induction of DM, control and diabetic rats were humanely euthanized with chloral hydrate according to the rules and regulations established by the Institutional Animal Ethics Committee. The ventricles of the heart were removed and processed for ghrelin immunohistochemistry using established method (1). Ghrelin was observed in both the sarcolemma and sarcoplasm of ventricular cardiomyocytes. The nuclei of cardiomyocytes were spared. The number of ghrelin-positive ventricular cardiomyocytes increased significantly (p < 0.05) after the onset of DM. Since it has been reported that ghrelin protects the heart by inhibiting apoptosis in cardiomyocytes, the increased cardiac tissue level of ghrelin observed in this study, may be a result of a compensatory mechanism that is established to help in restoring cardiac structure and function in the ailing heart.

Where applicable, experiments conform with Society ethical requirements