alexa Modulation of Cardiomyocyte and Hepatocyte Bioenergetics by Biguanides
ISSN: 2161-0495

Journal of Clinical Toxicology
Open Access

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Research Article

Modulation of Cardiomyocyte and Hepatocyte Bioenergetics by Biguanides

Saeeda Almarzooqi1*, Ali S. Alfazari2, Alia Albawardi1, Dhanya Saraswathiamma1, Hidaya Mohammed Abdul-Kader2, Sami Shaban3 and Abdul-Kader Souid4

1Department of Pathology, UAE University, Al-Ain, Abu Dhabi, United Arab Emirates

2Department of Medicine, UAE University, Al-Ain, Abu Dhabi, United Arab Emirates

3Department of Medical Education, UAE University, Al-Ain, Abu Dhabi, United Arab Emirates

4Department of Pediatrics, UAE University, Al-Ain, Abu Dhabi, United Arab Emirates

*Corresponding Author:
Saeeda Almarzooqi
Department of Pathology, UAE University
Al-Ain, Abu Dhabi, United Arab Emirates
Tel: +9-713-713-7471
Fax; +9-713-767-2022
E-mail: [email protected]

Received Date: April 08, 2014; Accepted Date: June 17, 2014; Published Date: June 20, 2014

Citation: Almarzooqi S, Alfazari AS, Albawardi A, Saraswathiamma D, Abdul-Kader HM, et al. (2014) Modulation of Cardiomyocyte and Hepatocyte Bioenergetics by Biguanides. J Clin Toxicol 4:203. doi: 10.4172/2161-0495.1000203

Copyright: © 2014, Almarzooqi S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Biguanides (metformin, buformin and phenformin) have been developed for oral treatment of non-insulindependent diabetes mellitus. Metformin, the drug of choice in this class, controls blood glucose primarily by lowering hepatic gluconeogenesis (e.g., decreasing glucagon-mediated hepatic glucose output). Its mode-of-action, however, is more complex and may involve “refining” cellular bioenergetics (improving energy efficiency) in various cell types including myocytes. Buformin and phenformin presumably have similar mechanisms of action. The main purpose of this in vitro study was to assess the effects of these drugs on bioenergetics - cellular respiration (mitochondrial O2 consumption) and ATP content - in tissue fragments from the heart muscle (cardiomyocytes) and liver (hepatocytes) of C57BL/6 mice. Cardiomyocyte respiration decreased by 10-26% in the presence of 100 μM metformin (p=0.093), buformin (p=0.028) or phenformin (p=0.015). Similar effects on cardiomyocyte respiration were noted with 1.0 mM drugs. Cardiomyocyte ATP, on the other hand, increased by 17-31% in the presence of 100 μM metformin (p=0.093), buformin (p=0.445) or phenformin (p=0.093). Hepatocyte respiration and ATP decreased by 11-26% and 8-25%, respectively in the presence of 1.0 mM drugs. Decreased respiration and ATP were also noted in hepatocytes exposed to 100 μM metformin for 1 ≤ t ≤ 6 hours (13% and 5%, respectively). Thus, the effects of biguanides on cardiomyocyte bioenergetics differed from that on hepatocyte bioenergetics. These findings suggest that biguanides regulate cardiomyocyte energy conversion, favoring better fuel efficiency (↓respiration/↑ATP). The drug effects in hepatocyte are ↓respiration/↓ATP, favoring less fuel production (↓hepatic gluconeogenesis). Biguanide activities in various tissues may be coupled.

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