Metformin use and the hepatic and renal toxicity
Abstract
Objectives
Metformin is an oral anti-diabetic that is commonly used in the treatment of type 2 diabetes mellitus. Metformin has been rarely associated with hepatic and renal toxicity and it is suggested that the hepatic toxicity is caused by the upregulation of hydrogen sulfide (H2S) as a result of changing the mitochondrial metabolism of H2S due to the inhibition of complex I by metformin. The renal toxicity is thought to be caused indirectly by the development of metformin associated lactic acidosis due to a pre-existing renal impairment.
This essay will include our findings on the molecular mechanism behind metformin’s toxic and beneficial effects on the liver and kidneys. Furthermore, the following questions are aimed to be answered:
Can the upregulation of H2S and lactate be the cause of the hepatic and renal injury, respectively, and how does this happen? What effects does the pre-existing renal impairment have on damage development? How does metformin exert its tissue-protective effects?
Results
From the data, we have found that metformin use is rarely associated with hepatic toxicity by which patients treated with metformin started to show signs of mixed type hepatocellular and cholestatic hepatic injury within two months after starting metformin treatment. Furthermore, the renal injury was found to occur in patients suffering from pre-existing renal impairments due to the development of lactic acidosis. On the other hand, we have found that metformin can be benefici
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