Metformin is one of a number of medications in the category known as the biguanide drugs. These drugs target the liver and keep it from releasing glucose into the bloodstream. Metformin is frequently prescribed to type II diabetics to aid in the control of their blood sugar levels. In healthy individuals, the liver releases glucose into the blood when more is needed for energy- for example, during times of strenuous exercise- but this function causes difficulties for diabetics who cannot absorb the sugar from their blood into the cells where it is needed.
Studies performed on diabetics have uncovered that those patients taking metformin experience a lower level of myocardial infarctions, or heart attacks, than those not using the medication. This decrease in cardiac ailments extends beyond what would be expected from the drug's ability to lower patients' blood glucose, as it was not evident in patients taking different types of medication that had similar effects on their overall blood sugar levels.. Further investigation showed that metformin usage stabilized general vascular function independent of its effects on sugar metabolism.
The drug's protective benefits appear to result from a series of biological interactions known as the AMPK-eNOS pathway. AMPK is a type of enzyme known as a protein kinase that is usually activated in cells as the result of oxidative stress, exercise, or a lack of glucose. However, it appears that metformin, in dosages frequently prescribed for diabetes, also activated AMPK which in turn lead to the production of nitric oxide by an enzyme known as eNOS.
A recent journal article showed how the increased levels of AMPK activation and nitric oxide induced by metformin lead to smaller size myocardial infarctions (or heart cell deaths) in both diabetic and non-diabetic mice. This gives clear evidence that metformin taken at commonly prescribed levels is beneficial to the heart for reasons unrelated to its effect on diabetes. As diabetes is one of the leading causes of heart disease, this news should come as a relief to the many type II diabetics who are already taking metformin as part of their daily routine.
References:
1. Owen MR, Doran E, Halestrap AP: Evidence that metformin exerts its anti-diabetic effects through inhibition of complex 1 of the mitochondrial respiratory chain. Biochem J 348 Pt 3:607–614, 2000
2. Verma S, Bhanot S, McNeill JH: Decreased vascular reactivity in metformin-treated fructose-hypertensive rats. Metabolism 45:1053–1055, 1996
3. Calvert JW, Gundewar S, Jha S, Greer JJ, Bestermann WH, Tian R, Lefer DJ: Acute metformin therapy confers cardioprotection against myocardial infarction via AMPK-eNOS-mediated signaling. Diabetes. 2008 Mar;57(3):696-705. Epub 2007 Dec 14.
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