Metformin, one of the most popular medications used in the front-line treatment of diabetes, appears to improve mitochondrial function in people with diabetes, reports a new study from researchers in Spain.
Mitochondria are what are known as organelles. Organelles are components of body cells that have a specific function to perform, such as storing genetic information or producing chemical energy. Sometimes mitochondria are referred to as the “powerhouses of the cell” because they help turn the energy contained in foods into energy that body can utilize. It’s estimated that mitochondria produce 90% of the energy required by the human body. Sometimes, however, mitochondria fail to do their work properly, often because of a disease, resulting in a condition called mitochondrial dysfunction, which is known to contribute to type 2 diabetes.
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For their study, the researchers collected data from 242 individuals recruited from the Endocrinology Department of the Hospital Universitari Doctor Peset in Valencia, Spain. The subjects were separated into three groups — 101 were volunteers without diabetes, 48 were people with type 2 diabetes who were not taking metformin, and 93 were people with diabetes who had been taking daily doses of 1700 milligrams of metformin for at least a year. The age of the subjects ranged from 35 to 70.
Metformin linked to improved mitochondrial function
The researchers determined that mitochondrial function improved in the participants using metformin compared to those not using it. Specifically, they found that people with diabetes not treated with metformin displayed more reactive oxygen species than the treated subjects. Reactive oxygen species (ROS) are unstable molecules, or free radicals, that react with other molecules in a cell. An excess of ROS can cause cell damage and even cell death. The study also reported that the metformin-treated patients showed “significantly lower” levels of two cytokines known as TNF-α and IL-6, which are both substances that promote the inflammation that appears to promote diabetes. Finally, the researchers theorized that “metformin diminishes leukocyte activation,” which is beneficial because the release of TNF-α from leukocytes “may inhibit insulin signaling and impair glucose uptake.”
The findings of the new study might have implications beyond diabetes because mitochondrial dysfunction might also contribute to other conditions — most notably atherosclerosis, which is commonly known as “hardening of the arteries.” According to study co-author Aranzazu Martínez de Marañón, PhD, “the message we want to spread with this article is that metformin, while far from being an exclusive treatment to regulate blood glucose levels, has several benefits on a cellular level. Specifically, it improves the state of mitochondria and the function of immune cells. This decreases the initial stages of the atherosclerotic process, a common complication in patients with Type-2 diabetes.”
As Víctor M. Víctor, another of the researchers, put it, “Our findings have significant clinical implications, as they back the idea that metformin plays a key role in modulating the inflammation that takes place in patients with Type 2 diabetes. Meanwhile, the study highlights the beneficial effects of this drug, which prevents mitochondrial dysfunction and deregulation … In this study we have shown that Type 2 diabetes is linked to mitochondrial dysfunction, and that metformin can modulate said effect.”
Want to learn more about metformin? Read “What to Know About Metformin,” “Diabetes Medicine: Metformin,” and “Metformin: The Unauthorized Biography.”