In a recent study published in Molecular Metabolism, researchers found the biological mechanism linking long-term arsenic exposure to diseases such as cancer and Type 2 diabetes.
The findings could result in potential new targets for drug development.
The study is from the University of Arizona. One author is Donna D. Zhang, Ph.D.
More than 34 million Americans have diabetes, according to the Centers for Disease Control and Prevention, and approximately 90-95% of them have Type 2 diabetes.
One of the main risk factors is environmental toxicant exposure, particularly chronic exposure to arsenic, which has been shown to affect insulin production and sensitivity, blood sugar levels, and lipid profiles, all common features of diabetes onset and progression.
Because arsenic is a natural metalloid found in soil, it can be one of the most significant contaminants in drinking water globally, especially when ingested at unsafe levels.
Arsenic is present in almost all groundwater sources in Arizona, particularly in rural areas. Combined with occupational exposures, such as mining, more than 160 million people worldwide are exposed to arsenic.
In the study, the team uncovered a biological mechanism by which chronic arsenic exposure led to insulin resistance and glucose intolerance, two key features of diabetes progression.
The study examined the effect of arsenic exposure on nuclear factor-erythroid 2 related factor 2 (NRF2) activation. NRF2 is the body’s governing regulator against oxidative stress.
Long-term oxidative stress, such as that caused by cigarette smoke, radiation, diets high in sugar, fat and alcohol, or environmental toxins, contributes to the development of a range of chronic conditions including cancer, diabetes and neurodegenerative disease.
Previously the team found that arsenic exposure results in the prolonged and uncontrolled activation of NRF2, which is a driver of cancer progression and resistance to anti-cancer therapy.
In this study, they found that arsenic exposure resulted in glucose intolerance and decreased insulin sensitivity.
The findings showed that prolonged NRF2 activation in response to arsenic increased glucose production in the liver and the release of that glucose to the bloodstream, which could represent a key driver of changes in systemic blood glucose.
The team hopes this study will serve as a foundation for future toxicant-driven diabetes research. The eventual goal is to generate effective preventive or interventive strategies to treat exposed populations.
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