Experts

Researchers Study Diabetes Atop Mount Everest

By Cheri Cheng | Update Date: Apr 15, 2014 11:44 AM EDT

In a new study, researchers used Mount Everest to help uncover new knowledge regarding type 2 diabetes. The team of British researchers found that low oxygen levels, known as hypoxia, could be tied to insulin resistance, which is a known risk factor for diabetes.

In order to test the effects of different oxygen levels in body, the researchers set out to conduct research atop Mount Everest. The researchers had examined 24 climbers who were a part of the 2007 Everest expedition. At the beginning of the expedition, the team measured blood sugar control, body weight and signs of inflammation at base camp, which sat at an altitude of 17,388 feet. The group was then divided in half with one half climbing up the mountain to 29,028 feet while the other half remained at base camp. Additional measurements were taken at week six and week eight.

The researchers found that when the climbers reached higher altitudes during weeks six and eight, they were exposed to hypoxia. These climbers also exhibited signs of insulin resistance, which occurs when the body cells do not respond to insulin, a hormone that is in charge of regulating blood sugar levels. The researchers measured markers of inflammation and oxidative stress in the participants' blood samples in order to determine whether or not they experienced with insulin resistance.

"These results have given us useful insight into the clinical problem of insulin resistance. Fat tissue in obese people is believed to exist in a chronic state of mild hypoxia because the small blood vessels are unable to supply sufficient oxygen to fat tissue," lead investigator, Mike Grocott, a professor of anesthesia and critical care at the University of Southampton, said reported by Philly. "The results suggest possible [treatments] to reduce progression towards full-blown diabetes, including measures to reduce oxidative stress and inflammation within the body."

The study was published in PLOS ONE.

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