Researchers in the United States have made a major new discovery in the fight against diabetes, and it may lead them to new treatments for the disease.
Diabetes affects millions of people around the world. The disease hampers the body's ability to produce insulin, which is used to regulate blood sugar levels. Without the needed insulin, sugar levels in the blood become too high, and this can lead to a host of complications, such as heart disease, kidney disease and even loss of limbs. There are a few types of diabetes, but there are two that are most common. Type 1 sufferers have the disease from birth and it causes insulin deficiency. Type 2 is acquired later in life (usually through poor diet) and it causes the body's cells to not use insulin efficiently, and it can also involve insulin deficiency.
Sufferers can manage the disease through injections of insulin, but the search has been on for a way to manage the disease more effectively or even cure it.
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It's been nearly 10 years since Dr. Anath Shalev, the director of the Comprehensive Diabetes Center at the University of Alabama, was able to point the finger at a specific protein, called TXNIP (or thioredoxin-interacting protein), as the culprit in causing diabetes. TXNIP is activated by the presence of sugars in our blood stream, and it sends out a flood of what are known as 'free radicals', which are known to damage the tissues in our bodies. Through her research, Shalev found that the chain reaction set off by TXNIP targets the insulin-producing cells in our pancreas (called 'beta cells'), and pushes them into premature cell death (apoptosis).
"We spent years confirming that TXNIP drives beta-cell death in both Type 1 and Type 2 diabetes," Shalev said in a UAB statement. "We were astounded to find that its action also contributes to a second major diabetic mechanism — the decrease seen in insulin production by beta cells — by a mechanism never before seen."
TXNIP does this by causing the beta cells to produce a small chunk of genetic code, called microRNA-204 which, in turn, interferes with another protein, called MAFA, which is responsible for turning on the beta cells' insulin production. Having discovered this TXNIP/microRNA-204/MAFA mode of action, this opens the door for researchers to find a way to interrupt it.
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So far, Shalev has reported that early tests have found a method of essentially quieting the TXNIP that has been activated by high blood sugar levels, without any apparent negative side effects. The next stage of the research is to search for a way to act against the microRNA-204, to prevent it from interfering with insulin production.
(Photo courtesy: Getty Images)
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