Diabetes and the Hormone of Darkness

Type 2 diabetes risk linked to mutations in the melatonin receptor gene

(RxWiki News) Sleep is tied to many aspects of your health. Some studies have found that poor sleep may even raise your risk of diabetes. Now, researchers have found another link between sleep and type 2 diabetes.

People with mutations in a gene involved with melatonin (a hormone that triggers sleep) may have a greater risk of developing diabetes. This finding could lead to new drugs that treat or prevent diabetes by targeting this gene.

"Eat healthy and get exercise to prevent diabetes."

While poor sleep has been tied to diabetes, no previous studies have pinpointed any mechanisms that link the biological clock to diabetes. Professor Philippe Froguel, of Imperial College London, and colleagues set out to see if the melatonin receptor gene played a role in diabetes risk.

Past research has shown that a lack of sleep or poor sleep quality can increase the risk of type 2 diabetes. 

Froguel and colleagues focused their research on something much smaller than the person at risk of diabetes. They looked at the receptor of a hormone called melatonin. Melatonin, which is sometimes called the "hormone of darkness," is produced by the body as light fades. It is basically a biological time-keeper, letting the body know when night has arrived.

Through a study of 7600 people with and without diabetes, the researchers found 40 rare mutations that change the protein structure of the melatonin receptor gene. Of these mutations, 14 stopped the receptor from working.

The researchers went on to show that people with these mutations - and who are thus melatonin-insensitive - are almost seven times more likely to develop diabetes.

These findings could be useful in the future development of drugs that treat and prevent diabetes.

This study also underlines the importance of genome sequencing as a way to personalize treatment for patients with diabetes. As there are many genetic causes of diabetes, each approach to treatment needs to be adjusted for each patient's specific condition.

The study by Froguel and colleagues appears in the journal Nature Genetics

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Review Date: 
January 30, 2012