Science

My body clock and I

Finally, a possible explanation for those self-inflicted Facebook/Youtube-laden all-nighters...

How many times have you ended up staring at Facebook at 3am on a Monday? If you’re me, the answer is too many to count. A lot of people out there have trouble keeping their sleeping pattern in check. It can be very detrimental to your life (and really annoying). It seems my body clock just wants to troll me constantly, smugly making me stumble bleary eyed out of bed after too little sleep. The recent freezing weather doesn’t help. It makes the warm confines of the covers look incredibly appealing.

A new study led by Imperial scientists has found a link between diabetes and a person’s body clock. To be less cryptically vague, the study found a link between the gene MTNR1B and type 2 diabetes. MTNR1B codes for MT2, a receptor for the hormone melatonin. Melatonin regulates the sleeping cycle and also the release of insulin, which is what regulates the level of sugar in the blood. The postulation is that mutations in the MT2 gene could disrupt both the sleeping cycle and the release of insulin. Thus, people with the mutations will not be able to control their blood sugar level correctly. Therein lies the link between the MT2 gene and diabetes and explains the connection between two seemingly unconnected things. A person carrying these mutations will not definitely develop type 2 diabetes, but the risk that they do, compared to someone without said mutations, is increased.

The study looked at 7,632 Europeans and included 2,186 individuals with type 2 diabetes. In total, the MT2 gene can have forty mutations; all were tested to see what the effect would be. Four of these, which are, luckily, very rare, were found to completely stop the melatonin from binding to MT2. These highly increased the risk of type 2 diabetes developing.

The hope is that this discovery and mechanistic link can be used to gauge the diabetes risk of an individual and tailor medical treatments to their needs, a small step towards personalised medicine.

From Issue 1511

17th Feb 2012

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