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Gene mutation gives mice 'night munchies'

28 May 2014
Appeared in BioNews 755

Genes responsible for night eating syndrome, where eating patterns are out of sync with sleeping schedules, have been found in a study on mice.

The research identifies a pair of genes that link eating habits to the body clock. Mutations in the PER2 gene have long been known to affect sleeping habits. Scientists investigating its sister gene, PER1, found that mice genetically engineered to have a defective copy of the gene were much more prone to eating when they should be sleeping.

'In the mice without PER1, there was no obvious defect in their sleep-wake cycles', said study author Dr Satchidananda Panda from the Salk Institute, California, USA. 'Instead, when we looked at their metabolism, we suddenly saw drastic changes'.

While mice with the PER2 mutation went to sleep at an earlier time, mice with the PER1 gene mutation overate and gained more weight when eating normal food. They also put on weight much more quickly when given a high-fat diet.

'We really never expected that we would be able to decouple the sleep-wake cycle and the eating cycle, especially with a simple mutation', said Dr Panda. 'It opens up a whole lot of future questions about how these cycles are regulated'.

The researchers believe that normally, the PER1 and PER2 genes are switched on and off at the same time, so that sleeping and eating patterns are in sync. But a mutation in PER1 means that this mechanism becomes misaligned, so the urge to eat strikes at odd hours.

When the team only gave the mice access to food at normal mealtimes, they found that they were able to maintain a normal weight. This means that the weight gain was due to the time that the meals were eaten rather than being a direct result of the mutation itself.

One to two percent of people are thought to have the syndrome, which has recently been classified as a type of eating disorder.

'For a long time, people discounted night eating syndrome as not real', said Dr Panda. 'These results in mice suggest that it could actually be a genetic basis for the syndrome'.

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