South Korea - A local team of scientists has discovered genes closely involved in regulating feeding behaviour, opening new possibilities for treating obesity and metabolic disorders.
Led by Yu Kweon, principal researcher at Korea Research Institute of Bioscience and Biotechnology's Aging Research Center, the team found that the fruit fly gene minibrain, or mnb, and mammalian functional equivalent DYRK1a gene control the expression of neuropeptides - proteins that transmit signals from nerve cells - involved in food intake regulation.
The results were published in the August issue of the peer-review journal PLoS Genetics.
In fruit flies, the mnb gene controls the expression of short neuropeptide F, or sNPF, while DYRK1a controls that of neuropeptide Y, or NPY.
Yu's research showed that the fruit fly and mammalian genes stimulate the production of the relevant proteins.
In the experiments, fruit flies with artificially enhanced mnb gene expression had 60 per cent larger daily food intake than control insects. In contrast, the food intake of flies with reduced mnb gene expression was about 30 per cent lower than those with normal levels of gene expression.
Similar results were also obtained in mice, with subjects with enhanced DYRK1a gene expression eating 20 per cent more.
In addition, Yu found that while DYRK1a acts in a positive feedback loop where NPY expression is increased with the rise in DYRK1a expression, the same process is dampened by insulin, the lack of which is the cause of Type 1 diabetes.
Although the involvement of sNPF and neuropeptide Y in food intake control has been known for some time, Yu and his team were the first to discover that the food intake-related genes are controlled by other genes.
"I researched the subject for nearly 10 years because the upstream control mechanisms (for sNPF and NPY) were unknown," Yu said.
"The discovery could provide an important step in developing new methods for treating obesity and metabolic disorders such as diabetes but its application will take more time."
In addition, this is the first time the DYRK1a gene has been shown to be involved in a molecular pathway other than those involved in Down syndrome.
Due to its location on chromosome 21, the DYRK1a is thought to play a role in Down syndrome, which manifests in individuals with three copies of the chromosome instead of the normal two.