Being a couch potato could be genetic say Aberdeen scientists
- 14 February 2014
- From the section NE Scotland, Orkney & Shetland
Being a couch potato could be due to a person's genetic make-up, according to new research.
Scientists from Aberdeen University, working with colleagues in China, have been looking at why some people are less inclined to exercise and more likely to put on weight.
The team said they had found a mutation in a gene which may explain it.
They said their findings raised hope of a personalised pill to reverse the problem being developed in the future.
The study, by researchers from the Chinese Academy of Sciences, Institute of Genetics and Developmental Biology (IGDB) in Beijing and the University of Aberdeen, has been published in the journal PLOS Genetics.
Fat, lazy mice
The scientists compared "normal" mice with mice that had a mutation in a gene called SLC35D3.
The researchers discovered that SLC35D3 produces a protein which plays a key signalling role in the system in the brain which is involved in regulating physical activity levels - the dopamine system.
They found that SLC35D3 seems to be important for transporting a type of dopamine receptor, from inside the cell where it is made to the cell surface.
However, mice with this gene mutated had far fewer of this type of dopamine receptor on their brain cell surfaces. Instead, the dopamine receptors were stuck within the cell.
This meant their signalling process was not functioning properly.
However, treating the mice with a drug that activates dopamine receptors reversed the problem - the mice became more active and lost their excess weight.
Prof Wei Li, from the IGDB, who led the study, said: "We discovered that mice with this gene mutation were typical couch potatoes.
"They walked only about a third as much as a normal mouse, and when they did move they walked more slowly.
"The mice became fat and they also developed other symptoms similar to a condition in people called 'metabolic syndrome' - a medical term for those with a combination of risk factors related to diabetes, high blood pressure and obesity."
He added: "What was of particular interest, was that what that when we gave the mice a drug that acted on the dopamine signalling system, the genetic defect could be overcome and the mice became more active and thinner."
The researchers then screened 400 overweight and obese Chinese patients with metabolic syndrome and found mutations in the SLC35D3 gene in two of them.
Prof John Speakman, who works between the University of Aberdeen and the IGDB, and was a co-author on the paper, added: "Although only about one in about 200 people may have these 'rare' mutations, there are a very large number of people worldwide that have metabolic syndrome.
"Consequently the population of sufferers that may benefit from being treated with dopamine receptor drugs runs into many millions of patients."
Prof Li added: "We are really excited about these findings. Medical treatments will in the future be tailored to fit a person's individual genetic make-up. "