’Couch potato’ gene discovered
A gene mutation may explain why some people are more likely than others to be couch potatoes, according to a new study which offers hope that in the future a personalised pill could counter the problem.
Scientists found that a mutation in a gene, which has a critical role in the brain, may explain why some people are less inclined to exercise and are more likely to put on weight and develop health problems.
Researchers from the Chinese Academy of Sciences, Institute of Genetics and Developmental Biology (IGDB) in Beijing and the University of Aberdeen in UK, 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 brain's dopamine system - this system is involved in a range of functions including regulation of physical activity levels.
They found that SLC35D3 seems to be important for transporting a type of dopamine receptor, from where they are made inside the cell, to the cell surface, where they can bind with dopamine.
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 that their signalling process was not functioning properly.
"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," said Professor Wei Li, of the IGDB.
"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," Li said.
"We discovered that SLC35D3 plays a critical role in transporting the dopamine 1 receptor from where it is made inside the cell, to the cell surface. Hence dopamine signalling in the mutant mice was significantly impaired," said Professor John Speakman, who works between the University of Aberdeen and the IGDB, and was a co-author on the paper.
"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," Li added.
The researchers then screened 400 overweight and obese Chinese patients with metabolic syndrome and found mutations in the SLC35D3 gene in two of them.
As the mice could be treated using a drug that acted on the dopamine receptor, the scientists suggest that in the future people with metabolic syndrome could possibly be screened to see if they have the relevant mutations.
The study is published in the journal PLOS Genetics. PTI
Scientists found that a mutation in a gene, which has a critical role in the brain, may explain why some people are less inclined to exercise and are more likely to put on weight and develop health problems.
Researchers from the Chinese Academy of Sciences, Institute of Genetics and Developmental Biology (IGDB) in Beijing and the University of Aberdeen in UK, 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 brain's dopamine system - this system is involved in a range of functions including regulation of physical activity levels.
They found that SLC35D3 seems to be important for transporting a type of dopamine receptor, from where they are made inside the cell, to the cell surface, where they can bind with dopamine.
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 that their signalling process was not functioning properly.
"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," said Professor Wei Li, of the IGDB.
"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," Li said.
"We discovered that SLC35D3 plays a critical role in transporting the dopamine 1 receptor from where it is made inside the cell, to the cell surface. Hence dopamine signalling in the mutant mice was significantly impaired," said Professor John Speakman, who works between the University of Aberdeen and the IGDB, and was a co-author on the paper.
"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," Li added.
The researchers then screened 400 overweight and obese Chinese patients with metabolic syndrome and found mutations in the SLC35D3 gene in two of them.
As the mice could be treated using a drug that acted on the dopamine receptor, the scientists suggest that in the future people with metabolic syndrome could possibly be screened to see if they have the relevant mutations.
The study is published in the journal PLOS Genetics. PTI
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