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Gene knock-out creates diabetes-free, mighty mice

14 November 2011

By George Frodsham

Appeared in BioNews 633

Mice that don't produce a certain protein in their fat cells do not develop type 2 diabetes despite an increase in weight, scientists report. In a separate study, the same research group also managed to double the physical performance of mice by removing the same protein from their muscle cells. In both studies, the team used a virus to knock out the gene coding for the protein in the relevant tissue.

In the first study, the researchers prevented production of the protein NCoR1 in the mice's fat cells. The mice had no resistance to insulin which would normally mean they would go on to develop type 2 diabetes. The knock-out mice also weighed 15 percent more than the control animals.

'The specimens that became obese via this treatment did not suffer from diabetes, unlike mice who become obese for other reasons', said author Professor Johan Auwerx of the Ecole Polytechnique Fédérale de Lausanne in Switzerland.

In the second study, the mice which had NCoR1 removed from their muscle cells were able to run 1,600 metres in two hours, versus the 800 metres run in the same time by untreated mice. 'Effectively, the mice go further, faster, on the same amount of gas', remarked Professor Auwerx.

The research may help to develop new methods of preventing or treating diabetes; it could also help to slow the degeneration of muscles in the elderly. 'In addition, we think that this could be used as a basis for developing a treatment for genetic muscular dystrophy', said Professor Auwerx.

NCoR1 normally has a role in controlling and limiting muscle growth. Without the protein, mitochondria – the energy-generating 'batteries' that power cells – can work for long periods at full speed.

Although it appears that the protein limits physical performance, Professor Auwerx cautioned against people attempting to use the discovery to improve their own physical capabilities. He told New Scientist: 'We only know what happens if it's knocked out either in fat or muscle, and it could have serious side effects on other organs'.

NCoR1 is also essential for fetal development, although its specific function has not been identified.


13 January 2014 - by Dr Shanya Sivakumaran 
Scientists have identified mutations in two genes that cause neonatal diabetes, a rare condition affecting around 1 in 100,000 births...
06 January 2014 - by Dr Charlotte Warren-Gash 
A gene variant increases the risk of type 2 diabetes in Latin American populations, according to a study in Nature...
20 August 2012 - by Dr Zara Mahmoud 
A large-scale statistical analysis of DNA from nearly 150,000 people of European descent has identified ten new regions of DNA that may help us understand the biological processes linked to glucose metabolism and insulin production in type 2 diabetes....
09 January 2012 - by Dr Marianne Kennedy 
Biotech company Osiris Therapeutics has this month released an optimistic update on its Phase II trial evaluating the use of adult stem cells for the treatment of type 1 diabetes, despite lacking positive results...

20 June 2011 - by Dr Rebecca Hill 
Scientists have discovered a way to bypass the type of mutation that causes about a third of human genetic diseases. Experiments in yeast have shown how chemical modifications can allow a cell's machinery to ignore mistakes in DNA known as nonsense mutations...
08 March 2010 - by Ruth Pidsley 
A team of researchers based at Ohio State University, USA, have used gene therapy to restore nerve and muscle function and prolong life in mice with a form of spinal muscular atrophy (SMA), a lethal childhood muscle-wasting disorder. Results from the study, published in the journal Nature Biotechnology, were so encouraging that the researchers hope to progress to human trials within two years...
01 June 2009 - by Dr Will Fletcher 
Transgenic mice containing a human speech gene could give clues about the evolution of language. A team from the Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany, replaced the mouse gene FOXP2 with the human equivalent - a gene implicated in speech problems, and thought to be linked...

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