Cause of insulin resistance in diabetics found

Last Updated: Monday, September 7, 2009 - 00:00

London: An international team of researchers have discovered a new gene that appears to affect how insulin works.

The new discovery could lead to better treatment of type 2 diabetes, and provide deeper insight into how this widespread disease develops.



The novel gene, called Insulin Receptor Substrate 1 (IRS1), affects how the body responds to insulin already in the bloodstream.




"Most of the genes that we``ve identified as diabetes risk genes to date reduce the function of the pancreas, specifically of beta cells in the pancreas that make insulin," Nature quoted Dr. Robert Sladek, of McGill University and the Genome Quebec Innovation Centre in Montreal, a corresponding author of the paper, as saying.




"IRS1 has to do with the function of the other tissues in the body. Rather than reduce production of insulin, this gene reduces the effect of insulin in muscles, liver and fat, a process called insulin resistance," he added.



The researchers analysed genetic material drawn from more than 6,000 French participants.



In addition to identifying the new gene, they have also found the genetic trigger, which leads to malfunction, in a totally unexpected place.



"It``s a single-nucleotide polymorphism (SNP, pronounced ``snip``), a single letter change in your DNA," said Sladek.




"What``s interesting about this particular SNP is that it``s not linked genetically to the IRS1 gene in any way; it``s about half-a-million base-pairs away, in the middle of a genetic desert with no known genes nearby.




“It causes a 40-per-cent reduction in the IRS1 gene, and even more important, a 40-per-cent reduction in its activity. Which means that even if insulin is present, it won``t work," he added.



Sladek says that it is possible that in diabetic patients, the signal to turn this gene on and off might be impaired.




The study has been published in Nature Genetics.

(ANI)



First Published: Monday, September 7, 2009 - 00:00

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