gene found that causes insulin resistance
- From: Big_I <autoclaveman2000@xxxxxxxxx>
- Date: Wed, 16 Sep 2009 19:54:08 -0700 (PDT)
Diabetes Advance: Researchers Find Gene That Causes Resistance to
Insulin
16-Sep-2009
September 2009 - A breakthrough by an international team of
researchers in Canada, France, the UK and Denmark has uncovered a new
gene that could lead to better treatment of type 2 diabetes, as well
as a better understanding of how this widespread disease develops.
Unlike most of the genes that have been shown to cause diabetes, the
new gene, called Insulin Receptor Substrate 1 (IRS1), doesn't affect
how insulin is created in the pancreas, but rather, how the body
responds to insulin already in the bloodstream, say the researchers,
whose work will be published in Nature Genetics Sept. 6.
"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," explained Dr. Robert Sladek of
McGill University and the Génome Québec Innovation Centre in Montreal,
a corresponding author of the paper.
"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."
Insulin, a hormone produced in the pancreas, enables the body's cells
to absorb glucose from food and turn it into energy. Different types
of diabetes are caused by the body's inability to produce sufficient
insulin, inability to use its own insulin properly, or a combination
of both factors.
"IRS1 is the first inside the cell that gets activated by insulin,"
Sladek continued. "It basically tells the rest of the cell, 'hey,
insulin is here, start taking in glucose from the blood!' If IRS1
doesn't work, the whole process is disrupted."
The research was conducted by an international team including Sladek,
Dr. Constantin Polychronakos of McGill's Faculty of Medicine; Dr.
Philippe Froguel of the CNRS and Lille 2 University in France and
Imperial College London; Dr. Oluf Pedersen of the University of
Copenhagen and Aarhus University in Denmark and their colleagues at
many institutions across Europe and North America.
This study, which used genetic material drawn from more than 6,000
French participants divided into two separate groups, represents the
final step in a series of collaborations between these researchers
that has redrawn our understanding of diabetes genetics. In this
instance, not only did the researchers pinpoint a new diabetes-linked
gene, they 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.
In genetic terms, it's halfway from Montreal to Halifax. And yet we
can see that 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."
"We would like to congratulate Rob Sladek and his group for this
breakthrough discovery. His work on the genetic basis of type 2
diabetes will certainly have an impact in the way clinicians diagnose
and treat diabetes patients and is paving the way for translational
research and personalized medicine," said Catalina Lopez-Correa, Vice-
president of Scientific Affairs at Genome Québec.
She added, "This discovery once again confirms the scientific
excellence and talent of Quebec's scientists and the key role that
genomics is playing in the study and treatment of complex diseases."
Sladek hopes this discovery may lead to new therapeutic lines of
attack in the future.
"It's possible that in diabetic patients, the signal to turn this gene
on and off might be impaired. But we might be able to use one of the
other pathways to turn it on," he said.
Source: McGill University
.
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