"Kurt" <kurtwheeling1965@hotmail.com> wrote in message
news:1171425829.254463.103980@a34g2000cwb.googlegr oups.com...
> http://diabetes.org/diabetesnewsarti...althewEDIT.xml
>
> or
>
> http://tinyurl.com/22rq96
>
> WASHINGTON (Reuters) - Researchers said on Sunday they had homed in on
> five areas of DNA that could account for 70 percent of the genetic
> risk for type 2 diabetes.
<snip>
Hi Kurt,
here is the news release :
http://www3.imperial.ac.uk/newsandev...13?newsid=5233
Imperial College London News Release
Under strict embargo for 18.00 London time / 13.00 US Eastern time Sunday 11
February 2007
The most important genes associated with a risk of developing type-2
diabetes have been identified, scientists report today in a new study. The
research, published online in Nature, is the first time the genetic makeup
of any disease has been mapped in such detail. It should enable scientists
to develop a genetic test to show an individual their likelihood of
developing diabetes mellitus type 2, commonly known as type-2 diabetes. The
researchers identified four loci, or points on individuals' genetic maps,
which corresponded to a risk of developing the disorder. The scientists,
from Imperial College London, McGill University, Canada, and other
international institutions, believe their findings explain up to 70% of the
genetic background of type-2 diabetes. In addition, one of the genetic
mutations which they detected might further explain the causes behind type-2
diabetes, potentially leading to new treatments. The research revealed that
people with type-2 diabetes have a mutation in a particular zinc transporter
known as SLC30A8, which is involved in regulating
insulin secretion. Type-2
diabetes is associated with a deficiency in insulin and the researchers
believe it may be possible to treat it by fixing this transporter.
Here is the abstract from the original publication :
Nature Advance online publication 11 Februari 2007
A genome-wide association study identifies novel risk loci for type 2
diabetes
Type 2 diabetes mellitus results from the interaction of environmental
factors with a combination of genetic variants, most of which were hitherto
unknown. A systematic search for these variants was recently made possible
by the development of high-density arrays that permit the genotyping of
hundreds of thousands of polymorphisms. We tested 392,935 single-nucleotide
polymorphisms in a French case-control cohort. Markers with the most
significant difference in genotype frequencies between cases of type 2
diabetes and controls were fast-tracked for testing in a second cohort. This
identified four loci containing variants that confer type 2 diabetes risk,
in addition to confirming the known association with the TCF7L2 gene. These
loci include a non-synonymous polymorphism in the zinc transporter SLC30A8,
which is expressed exclusively in insulin-producing b-cells, and two linkage
disequilibrium blocks that contain genes potentially involved in b-cell
development or function (IDE-KIF11-HHEX and EXT2-ALX4). These associations
explain a substantial portion of disease risk and constitute proof of
principle for the genome-wide approach to the elucidation of complex genetic
traits.
hth
Gys