[acb-diabetics] gen from parent can determine if you are susject to type 2

[Patricia LaFrance-Wolf]

20 December, 2009

 and appeared in  

Issue 501

Diabetes Risk Depends on Which Parent a DNA Variant Is Inherited From

Icelandic biologists have discovered that the genetic risk of several common
diseases, like Type 2 diabetes and cancer, can depend on which parent a DNA

variant is inherited from.    

The finding may help explain part of a serious gap in understanding the
genetics of common diseases. Using an extensive genealogy that includes
almost all

the present population of Iceland and many in previous generations, the
Reykjavik company DeCode Genetics managed to distinguish which chromosomes
came

from the father and which from the mother in some 40,000 people. 

The company then ran standard tests, known as genome wide association
studies, the tool that scientists have hoped would track down the roots of
common

diseases and fulfill the promise of the Human Genome Project. 

But with most of these common diseases, the tests have so far identified
genetic variants that account for only a small percentage of the risk. This
is

in contrast to simple diseases, most of them rare, where a single gene is
the cause and the disease has a clear family pedigree.  

The failure has left biologists puzzled about the missing heritability,
which some have jokingly attributed to "dark matter" within the human
genome, an

analogy with the dark matter invoked by cosmologists to explain the missing
mass of the universe. 

Some experts believe the missing risk might be carried in a large number of
rare DNA variants not included in current scans of patients' genomes.
Because

it costs too much to decode all three billion units of DNA in a patient's
genome, biologists use chips that scan just the 500,000 sites where
variation

is most common. These sites were expected to explain the genetic component
of common diseases like cancer or schizophrenia, but mostly do not do so. 

Another explanation is that the missing heritability lies in aspects of cell
biology that are not yet understood.  

DeCode scientists have found one such instance. They report in Friday's 

Nature

 that a DNA variant increases a person's risk of Type 2 diabetes by 30
percent if inherited from the father, but reduces the risk by 10 percent if
it comes

from the mother.  

Because the two effects tend to cancel each other out, they have not been
picked up by the standard tests that do not identify the parental origin of
each

section of DNA. 

DeCode found that five of seven variants tested made different contributions
to disease depending on the parent of origin. In most cases the effect was

of differing degrees of severity, depending on the parent involved. 

To increase the chances of seeing such an effect the researchers tested
known disease-associated variants that lay close to so-called imprinted
genes, ones

where the copy from one parent is suppressed. They now plan to survey the
rest of the genome. 

Kari Stefansson, DeCode's chief executive, said he could not predict how
large a percentage of the missing heritability the parent-of-origin effect
might

account for. "But I think it's going to be substantial," he said. 

Dr. Stefansson said that its access to the Icelandic genealogical database
would give it an advantage in searching for disease genes in circumstances
where

it is essential to know the genetic structure of a population. 

Mark Daly, a medical geneticist at Massachusetts General Hospital, said that
DeCode's result was "a significant finding" and that it confirmed the idea

that effects of this nature would account for some of the missing
heritability.  

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This article originally posted 20 December, 2009 and appeared in  

Issue 501

 

Diabetes Risk Depends on Which Parent a DNA Variant Is Inherited From

Icelandic biologists have discovered that the genetic risk of several common
diseases, like Type 2 diabetes and cancer, can depend on which parent a DNA

variant is inherited from.    

 

The finding may help explain part of a serious gap in understanding the
genetics of common diseases. Using an extensive genealogy that includes
almost all

the present population of Iceland and many in previous generations, the
Reykjavik company DeCode Genetics managed to distinguish which chromosomes
came

from the father and which from the mother in some 40,000 people. 

 

The company then ran standard tests, known as genome wide association
studies, the tool that scientists have hoped would track down the roots of
common

diseases and fulfill the promise of the Human Genome Project. 

 

But with most of these common diseases, the tests have so far identified
genetic variants that account for only a small percentage of the risk. This
is

in contrast to simple diseases, most of them rare, where a single gene is
the cause and the disease has a clear family pedigree.  

 

The failure has left biologists puzzled about the missing heritability,
which some have jokingly attributed to "dark matter" within the human
genome, an

analogy with the dark matter invoked by cosmologists to explain the missing
mass of the universe. 

 

Some experts believe the missing risk might be carried in a large number of
rare DNA variants not included in current scans of patients' genomes.
Because

it costs too much to decode all three billion units of DNA in a patient's
genome, biologists use chips that scan just the 500,000 sites where
variation

is most common. These sites were expected to explain the genetic component
of common diseases like cancer or schizophrenia, but mostly do not do so. 

 

Another explanation is that the missing heritability lies in aspects of cell
biology that are not yet understood.  

 

DeCode scientists have found one such instance. They report in Friday's
Nature that a DNA variant increases a person's risk of Type 2 diabetes by 30
percent

if inherited from the father, but reduces the risk by 10 percent if it comes
from the mother.  

 

Because the two effects tend to cancel each other out, they have not been
picked up by the standard tests that do not identify the parental origin of
each

section of DNA. 

 

DeCode found that five of seven variants tested made different contributions
to disease depending on the parent of origin. In most cases the effect was

of differing degrees of severity, depending on the parent involved. 

 

To increase the chances of seeing such an effect the researchers tested
known disease-associated variants that lay close to so-called imprinted
genes, ones

where the copy from one parent is suppressed. They now plan to survey the
rest of the genome. 

 

Kari Stefansson, DeCode's chief executive, said he could not predict how
large a percentage of the missing heritability the parent-of-origin effect
might

account for. "But I think it's going to be substantial," he said. 

 

Dr. Stefansson said that its access to the Icelandic genealogical database
would give it an advantage in searching for disease genes in circumstances
where

it is essential to know the genetic structure of a population. 

 

Mark Daly, a medical geneticist at Massachusetts General Hospital, said that
DeCode's result was "a significant finding" and that it confirmed the idea

that effects of this nature would account for some of the missing
heritability

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