SI
SI
discoversearch

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor.  We ask that you disable ad blocking while on Silicon Investor in the best interests of our community.  If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.
Biotech / Medical : Ligand (LGND) Breakout!
LGND 203.18-1.4%Nov 28 9:30 AM EST

 Public ReplyPrvt ReplyMark as Last ReadFilePrevious 10Next 10PreviousNext  
To: David L. Hachey who wrote (15886)2/26/1998 8:52:00 AM
From: Henry Niman  Read Replies (1) of 32384
 
Here's what Reuters had to say:

Wednesday February 25 6:15 PM EST

Gene Linked To Type 2 Diabetes

NEW YORK (Reuters) -- Researchers reporting in the current issue of the journal Nature say they
may have discovered a gene that plays a role in the development of adult-onset, type 2 diabetes.

"Functional abnormalities in (the) IRS-2 (gene) could be involved in the pathogenesis of this human
disease," according to researchers at the Howard Hughes Medical Institute at Harvard Medical
School, in Boston, Massachusetts.

Problems with both the secretion and action of insulin are markers of type 2 diabetes mellitus, the
form of the disease which occurs in adults and accounts for 95% of all cases of diabetes. But
scientists have so far been unable to pinpoint an underlying mechanism responsible for both of these
types of insulin-related malfunction.

Research into the IRS-2 gene may help solve that puzzle. The Boston scientists say the gene is linked
to the function of insulin receptor substrates (IRS), specific proteins which help regulate the cell's
ability to produce and respond to insulin and other diabetes-related compounds.

The researchers bred a strain of mice lacking the IRS-2 gene, and compared the medical history of
those mice with that of normal mice.

None of the mice exhibited diabetic symptoms in the first few weeks after birth. However, the study
authors say the gene-deficient mice developed high blood sugar levels by 3 to 6 weeks of age, "and
at 6 to 8 weeks of age these mice exhibited marked glucose (blood sugar) intolerance...." By 10
weeks, they say the gene-deficient mice were "overtly diabetic," displaying marked abnormalities in
both insulin secretion and insulin action.

The investigators note that "this combination of features is a hallmark of human type 2 diabetes."
They say the exact mechanisms involved in this gene-related breakdown of insulin function remains
unknown, and requires further study. SOURCE: Nature (1998;391:900-904)
Report TOU ViolationShare This Post
 Public ReplyPrvt ReplyMark as Last ReadFilePrevious 10Next 10PreviousNext