[acb-diabetics] ionteresting article

[Patricia LaFrance-Wolf]

Click here to find out more! frame end

 

Researchers  also found several cocktails of molecules that drive human beta
cells to replicate, as well as important differences between mouse and human

beta cells that could influence how these approaches are best used to treat
diabetes, which is caused by insufficient insulin production leading to
abnormal

blood sugar levels. 

 

"Our team was the first to show that adult human beta cells can be induced
to proliferate or grow at substantial rates, which no one thought possible
before,"

said senior author Andrew F. Stewart, M.D., professor of medicine and chief
of the Division of Endocrinology and Metabolism, University of Pittsburgh
School

of Medicine, PA. "Now our effort has been to unravel these regulatory
pathways to find the most effective strategy that will allow us to treat -
and perhaps

cure - diabetes by making new insulin-producing cells." 

 

In a series of experiments, lead author Nathalie M. Fiaschi-Taesch, Ph.D.,
assistant professor of endocrinology, and the team discovered that combining

elevated amounts of the regulatory molecules cdk4 or cdk6 with a variety of
D-cyclin proteins, particularly cyclin D3, stimulates human beta cell
replication

in test tubes. 

 

"We didn't expect cyclin D3 to ramp up beta cell replication so strongly
when it was used with either cdk4 or cdk6," Dr. Fiaschi-Taesch said. "There
was

no known role for cyclin D3 in human beta cell physiology."

 

Cyclin D2 is present in and essential for rodent beta cell replication and
function, but the team showed that molecule is barely detectable in human
cells,

and beta cell replication could be sustained for at least four weeks in a
model in which mice were transplanted with human beta cells engineered to
overproduce

cdk6. Blood sugar normalized in the diabetic mice transplanted with
surprisingly small numbers of human beta cells, indicating that the cells
functioned

properly to produce needed insulin. 

 

Mice don't appear to make cdk6 naturally, but they do have cdk4 and cyclins
D1 and D2, so standard rodent studies of beta replication might have led
scientists

to pursue the wrong molecules in their quest to stimulate human beta cell
replication, Dr. Stewart noted. 

 

He and his colleagues continue to explore many other regulatory proteins
that could play a role in encouraging or thwarting beta cell replication.

 

Diabetes, July 2010

-------------- next part --------------
An HTML attachment was scrubbed...
URL: <http://www.acb.org/pipermail/acb-diabetics/attachments/20100808/a1149899/attachment.htm>