人产胰岛素的beta细胞的复制就能够维持四周以上

核心提示:
据匹兹堡大学医学院的研究人员报道,在小鼠糖尿病模型上,只需要一个刺激分子,人产胰岛素的beta细胞的复制就能够维持四周以

据匹兹堡大学医学院的研究人员报道,在小鼠糖尿病模型上,只需要一个刺激分子,人产胰岛素的beta细胞的复制就能够维持四周以上。

他们也发现几种分子的混合物也能使人的beta细胞复制,这也是人beta细胞核小鼠beta细胞之间的重要区别。这一结果可能被用于治疗糖尿病。

研究者之一医学博士Andrew
F.Stewart介绍说:”我们的研究小组是最先证明成人beta细胞能够被诱导和大量增殖的,这在以前被认为是不可能的。现在我们的努力已经揭示了这些复杂调控过程中的一部分,这将是我们能够通过生产新的beta细胞来治疗或者治愈糖尿病。

通过一系列的实验,M.Fiashi-Taesch博士和研究小组发现了调节分子cdk4或cdk6的量是与D-细胞周期蛋白特别是细胞周期蛋白D-3的同时增加,刺激了试管中人类的beta细胞增殖。Fiaschi-Taesch
博士说:”我们之前没有想到D3细胞周期蛋白和cdk4或cdk6能够如此强烈地刺激beta细胞的复制。之前并不清楚对D3细胞周期蛋白在beta细胞生理中作用。

One molecule, many more insulin-producing cells to treat diabetes, says Pitt team

July 28, 2010

With a single stimulatory molecule, human insulin-producing beta cell
replication can be sustained for at least four weeks in a mouse model of
diabetes, according to researchers at the University of Pittsburgh
School of Medicine in Diabetes, a journal of the American Diabetes
Association.

They 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 authorAndrew F. Stewart, M.D.,
professor of medicine and chief of the Division of Endocrinology and
Metabolism, Pitt School of Medicine. “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.

Provided by University of Pittsburgh

关键词:糖尿病 beta细胞 细胞周期蛋白D3

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