s******9
发帖数: 283 | 1 http://www.cell.com/abstract/S0092-8674%2813%2900449-2
Researchers at the Harvard Stem Cell Institute (HSCI) have discovered a
hormone that holds promise for a dramatically more effective treatment of
type 2 diabetes, a metabolic illness afflicting an estimated 26 million
Americans. The researchers believe that the hormone might also have a role
in treating type 1, or juvenile, diabetes.
The work was published today by the journal Cell as an early online release.
It is scheduled for the May 9 print edition of the journal.
The hormone, called betatrophin, causes mice to produce insulin-secreting
pancreatic beta cells at up to 30 times the normal rate. The new beta cells
only produce insulin when called for by the body, offering the potential for
the natural regulation of insulin and a great reduction in the
complications associated with diabetes, the leading medical cause of
amputations and non-genetic loss of vision.
The researchers who discovered betatrophin, HSCI co-director Doug Melton and
postdoctoral fellow Peng Yi, caution that much work remains to be done
before it could be used as a treatment in humans. But the results of their
work, which was supported in large part by a federal research grant, already
have attracted the attention of drug manufacturers.
“If this could be used in people,” said Melton, Harvard’s Xander
University Professor and co-chair of the University’s Department of Stem
Cell and Regenerative Biology, “it could eventually mean that instead of
taking insulin injections three times a day, you might take an injection of
this hormone once a week or once a month, or in the best case maybe even
once a year.”
Type 2 diabetes, a disease associated with the national obesity epidemic, is
usually caused by a combination of excess weight and lack of exercise. It
causes patients to slowly lose beta cells and the ability to produce
adequate insulin. One recent study has estimated that diabetes treatment and
complications cost the United States $218 billion annually, or about 10
percent of the nation’s entire health bill.
“Our idea here is relatively simple,” Melton said. “We would provide this
hormone, the type 2 diabetic will make more of their own insulin-producing
cells, and this will slow down, if not stop, the progression of their
diabetes. I’ve never seen any treatment that causes such an enormous leap
in beta cell replication.”
Though Melton sees betatrophin primarily as a treatment for type 2 diabetes,
he believes it might play a role in the treatment of type 1 diabetes as
well, perhaps boosting the number of beta cells and slowing the progression
of that autoimmune disease when it’s first diagnosed.
“We’ve done the work in mice,” Melton said, “but of course we’re not
interested in curing mice of diabetes, and we now know the gene is a human
gene. We’ve cloned the human gene and, moreover, we know that the hormone
exists in human plasma; betatrophin definitely exists in humans.”
While Melton was clear about the need for more research before the hormone
could be available as a drug, he also said that betatrophin could be in
human clinical trials within three to five years, an extremely short time in
the normal course of drug discovery and development.
Working with Harvard’s Office of Technology Development, Melton and Yi
already have a collaborative agreement with Evotec, a German biotech firm
that now has 15 scientists working on betatrophin, and the compound has been
licensed to Janssen Pharmaceuticals, a Johnson & Johnson company that now,
too, has scientists working to move betatrophin toward the clinic.
But were it not for the federal funding of basic science research, there
would be no betatrophin. A Melton proposal titled “Searching for Genes and
Compounds That Cause Beta Cell Replication” impressed National Institutes
of Health grant reviewers, and received federal funding for 80 percent of
the work leading to the discovery of betatrophin.
“At a time of great uncertainty for federal research funding, the discovery
of betatrophin is a reminder of the importance of basic research,” said
Harvard Provost Alan Garber. “Were it not for a National Institutes for
Health grant, this promising new approach to treating diabetes might never
have come to light.”
As is often the case in basic science research, serendipity played a role in
the discovery of betatrophin, which Melton and Yi originally called Rabbit
because they discovered it during the Chinese Year of the Rabbit, and
because it makes beta cells multiply so quickly.
For more than 15 years the major focus of Melton’s work has been not type 2
diabetes but the less common type 1, or juvenile diabetes, which he began
focusing on when his son was diagnosed with it as an infant. (The disease
later was also diagnosed in his daughter.) Additionally, most of Melton’s
work has involved using stem cells, the fundamental building blocks of all
human organs, as disease treatments and targets for drug discoveries. But
stem cells played no direct role in the discovery of betatrophin. It was,
rather, a classic example of scientists with sufficient resources asking
questions, and pursuing answers, that fell outside the usual scope of their
laboratories and institutes.
“I would like to tell you this discovery came from deep thinking and we
knew we would find this, but it was more a bit of luck,” explained Melton,
who in addition to his roles at Harvard is a Howard Hughes Medical Institute
investigator. “We were just wondering what happens when an animal doesn’t
have enough insulin. We were lucky to find this new gene that had largely
gone unnoticed before.
“Another hint came from studying something that people know about but don’
t think much about, which is: What happens during pregnancy?” he said, “
When a woman gets pregnant, her carbohydrate load, her call for insulin, can
increase an enormous amount because of the weight and nutrition needs of
the fetus. During pregnancy, there are more beta cells needed, and it turns
out that this hormone goes up during pregnancy. We looked in pregnant mice
and found that when the animal becomes pregnant this hormone is turned on to
make more beta cells.”
Melton and Yi have been working on the project for more than four years. But
the big breakthrough came on Feb. 10, 2011. “I was just sitting there at
the microscope looking at all these replicating beta cells,” said Yi, and
he could barely believe his eyes. He said he never had “seen this kind of
dramatic replication.”
At first unsure whether to repeat the experiment or to tell Melton right
away, Peng said he rushed into Melton’s office, printed out the image he
was seeing, and showed it to Melton, telling him they probably had a
breakthrough. “I showed him this picture and told him this is a secreted
protein, and he was really, really excited about this result.”
“I remember this very well,” Melton recalled. “It’s a black-and-white
picture where you’re looking at a section, like a section through a sausage
, of the whole pancreas. When you normally look at a black-and-white
picture of that, it’s very hard to tell where the beta cells are, the
insulin cells.
“But in this test,” he continued, “any cell that was dividing would shine
up bright and white, like a sparkle. He showed me this picture where the
whole pancreas is largely black, but then there were these clusters, like
stars of these white dots, which turned out to be all over the islets, the
place where the beta cell sits. I still keep that black-and-white picture.
We have much fancier color ones, but I like the black-and-white picture,
because it’s one of those moments when you know something interesting has
happened. This is not by accident. I’ve never seen any treatment that
causes such an enormous leap … in beta cell replication.”
The following morning, when Yi sat down at his lab bench, there was a formal
-looking, cream-colored envelope lying on the brown surface of the bench. He
opened it up, and took from the envelope a handwritten note from Melton. It
read:
“Dear Peng, I can hardly sleep — I am so excited by your result. It’s a
tribute to your hard work and hard thinking. Can’t wait to see the data
from the repeat. Doug.” | a****k
发帖数: 1130 | 2 顶~ :)
release.
cells
【在 s******9 的大作中提到】
: http://www.cell.com/abstract/S0092-8674%2813%2900449-2
: Researchers at the Harvard Stem Cell Institute (HSCI) have discovered a
: hormone that holds promise for a dramatically more effective treatment of
: type 2 diabetes, a metabolic illness afflicting an estimated 26 million
: Americans. The researchers believe that the hormone might also have a role
: in treating type 1, or juvenile, diabetes.
: The work was published today by the journal Cell as an early online release.
: It is scheduled for the May 9 print edition of the journal.
: The hormone, called betatrophin, causes mice to produce insulin-secreting
: pancreatic beta cells at up to 30 times the normal rate. The new beta cells
| w***a
发帖数: 4361 | 3 这个很cool呀，CNS上为数不多的马上就有希望上临床试验的study
一共就三个作者，一作还是中国WSN，很赞。
release.
cells
【在 s******9 的大作中提到】
: http://www.cell.com/abstract/S0092-8674%2813%2900449-2
: Researchers at the Harvard Stem Cell Institute (HSCI) have discovered a
: hormone that holds promise for a dramatically more effective treatment of
: type 2 diabetes, a metabolic illness afflicting an estimated 26 million
: Americans. The researchers believe that the hormone might also have a role
: in treating type 1, or juvenile, diabetes.
: The work was published today by the journal Cell as an early online release.
: It is scheduled for the May 9 print edition of the journal.
: The hormone, called betatrophin, causes mice to produce insulin-secreting
: pancreatic beta cells at up to 30 times the normal rate. The new beta cells
| g*****n
发帖数: 250 | 4 用这个治疗糖尿病？太扯了吧。那激素刺激beta细胞分裂，可糖尿病不是细胞分裂的问
题。一型糖尿病是细胞死亡. 你增加多少还不都得死。二型糖尿病是因为胰岛素不能被
利用，导致细胞过度劳累。这些问题不解决，细胞增加多少还不得死多少。 | s********e
发帖数: 1596 | 5 就是起延缓的作用吧。如果真是一针管半年一年的话大概还是有市场的：）
【在 g*****n 的大作中提到】
: 用这个治疗糖尿病？太扯了吧。那激素刺激beta细胞分裂，可糖尿病不是细胞分裂的问
: 题。一型糖尿病是细胞死亡. 你增加多少还不都得死。二型糖尿病是因为胰岛素不能被
: 利用，导致细胞过度劳累。这些问题不解决，细胞增加多少还不得死多少。
| w***a
发帖数: 4361 | 6 太扯了？
对于糖尿病这种每年400多个billion dollar的market，
任何哪怕一点点的进步，都是巨大的商业利益。
压根就不可能有药到病除的玩意儿。
【在 g*****n 的大作中提到】
: 用这个治疗糖尿病？太扯了吧。那激素刺激beta细胞分裂，可糖尿病不是细胞分裂的问
: 题。一型糖尿病是细胞死亡. 你增加多少还不都得死。二型糖尿病是因为胰岛素不能被
: 利用，导致细胞过度劳累。这些问题不解决，细胞增加多少还不得死多少。
| b******y
发帖数: 627 | | s******9
发帖数: 283 | 8 http://www.cell.com/abstract/S0092-8674%2813%2900449-2
Researchers at the Harvard Stem Cell Institute (HSCI) have discovered a
hormone that holds promise for a dramatically more effective treatment of
type 2 diabetes, a metabolic illness afflicting an estimated 26 million
Americans. The researchers believe that the hormone might also have a role
in treating type 1, or juvenile, diabetes.
The work was published today by the journal Cell as an early online release.
It is scheduled for the May 9 print edition of the journal.
The hormone, called betatrophin, causes mice to produce insulin-secreting
pancreatic beta cells at up to 30 times the normal rate. The new beta cells
only produce insulin when called for by the body, offering the potential for
the natural regulation of insulin and a great reduction in the
complications associated with diabetes, the leading medical cause of
amputations and non-genetic loss of vision.
The researchers who discovered betatrophin, HSCI co-director Doug Melton and
postdoctoral fellow Peng Yi, caution that much work remains to be done
before it could be used as a treatment in humans. But the results of their
work, which was supported in large part by a federal research grant, already
have attracted the attention of drug manufacturers.
“If this could be used in people,” said Melton, Harvard’s Xander
University Professor and co-chair of the University’s Department of Stem
Cell and Regenerative Biology, “it could eventually mean that instead of
taking insulin injections three times a day, you might take an injection of
this hormone once a week or once a month, or in the best case maybe even
once a year.”
Type 2 diabetes, a disease associated with the national obesity epidemic, is
usually caused by a combination of excess weight and lack of exercise. It
causes patients to slowly lose beta cells and the ability to produce
adequate insulin. One recent study has estimated that diabetes treatment and
complications cost the United States $218 billion annually, or about 10
percent of the nation’s entire health bill.
“Our idea here is relatively simple,” Melton said. “We would provide this
hormone, the type 2 diabetic will make more of their own insulin-producing
cells, and this will slow down, if not stop, the progression of their
diabetes. I’ve never seen any treatment that causes such an enormous leap
in beta cell replication.”
Though Melton sees betatrophin primarily as a treatment for type 2 diabetes,
he believes it might play a role in the treatment of type 1 diabetes as
well, perhaps boosting the number of beta cells and slowing the progression
of that autoimmune disease when it’s first diagnosed.
“We’ve done the work in mice,” Melton said, “but of course we’re not
interested in curing mice of diabetes, and we now know the gene is a human
gene. We’ve cloned the human gene and, moreover, we know that the hormone
exists in human plasma; betatrophin definitely exists in humans.”
While Melton was clear about the need for more research before the hormone
could be available as a drug, he also said that betatrophin could be in
human clinical trials within three to five years, an extremely short time in
the normal course of drug discovery and development.
Working with Harvard’s Office of Technology Development, Melton and Yi
already have a collaborative agreement with Evotec, a German biotech firm
that now has 15 scientists working on betatrophin, and the compound has been
licensed to Janssen Pharmaceuticals, a Johnson & Johnson company that now,
too, has scientists working to move betatrophin toward the clinic.
But were it not for the federal funding of basic science research, there
would be no betatrophin. A Melton proposal titled “Searching for Genes and
Compounds That Cause Beta Cell Replication” impressed National Institutes
of Health grant reviewers, and received federal funding for 80 percent of
the work leading to the discovery of betatrophin.
“At a time of great uncertainty for federal research funding, the discovery
of betatrophin is a reminder of the importance of basic research,” said
Harvard Provost Alan Garber. “Were it not for a National Institutes for
Health grant, this promising new approach to treating diabetes might never
have come to light.”
As is often the case in basic science research, serendipity played a role in
the discovery of betatrophin, which Melton and Yi originally called Rabbit
because they discovered it during the Chinese Year of the Rabbit, and
because it makes beta cells multiply so quickly.
For more than 15 years the major focus of Melton’s work has been not type 2
diabetes but the less common type 1, or juvenile diabetes, which he began
focusing on when his son was diagnosed with it as an infant. (The disease
later was also diagnosed in his daughter.) Additionally, most of Melton’s
work has involved using stem cells, the fundamental building blocks of all
human organs, as disease treatments and targets for drug discoveries. But
stem cells played no direct role in the discovery of betatrophin. It was,
rather, a classic example of scientists with sufficient resources asking
questions, and pursuing answers, that fell outside the usual scope of their
laboratories and institutes.
“I would like to tell you this discovery came from deep thinking and we
knew we would find this, but it was more a bit of luck,” explained Melton,
who in addition to his roles at Harvard is a Howard Hughes Medical Institute
investigator. “We were just wondering what happens when an animal doesn’t
have enough insulin. We were lucky to find this new gene that had largely
gone unnoticed before.
“Another hint came from studying something that people know about but don’
t think much about, which is: What happens during pregnancy?” he said, “
When a woman gets pregnant, her carbohydrate load, her call for insulin, can
increase an enormous amount because of the weight and nutrition needs of
the fetus. During pregnancy, there are more beta cells needed, and it turns
out that this hormone goes up during pregnancy. We looked in pregnant mice
and found that when the animal becomes pregnant this hormone is turned on to
make more beta cells.”
Melton and Yi have been working on the project for more than four years. But
the big breakthrough came on Feb. 10, 2011. “I was just sitting there at
the microscope looking at all these replicating beta cells,” said Yi, and
he could barely believe his eyes. He said he never had “seen this kind of
dramatic replication.”
At first unsure whether to repeat the experiment or to tell Melton right
away, Peng said he rushed into Melton’s office, printed out the image he
was seeing, and showed it to Melton, telling him they probably had a
breakthrough. “I showed him this picture and told him this is a secreted
protein, and he was really, really excited about this result.”
“I remember this very well,” Melton recalled. “It’s a black-and-white
picture where you’re looking at a section, like a section through a sausage
, of the whole pancreas. When you normally look at a black-and-white
picture of that, it’s very hard to tell where the beta cells are, the
insulin cells.
“But in this test,” he continued, “any cell that was dividing would shine
up bright and white, like a sparkle. He showed me this picture where the
whole pancreas is largely black, but then there were these clusters, like
stars of these white dots, which turned out to be all over the islets, the
place where the beta cell sits. I still keep that black-and-white picture.
We have much fancier color ones, but I like the black-and-white picture,
because it’s one of those moments when you know something interesting has
happened. This is not by accident. I’ve never seen any treatment that
causes such an enormous leap … in beta cell replication.”
The following morning, when Yi sat down at his lab bench, there was a formal
-looking, cream-colored envelope lying on the brown surface of the bench. He
opened it up, and took from the envelope a handwritten note from Melton. It
read:
“Dear Peng, I can hardly sleep — I am so excited by your result. It’s a
tribute to your hard work and hard thinking. Can’t wait to see the data
from the repeat. Doug.” | a****k
发帖数: 1130 | 9 顶~ :)
release.
cells
【在 s******9 的大作中提到】
: http://www.cell.com/abstract/S0092-8674%2813%2900449-2
: Researchers at the Harvard Stem Cell Institute (HSCI) have discovered a
: hormone that holds promise for a dramatically more effective treatment of
: type 2 diabetes, a metabolic illness afflicting an estimated 26 million
: Americans. The researchers believe that the hormone might also have a role
: in treating type 1, or juvenile, diabetes.
: The work was published today by the journal Cell as an early online release.
: It is scheduled for the May 9 print edition of the journal.
: The hormone, called betatrophin, causes mice to produce insulin-secreting
: pancreatic beta cells at up to 30 times the normal rate. The new beta cells
| w***a
发帖数: 4361 | 10 这个很cool呀，CNS上为数不多的马上就有希望上临床试验的study
一共就三个作者，一作还是中国WSN，很赞。
release.
cells
【在 s******9 的大作中提到】
: http://www.cell.com/abstract/S0092-8674%2813%2900449-2
: Researchers at the Harvard Stem Cell Institute (HSCI) have discovered a
: hormone that holds promise for a dramatically more effective treatment of
: type 2 diabetes, a metabolic illness afflicting an estimated 26 million
: Americans. The researchers believe that the hormone might also have a role
: in treating type 1, or juvenile, diabetes.
: The work was published today by the journal Cell as an early online release.
: It is scheduled for the May 9 print edition of the journal.
: The hormone, called betatrophin, causes mice to produce insulin-secreting
: pancreatic beta cells at up to 30 times the normal rate. The new beta cells
| | | g*****n
发帖数: 250 | 11 用这个治疗糖尿病？太扯了吧。那激素刺激beta细胞分裂，可糖尿病不是细胞分裂的问
题。一型糖尿病是细胞死亡. 你增加多少还不都得死。二型糖尿病是因为胰岛素不能被
利用，导致细胞过度劳累。这些问题不解决，细胞增加多少还不得死多少。 | s********e
发帖数: 1596 | 12 就是起延缓的作用吧。如果真是一针管半年一年的话大概还是有市场的：）
【在 g*****n 的大作中提到】
: 用这个治疗糖尿病？太扯了吧。那激素刺激beta细胞分裂，可糖尿病不是细胞分裂的问
: 题。一型糖尿病是细胞死亡. 你增加多少还不都得死。二型糖尿病是因为胰岛素不能被
: 利用，导致细胞过度劳累。这些问题不解决，细胞增加多少还不得死多少。
| w***a
发帖数: 4361 | 13 太扯了？
对于糖尿病这种每年400多个billion dollar的market，
任何哪怕一点点的进步，都是巨大的商业利益。
压根就不可能有药到病除的玩意儿。
【在 g*****n 的大作中提到】
: 用这个治疗糖尿病？太扯了吧。那激素刺激beta细胞分裂，可糖尿病不是细胞分裂的问
: 题。一型糖尿病是细胞死亡. 你增加多少还不都得死。二型糖尿病是因为胰岛素不能被
: 利用，导致细胞过度劳累。这些问题不解决，细胞增加多少还不得死多少。
| b******y
发帖数: 627 | | a******u
发帖数: 211 | |
|
