Gr8 work...
I am M.D. Pharmacology
, wrking as Asst. Prof pharma in pvt Medical college in jaipur.
I did my thesis on diabetic pts in hospital. Worked hard that time and now I am also consultant diabetologist doing PP..
Dr. Neelesh Arya
Pls visit my different posts in Pharmacology
Career forum and DocIndia.
Gr8 work...
I am M.D. <a href="http://www.rxpgonline.com/forum100.html">Pharmacology
</a>
, wrking as Asst. Prof pharma in pvt Medical college in jaipur.
I did my thesis on diabetic pts in hospital. Worked hard that time and now I am also consultant diabetologist doing PP..
Dr. Neelesh Arya
Pls visit my different posts in <a href="http://www.rxpgonline.com/forum100.html">Pharmacology
</a>
Career forum and DocIndia.
thankzzzz........even i'm doin a work on diabetes...so wht topic exactly did u focous on
Disclaimer "This research news has been taken from a reputed news website. It has not been modified or recreated in way, as to preserve the authenticity of it. No Copyright Infringement is intended. This information is posted here for read-only basis. No part of this news is to be reproduced elsewhere, unless due credit is given to the original source and author.
Stem Cell Therapy Controls Diabetes in Mice
By ANDREW POLLACK
Published: February 21, 2008
Scientists reported on Wednesday that they were able to control diabetes in mice by harnessing human embryonic stem cells. The work raised the prospect that the embryonic cells might one day be used to provide insulin-producing replacement cells to treat the disease in people.
The scientists, at the biotechnology company Novocell, turned the stem cells into cells that produced insulin in the mice. Those cells kept blood sugar in check after the mice’s own insulin-producing cells were destroyed.
“For those who say there is not much evidence that embryonic stem cells can cure diabetes, there you go,” said Dr. Camillo Ricordi, director of the Diabetes Research Institute at the University of Miami, who was not involved in the research.
Still, a small number of the mice developed tumors, and some experts said the cells might not be well-characterized enough for use in people. In any event, Novocell said it would be several years before any human tests could begin.
Doctors are already experimenting with transplants of insulin-producing islet cells from cadavers for patients with Type 1 diabetes, a disease that destroys a person’s own islet cells. In some cases, the transplant recipients have not needed daily injections of insulin, at least for a while.
But there are too few donors to provide cell replacement to more than a small percentage of diabetics. Embryonic stem cells, which can potentially be turned into any type of cell in the body, could be a source of islet cells.
Novocell, which is based in San Diego, reported in 2006 that its researchers had turned human embryonic stem cells into insulin-producing cells in culture dishes, something others have also reported doing. But Novocell’s cells did not vary insulin production in response to glucose, a crucial requirement for implantation.
In the latest work, published online Wednesday by Nature Biotechnology, the researchers got assistance from the mice themselves. Instead of implanting the insulin-producing cells into mice, they implanted precursor cells that were a step short of developing into insulin-producing cells.
The mice’s bodies apparently provided the proper signals to turn the implanted cells into functioning insulin-producing cells in about 90 days.
When the scientists used a toxin to destroy the mice’s own islet cells, the animals that had received the human cells continued to produce insulin and control their blood sugar while mice without the implants quickly became diabetic. After about 100 days, the scientists removed the implanted cells from the mice, and blood sugar levels shot up.
“This for the first time validates that you can use human embryonic stem cells to produce fully functional human islets,” said Emmanuel E. Baetge, the chief scientific officer of Novocell and senior author of the report.
But Dr. Mark A Magnuson, a professor at Vanderbilt University and director of its stem cell biology center, said the Food and Drug Administration might not allow the transplant into people of cellular material that would have to “mature” in the body.
“Would this happen reproducibly in different people, and would it be the same in all transplant sites?” Dr. Magnuson said in an e-mail message. “If it wasn’t totally predictable, could there be adverse effects, such as tumors?”
Indeed, in the Novocell experiment, 7 of the 105 mice with the implants developed a sort of tumor called teratomas. Dr. Baetge said Novocell could probably have reduced or eliminated the teratomas if it had purified the cells before implanting them.
MY OPINION: These researches have been going on for the past few years, only only in USA , but also in other countries as well. No doubt the prospect of providing stem cell therapy for diabetics will be a boon, but there is a dearth of stem cell providers. Also the side effects, like tumours seem bad enough, but if the procedure were to be sophisticated, I am sure this side effect could be minimised. Since controlled human trials will be held after a long duration, one can only hope we are going in the right direction and keep our hopes pinned on this therapy. For now, the best recourse is to avoid getting diabetes, or if afflicted with diabetes, then to effectively manage it.
[/b]
Main Category: Diabetes
Also Included In: Obesity / Weight Loss / Fitness; Liver Disease / Hepatitis; Biology / Biochemistry
Article Date: 07 Mar 2008 - 4:00 PST
Continually revved up insulin production, the kind that results from overeating and obesity, slowly dulls the body's response to insulin. As a result, blood sugar levels start to creep up, setting the stage for diabetes-associated complications such as blindness, stroke and renal failure. To make matters even worse, chronically elevated blood sugar concentrations exacerbate insulin resistance.
The vicious circle gets rolling, researchers at the Salk Institute for Biological Studies discovered, when out-of-control blood sugar levels disable the molecular switch that normally shuts off sugar production in the liver in response to rising levels of insulin.
Their findings, published in the March 7 issue of Science suggest that appropriate inhibitors of the enzymatic pathway that blocks the "sugar-off"-switch might be useful in lowering glucose levels in diabetic individuals and reducing long-term complications associated with the disease.
"The islet cells in the pancreas can compensate with increased insulin production only for so long when confronted with chronic obesity and inactivity," says Marc Montminy, Ph.D., a professor in the Clayton Foundation Laboratories for Peptide Biology, who led the study. "As a result glucose levels start to rise causing a host of problems."
Just like a flex-fuel vehicle that can run on either gasoline or ethanol, the human body can switch between different types of fuel: During the day the body mostly burns glucose, and during the night or prolonged fasting, it burns primarily fat. But neither flex-fuel engines nor human brains can run on ethanol or fat alone - a little bit of gasoline or glucose needs to be thrown into the mix to keep either one of them humming.
Three years ago, Montminy discovered a "fasting switch" called CRTC2 (formerly known as TORC2) that flips on glucose production in the liver when blood glucose levels run low during the night. After a meal, the hormone insulin normally shuts down CRTC2 ensuring that blood sugar levels don't rise too high.
In many patients with type II diabetes, however, CRTC2 no longer responds to rising insulin levels and as a result the liver acts like a sugar factory on overtime, churning out glucose throughout the day, even when blood sugar levels are high. The Salk researchers were interested in the molecular mechanism that leads to the breakdown of the normally tightly regulated FEEDBACK
loop.
Mice whose livers light up - courtesy of the luciferase gene, which produces the glow in fireflies - as soon as CRTC2 is turned on, led post-doctoral fellow and first author Renaud Dentin, Ph.D., onto the trail of the hexosamine biosynthetic pathway. Activation of the pathway promotes the addition of sugar molecules to proteins, a process also known as O-glycosylation. "It had been known that increases in the concentration of circulating glucose activate the hexosamine biosynthetic pathway," says Dentin. "But we had no idea that the resulting O-glycosylation would lock CRTC2 in the 'on'-position."
Normally, the rise in insulin after a meal activates a liver enzyme called SIK2. The enzyme chemically tags CRTC2 with a phosphate group, marooning the protein outside the cell's nucleus. Unable to reach the genes involved in gluconeogenesis, CRTC2 is powerless to turn them on and glucose production in the liver ceases.
In the presence of excessive glucose levels, however, the hexosamine biosynthetic pathway is activated and blocks crucial phosporylation sites on CRTC2 by adding sugar molecules instead. CRTC2 can no longer be phosphorylated in response to rising insulin levels and is now free to slip into the nucleus and keep the gluconeogenic program going.
Shutting down the O-glycosylation pathway should then get the body's own glucose production under control, the researchers reasoned. Just as predicted, glucose tolerance and insulin sensitivity markedly improved in insulin resistant diabetic mice and mice fed a high fat diet - who both suffered from hyperglycemia - when Dentin and his colleagues decreased the activity of the hexosamine biosynthetic pathway in the liver of these animals.
"What I really would like to do is to use the glowing mice to screen for drugs that decrease gluconeogenesis," says Montminy. "Imagine hyperglycemic mice whose livers light up because CRTC2 is on all the time. When you feed them a drug that inhibits O-glycosylation the light dims and you know you have compound that's effective in living animals and you know how it works."
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Article adapted by Medical News Today from original press release.
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Researchers who also contributed to the study include research assistant Susan Hedrick, in the Clayton Foundation Laboratories for Peptide Biology at the Salk Institute, Jianxin Xie, Ph.D., at Cell Signaling Technology in Danvers, Massachusetts, and professor John Yates III, Ph.D., at the Scripps Research Institute in La Jolla, California.
This work was supported by NIH grant RO1 GM037828, by the Clayton Medical Research Foundation, Inc., and by the Kiekhefer Foundation.
The Salk Institute for Biological Studies in La Jolla, California, is an independent nonprofit organization dedicated to fundamental discoveries in the life sciences, the improvement of human health and the training of future generations of researchers. Jonas Salk, M.D., whose polio vaccine all but eradicated the crippling disease poliomyelitis in 1955, opened the Institute in 1965 with a gift of land from the City of San Diego and the financial support of the March of Dimes.
Source: Gina Kirchweger
Salk Institute
Edit : Footnote containing Personal Opinion or Personal Reference needed
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University of Queensland researchers are developing a simple test that may predict whether a child will develop Type 1 diabetes.
Professor Ranjeny Thomas and her colleagues from UQ's Diamantina Institute for Cancer, Immunology and Metabolic Medicine, have identified a cellular pathway known as NF-kappa B that is activated in blood cells of people with Type 1 diabetes.
"Blood cells are the major infection and immune-control cells of the body, called monocytes and dendritic cells," Professor Thomas said.
"Monocytes from healthy people are 'quiet' in the blood and if we expose them to infection outside the body, the NF-kappa B pathway gets activated.
"In individuals with Type 1 diabetes, we found monocyte NF-kappa B was already activated in the blood, and when exposed to infection the pathway shut down. This tells us something fundamental about the problems of immune control that cause diabetes to develop in children.
"As a spin off, by simply taking blood, we hope to now be able to identify if a child will develop diabetes.
Professor Thomas said Type 1 diabetes is caused by problems in the immune system, so that the pancreas is not tolerated - like an organ rejection.
"In a similar way, people with rheumatoid arthritis don't tolerate their own joints, and they get inflamed, sore and swollen," she said.
"The pancreas of diabetics doesn't get sore but it gets inflamed, and then stops producing the hormone insulin. Insulin is needed to control blood sugar."
She said the test would target families with a history of diabetes with the aim of picking up other children at risk.
"Currently available tests pick up this risk rather late and in relatively few people, when there is already evidence of intolerance of the pancreas. We are investigating at what stage our test becomes abnormal," she said.
"With various trials of vaccines for diabetes underway, the potential is there to identify and intervene in children at risk of Type 1 diabetes before it occurs.
"But what is also important, is that we are in a position to really investigate why the immune system loses control before the disease starts. That fundamental understanding will bring the vaccines of the future."
The research has been published this week in the Journal of Immunology.
Edit: Disclaimer, original source, reference and footnote absent in this post. Post will be edited or deleted within the next 1-2 weeks, unless the author of this post decides to add the relevant information. Posts without disclaimers and quotations about original sources are not acceptable in this forum anymore. [/b]
Shravani, I have requested you to add a disclaimer and a footnote already. If you dont add it the next time, i shall edit or delete your posts.
Please adhere to the rules of the forum, let's keep it professional. And plase give due credit to the original sources.
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