Two Asian companies--BioLineRx of Israel and JHL Biotech of Taiwan--have agreed to collaborate on the development and marketing of BL-9020, a monoclonal antibody that could become a significant means of treatment for early-stage type 1 diabetes.
File this news under "potential breakthrough you didn't see coming." Researchers have tried--and seem to have succeeded--in slowing the destruction of beta cells by treating recently diagnosed people with type 1 diabetes with alefacept, a drug usually prescribed to treat psoriasis, a disorder that leaves skin red and itchy.
People with type 2 diabetes and those heading toward that diagnosis may face a quicker decline in their beta cell function than previously understood, according to a new study published in the Journal of Clinical Endocrinology & Metabolism. That means the progress and challenges for such patients may progress more quickly than doctors expects and need more aggressive treatment.
Type 1 diabetes doesn't happen all at once. Scientists have shown that it's usually a gradual process, in which the insulin-producing beta cells eventually fade out. So wouldn't it be marvelous if the function of those beta cells could be preserved, allowing people newly diagnosed with diabetes to produce some of their own insulin for a longer time?
Israeli researchers believe that they have found a way to increase the survival and effectiveness of insulin-producing pancreatic cells transplanted into diabetic mice. The technique, developed by scientists at the Technion-Israel Institute of Technology in Haifa and Ben-Gurion University of the Negev in Beersheba, involves surrounding the transplanted beta cells with a three-dimensional latticework of nurturing blood vessels called "engineered tissue."
Low doses of metformin and rosiglitazone seem to delay the onset of type 2 in prediabetic people who have impaired glucose tolerance, according to a Canadian study. However, although the drug combination was effective over the first year of the study in helping to control glucose levels and insulin resistance, it was not effective subsequently in delaying the onset of insulin resistance and pancreatic beta cell deterioration.
Over the last decade, dramatic changes have occurred in our understanding of the onset and progression of prediabetes. Lightning speed changes have also occurred regarding the therapies available to achieve optimal blood glucose control. Even with all of this change, however, many old dogmas hang on. It's time to become aware of the new realities. In this article, I focus on two common old dogmas and the new realities.
Every year four million baby teeth fall out, and 1.4 million wisdom teeth are pulled out of our collective mouth. Until recently, the only entity really interested in all those teeth was the tooth fairy. But all that changed in the year 2000, with the discovery that dental pulp contains adult stem cells. In the not-too-distant future, those stem cells might be used for growing new islet cells to cure diabetes. The problem is, how to keep the teeth nice and fresh until that hoped-for day. That's where Provia Laboratories comes in, with their Store-A-Tooth service.
The final patient has performed the last visit of the main study period in Diamyd Medical's European Phase III study. Treatment with the antigen based therapy Diamyd® is made to investigate whether beta cell function and thereby blood sugar control can be preserved in children and adolescents with new onset type 1 diabetes. The top line results from this study are expected to be reported as planned, in late spring 2011.
INDIANAPOLIS and NEW YORK - Eli Lilly and Company and the Juvenile Diabetes Research Foundation (JDRF) today announced that they have signed an agreement to fund early-stage research that could enable patients with type 1 diabetes to regenerate insulin-producing cells destroyed by the disease.
(Reuters) - Stem cells can be transformed into the pancreatic cells needed to treat diabetes and into complex layers of intestinal tissue, scientists demonstrated in two experiments reported on Sunday.
"The objective of this clinical trial (research study) is to determine if the medications can rescue the few beta cells that remain soon after the diagnosis of type 1 diabetes; and whether new beta cells can even be regenerated," commented Alex Rabinovitch, MD, Principal Investigator of the trial and Associate Director of The Sanford Project. "The investigational combinations of these medications could possibly allow patients to decrease or no longer need to inject insulin to keep their blood levels under proper control."
Over 80 years ago, famed diabetologist Elliot Joslin said about the treatment of patients with type 1 diabetes: "Ketoacidosis may kill a patient, but frequent hypoglycemic reactions will ruin him." Unfortunately, hypoglycemia continues to be the most difficult problem facing most patients, families, and caregivers who deal with the management of type 1 diabetes on a daily basis. Frequent hypoglycemia episodes not only can "ruin," or adversely impact the quality of life for patients, but also, when severe, can cause seizures, coma, and even death.
Dr. Richard Hays announced today that he is now recruiting children with newly diagnosed type 1 diabetes for Protégé Encore, a randomized, placebo-controlled Phase III clinical trial. This is the second of two Phase III studies testing the safety and efficacy of an investigational drug called teplizumab. The first study, known as Protégé, has completed enrollment of more than 530 subjects with type 1 diabetes. There is currently no approved therapy to slow the progression of type 1 diabetes.
Osiris Therapeutics announced that it has been granted Orphan Drug designation from the U.S. Food and Drug Administration (FDA) for Prochymal as a treatment for type 1 diabetes mellitus. The FDA instituted the Orphan Drug Act to promote the development of treatments for underserved patient populations. To be eligible for Orphan Drug designation, the treatment must target a disease that affects fewer than 200,000 new patients per year in the United States.
NEW YORK, April 27, 2010 - The Juvenile Diabetes Research Foundation announced today that it is partnering with Living Cell Technologies (LCT), a New Zealand-based biotechnology company focused on developing cell based therapeutics, in a Phase II clinical trial to study the safety and effectiveness of transplanting encapsulated insulin-producing cells from pigs as a treatment for type 1 diabetes with significant hypoglycemia unawareness.
Healthy, insulin-producing beta cells in the pancreas have a relatively long life and typically do not replicate under normal conditions. Any loss of beta cells, therefore, is usually permanent. In the case of type 1 diabetes, for example, the destruction of beta cells by the body's own immune system is permanent.
You may not have heard of GAD, but it's a hot topic in the world of type 1 diabetes research. GAD, which stands for glutamic acid decarboxylase, is an enzyme in the brain and the pancreas that plays several roles in the body. As an enzyme, it converts the excitatory amino acid glutamate into the inhibitory neurotransmitter GABA, which nerve cells use to communicate. But it also has a less helpful role, as an autoantigen (an element of self that provokes the generation of antibodies) in autoimmune diabetes.
An enzyme that destroys pancreatic beta cells in lab mice has now been observed in human beta cells. Because scientists already know how to delete the mouse gene that produces the enzyme, they are hopeful that the same therapy can eventually be applied to people with type 1 diabetes. If so, it would be one of the most powerful therapies yet for addressing the destruction of insulin-producing beta cells that causes type 1.
A hormone responsible for the body's stress response is also linked to the growth of insulin-producing cells in the pancreas, according to JDRF- funded researchers at the Salk Institute for Biological Studies in California. The findings are the latest advances to underscore the potential for regeneration as a key component of a possible cure for type 1 diabetes.
Researchers at RIKEN and Fukuoka University have pinpointed the mechanism responsible for early rejection of transplanted pancreatic islet cells in the treatment of type 1 diabetes. A new system based on this mechanism has been shown to vastly increase transplant efficiency, setting the stage for the development of powerful new treatment techniques.
WASHINGTON (Reuters) - Researchers have transformed ordinary mouse skin cells directly into neurons, bypassing the need for stem cells or even stemlike cells and greatly speeding up the field of regenerative medicine.
An international research consortium has found 13 new genetic variants that influence blood glucose regulation, insulin resistance, and the function of insulin-secreting beta cells in populations of European descent. Five of the newly discovered variants increase the risk of developing type 2 diabetes, the most common form of diabetes.
BOSTON, Mass. - Dec. 23, 2009 - Cells in your body are constantly churning out poisonous forms of oxygen (oxidants) and mopping them up with a countervailing force of proteins and chemicals (anti-oxidants). This balancing act of oxidative stress is particularly likely to go haywire in beta cells, the insulin-producing cells that malfunction and then start to die off in type 2 diabetes.
Rituxamab, a drug that treats lymphoma and rheumatoid arthritis, may soon be used to help combat the destruction of pancreatic beta cells in newly diagnosed cases of type 1 diabetes. Researchers at Indiana University have found that the drug, originally developed and sold by Genentech as Rituxan, temporarily slows or stops the destruction of the 10 or 20 percent of beta cells that type 1s typically have remaining when they are first diagnosed.
NEW YORK, Dec. 17, 2009 - The Juvenile Diabetes Research Foundation, a leader in setting the agenda for diabetes research worldwide, said today that it will begin working with The Johnson & Johnson Corporate Office of Science and Technology, and its affiliates, to speed the development of drug targets and pathways to promote the survival and function of insulin-producing cells in people who have diabetes. The program will look to fund research at academic centers around the world that could eventually lead to novel drug targets and industry collaborations for the treatment of type 1 diabetes.
WASHINGTON, Dec. 15 /PRNewswire-USNewswire/ -- A 21-year old Airman severely wounded in Afghanistan is recovering at Walter Reed Army Medical Center after several surgeries and an unprecedented transplant.
One thing that really frustrates people with diabetes mellitus is the biopharma industry's focus on treatments rather than cures. A cure is what the diabetes community wants, not another band-aid. So the existence of a biopharma company that calls itself "CureDM" is promising, and its first product, Pancreate, seems to be on its way to fulfilling that promise.
By reprogramming skin cells from people with type 1 diabetes, scientists have produced beta cells that secrete insulin in response to changes in glucose levels. Dr. Douglas Melton and his colleagues at the Harvard Stem Cell Institute started by using the skin cells to generate induced pluripotent stem (iPS) cells. Once they had iPS cells, the researchers manipulated them into developing into pancreatic islet (beta) cells.
Our genes are like a recipe for a human. It's a very complicated recipe, determining how much of this protein and how much of that enzyme need to be added into the mix in order for us to function properly, but our genes are pretty good at getting it right. Although we are still learning how the recipe works, what ingredients (gene products) are involved, and when are they are produced, our knowledge is growing fast.
A study from Massachusetts General Hospital and Harvard Medical School in Boston says that magnetic resonance imaging could become a useful tool for diagnosing diabetes and helping doctors determine the proper course of treatment.
A protein that builds up in the pancreases of baboons and leads to the suppression of insulin-producing beta cells, may provide one of the most significant indicators yet for predicting the onset of type 2 diabetes.
Of all the quests that researchers have undertaken in search of a cure or decisive treatment for type 1 diabetes, the search for a vaccine has to be the boldest. But how would you develop such a vaccine, and how would it work?
Researchers funded by the Juvenile Diabetes Research Foundation have found two chemical compounds that can trigger the growth of insulin-producing beta cells in the pancreas. The discovery could become the basis for medicines designed to regenerate the pancreas in people with type 1 diabetes.
A team of five seniors and two freshmen at Johns Hopkins University has devised a little "pouch" to hold microcapsules of beta cells in the portal vein, from which the cells can send out insulin while safely protected inside. It's made by sandwiching a porous cylinder of nylon mesh between two cylindrical metal stents, similar to the ones that are used to keep clogged blood vessels open.
A new study out of London and Paris indicates in the developing embryo, beta cells form in the pancreas in response to the presence of glucose. Glucose triggers a gene called Neurogenin3 to switch on another gene, neuroD, which is critical for the normal development of beta cells. If glucose levels are low, the gene doesn't switch on and the beta cells don't develop.
A team of five seniors and two freshman at Johns Hopkins University has devised a little “pouch” to hold microcapsules of beta cells in the portal vein, from which the cells can send out insulin while safely protected inside.
Novocell, Inc., a San Diego, California-based stem cell engineering company, announced on October 19, 2006, the development of a process that “efficiently converts human embryonic stem cells into insulin-producing pancreatic endocrine cells.”
I just discovered your May 2005 article, “Why Did the JDRF Try to Discredit Cure Research?” That, and lingering resentment over my own futile correspondence with Van Etten and Ahearn, inspired me to dig deeper into some points you made and some reasonable suspicions your article aroused.
Five years ago, when Dana Elias, PhD, first clutched a publication reporting that a synthetic peptide had halted beta-cell destruction in mice that already were showing high blood-glucose levels, she felt a shiver of excitement. She had helped develop the synthetic peptide, called DiaPep277.
The precursor to insulin produced by the pancreas's beta cells is a peptide chain known as proinsulin. Made up of amino acids bound into a u-shape by a connecting polypeptide, proinsulin is stored in beta cells until a glucose load demands the release of insulin. At this point, the connecting molecule is broken off the bottom of the "u"-its shape earning it the moniker C-peptide-freeing the insulin molecule for secretion.
Scientists at the University of California at San Diego recently announced that they have successfully grown beta cells that can produce insulin. The finding may eliminate one of the biggest obstacles in making islet transplantation a viable treatment for diabetes.
A promising drug trial at the Naomi Berrie Diabetes Center at New York's Columbia Presbyterian Medical Center needs children, aged 8 and older, who have recently been diagnosed with type 1 diabetes, to participate.
Dr. David Matthews, chairman of the Oxford Center for Diabetes, Endocrinology and Metabolism, says beta-cell deterioration is "virtually inevitable" in persons with type 2 diabetes. He urges doctors who treat type 2s to refrain from telling them that they only have "mild diabetes," and instead tell them that they are still at considerable risk for diabetic complications.
Q: I just finished reading the November 1998 issue of DIABETES HEALTH regarding the Juvenile Diabetes Foundation (JDF) islet transplantation $20 million advance. I didn't see anything about the cloning of islets, however, which I had read about in a previous issue of DIABETES HEALTH. I am curious to know how realistic the cloning process is, and when we might see it actually take place.
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