Islet transplantation is an exciting frontier of diabetes research as it can reverse diabetes. A recent study from researchers at the University of Alberta in Edmonton showed promising results when a combination of intensive insulin and heparin is used to garner better success of islet transplantation from a single donor.

Due to inefficiencies in islet harvest, islet transplants usually require harvesting from more than one donor. Not only does the drug combination yield more islets from a single donor, early results suggest patients receiving islets from one donor realize longer insulin independence. Study researchers hypothesized heparin, an anticoagulant, could prevent damage from clotting, while intensive insulin could relieve stress and inflammation on the islets during transplantation.

13 patients received the insulin/heparin (IH) combination. 6 of the 13 IH patients (46%) were able to give up insulin treatments. This was compared to a previous 66-patient cohort that had received islet transplants via intraportal cultured islet-alone infusions, followed by immune system suppression via three different drugs. Of these 66 patients, only 5 (8%) were able to give up insulin. Furthermore, 55% of patients reaching insulin dependence via one donor maintained independence after 60 months, compared to only 9% of patients receiving islets from more than one donor.

To learn more about the metabolic wonders of islets of Langerhan, please see this previous post.

Novocell is the first company to use polyethylene glycol (PEG) to encapsulate clusters of insulin-producing cells. This biocompatible substance allows glucose and insulin to pass freely through the coating while preventing the body's immune system from destroying the islets.

The encapsulated islets release human insulin through natural mechanisms in response to the recipient's blood glucose. The islet cells used in this study are isolated from human cadavers. The implant procedure is performed under local anesthesia and the encapsulated islets are injected into a surgically formed micropocket in the subcutaneous tissues of the thigh or lower abdomen of the recipient. The patients received temporary low dose cyclosporine (50-100 ng/ml 12hr trough) and did not receive any other form of immunosuppression.

At the American Diabetes Association 66th Annual Scientific Session in June -- Novocell announced the progress of the study. No adverse events had occurred -- no news is good news. In addition, the company also has the fortune of existing in California - where they can prosper on further stem cell research. Novocell has developed a process that efficiently converts human embryonic stem cells into insulin-producing cells. Novocell believes this study will demonstrate the safety and efficacy of the encapsulation technology that can be used with the unlimited source of insulin-producing cells developed from stem cells to treat patients with diabetes.

The Edmonton Protocol has been temporarily put on hold due to fears the human form of mad cow disease might infect patients.

The source of an enzyme used in transplants was reported to derive from cow brains. Transplants of these treated islets have been put on hold until a source for this enzyme can be found that doesn't use cow brains. Dr. James Shapiro, the surgeon who developed the Edmontol Protocol said, "we just decided to put the program on hold". Shapiro and his team transplant healthy islet cells into the pancreas of people with Type 1 diabetes. The healthy cells allow recipients to again begin producing insulin crucial to the body's ability to regulate sugar digestion.

The National Institutes of Health was creating a similar program in the United States when it discovered that one of the biomedical compounds that Shapiro's team has been using depends on cow brains. Roche Applied Sciences was selling the team an enzyme that allows doctors to extract healthy islet cells. But Roche was buying the bacteria that secretes the enzyme from a third company, which grew the bacteria using fat from cow brains. Roche spokeswoman Michele Beaubien said from Montreal that the enzyme is sold for research purposes only.

The more I learn these days about medicine and how it is applied to diabetes - the more I feel as though everything is for research purposes only. Don't you? As Yogi Berra said, "it ain't over till it's over". A big thanks to Dave of No Sugar Tonight for bringing this story to my attention.

Living Cell Technologies has been given the go ahead to conduct clinical trials of its DiabeCell diabetes product in New Zealand.

DiabeCell is a porcine islet cell product for the treatment of insulin- dependent diabetes. The pig cells are injected into the body without any immunosuppressant drugs. The cells produce insulin to help regulate blood glucose levels appropriate to the amount of glucose detected in the blood stream of the diabetic recipient.

The Medical Director of Living Cell Technologies explains that DiabeCell offers considerable advantages over other available treatments in addition to the fact there is no need for immuno-suppressive drugs. Anther problem of islet transplants is the strain on the supply of islets. This is not a problem with the DiabeCell because their supply of cells derive from natural biocertified pig herds, unlike human organ donors.

LCT's application is to conduct the clinical trial of its DiabeCell product on 8 long standing Type 1 diabetics. The clinical trial is expected to be approximately 12 months in duration. This will then be followed by a trial on a larger scale. The trial will be conducted at a New Zealand hospital and involves the simple injection of encapsulated islets into the abdomen of the diabetic patients. It is anticipated that the trial would start by the end of 2007.

Hold on to your seats, folks. This story is pretty controversial but fascinating enough to make an appearance on Prime Time television 2x tonight on the evening news! A treatment involving the annihilation of the immune system, followed by a period of rebuilding the immune system is being tested in Brazil as a cure for type 1 diabetes.

The patients involved were newly diagnosed with type 1 diabetes, and between the ages of 14 to 31 years old. The 15 diabetics were treated at a bone marrow center at the University of Sao Paulo. Timing is key in this method of therapy because if you wait too long - the window of opportunity where the body's ability to repair itself closes. The procedure involves stimulating the body to produce new stem cells and harvesting them from the patient's blood. Next comes several days of high-dose chemotherapy, which shuts down the patient's immune system. This also stops destruction of the few remaining insulin-producing cells in the body. This requires hospitalization and potent drugs to fend off infection. The harvested stem cells, when injected back into the body, build a new healthier immune system that does not attack the insulin-producing cells. Patients were hospitalized for about three weeks. Many had side effects including nausea, vomiting and hair loss.

For the record (and the Freedom of Information Act) the study was partly funded by the Brazilian Ministry of Health, Genzyme Corp. and a maker of blood sugar monitoring products.

Just like a referee to normalize play throughout the game - DiaKine Therapeutics is developing ways to normalize the body's immune system.

The new drugs modulate cytokines, part of the body's immune system, which mistakenly attack normal organs and tissue and cause diseases such as: diabetes, multiple sclerosis and inflammatory bowel disease. Research by Dr. Nadler and his collaborators published in 2006 showed that controlling certain cytokines can arrest the progression of, or reverse, type 1 diabetes in an animal model.

The company's first product, IsletLifeLSF Media 1 is designed to improve the viability and insulin producing capabilities of harvested islet cells prior to transplant. This would potentially improve the success rate of the procedure. Additional therapeutics under development by DiaKine include: adjunct therapy to islet cell transplants, halting the progression of type 1 diabetes in newly diagnosed adults, treatment and prevention of Latent Autoimmune Diabetes of Adults (LADA), treatment and prevention of insulin requiring type 2 diabetic, treatment and prevention of diabetes complications.

It all sounds like good stuff in the works. Keep an eye on the progress and press releases of DiaKine, as well as their research partner - the Diabetes Research Institute. A lot is happening these days. What else have you seen or heard about in the autoimmune arena?

For thousands of years, Ayurveda has used meshashringi as a treatment for adult-onset diabetes, a condition once described as "honey urine". Meshashringi is a climbing plant that grows in the tropical forests of India and could be just the thing to combat high blood sugar.

Thousands of years ago, type 2 diabetes was treated with meshashringi. The plant's sugar-destroying property was released when a person chewed on one or two leaves. Meshashringi was said to "paralyse" a person's tongue to sweet and bitter tastes. This taste-blocking reaction lasted for several hours. Meshashringi blocked sugar in the digestive system, resulting in a decrease in blood sugar. This is known as a hypoglycemic effect. This action has been studied since the late 1930s.

Recent studies have shown that meshashringi helped control blood sugar levels by stimulating insulin release from the beta cells. Meshashringi enhanced natural insulin production, which was evidenced by an increase in levels of C-peptide. C-peptide is the connecting peptide that is found along the amino acid chains in natural insulin (insulin produced in the islets). When insulin is cleaved apart, the connecting peptide disengages and floats off to preserve and protect the body's cells from microvascular damage resulting in diabetic complications like blindness, kidney disease, and neuropathy.

Another study found that 400 mg a day of meshashringi produced similar results for non insulin-dependent diabetics. Fasting blood glucose, A1c and glycosylated plasma protein were significantly reduced compared to baseline values after 18-20 months of treatment. By the end of the treatment period, cholesterol, triglycerides, phospholipids and free fatty acid levels were also significantly reduced. It is possible that the blood sugar lowering effects of meshashringi are mediated through their cortisol inhibiting potency. Clinical trials have recorded the benefits of meshashringi in diabetic patients where 400 mg a day reduced insulini requirements by about 50% in insulin-dependent diabetics.

Hello? Did that study say I might be able to cut my daily insulin requirements in HALF? Where on Earth (besides the Saharan terrain of Africa and the jungles of India) can I find this green Goddess? Somebody clear the fog in my head - does India even have jungles? I'm not a Globe-trotter (not yet, anyway). Irrational fear of turbulance.

Chat live with Dr. Pugliese, an expert on the immunology and genetics of diabetes at The Diabetes Research Institute. His work has been focused on preventing the autoimmune attack that leads to diabetes. This research is very important for future prevention strategies, as well as stopping autoimmune destruction of transplanted islets.

Dr. Pugliese's has studied the role of the thymus gland in the immune system and he describes it as the "school for the immune system". All immune cells are forced to pass through the thymus gland where they are exposed to the antigens present throughout the body. Immune cells that bind to these normal antigens are destroyed, thereby preventing the later destruction of healthy cells. If no binding occurs, then the cell is deemed to be friendly to host tissue and is released to become part of the immune system. The insulin producing cells of the body - islets -- are not the only body cells that release insulin. Dr. Pugliese's research has shown that there are other cells that release tiny amounts of insulin, but not in response to blood glucose. These cells present insulin to the visiting immune cells in the thymus, and any immune cell that binds is killed. It is believed that a low insulin output in these decoy cells in people who develop diabetes may be the reason that immune cells are allowed to live that will later track insulin back to its source and destroy healthy islets. In people who have the genetic markers that protect against diabetes, these cells secrete more insulin than they do in people with genes that pre-dispose them to diabetes. The more insulin in the thymus, the more likely that insulin-specific autoreactive lymphocytes will be killed, with fewer chances of developing diabetes.

Confused yet? Yeah, me too - but my confusion feeds my insatiable curiosity. That is precisely why I will be joining the rescheduled chat with Dr. Pugliese. Please, be there on March 15th at 9pm Eastern Standard Time on Diabetes Talkfest. Make it a date: you, me, Dr. P and the most informed people in the diabetes community. Once again, thanks to Gina and Jon for Linking Diabetics Coast to Coast!

The Spring Point Project is a nonprofit organization created to increase the availability of islet tissue for diabetes care by cultivating medical-grade pigs for islet xenotransplantation.

Dr. Bernhard Hering is the scientific director of the Diabetes Institute for Immunology & Transplantation at the University of Minnesota. He believes the shortage of human donor organs greatly limits the applicability of islet transplants. Of course he does. In 2004, President Bush directed the Diabetes Research Work Group, created by Congress, to develop a comprehensive plan for diabetes research. One of the outgrowths has been the establishment of the NIH (National Institute of Health) Clinical Islet Transplant Consortium. Spring Point Project's consultant Dr. Bernhard Hering, M.D., is one of only five researchers worldwide appointed to serve on it. Hold the cornmeal, Wilbur. Who else has a seat in the NIH panel?These medical-grade pig islets require immunosuppression drugs to sustain the life of the islets without another autoimmune attack taking place. A statement from the faq page on The Spring Point Project site states, "Pig islet graft survival was made possible with a novel immunosuppressive protocol." Okay. Minor detail but very important when you weigh your options.

The Spring Point Project says human trials are slated to begin in 2008. Funny-- that is the same time Massachusetts General Hospital's human trials for Dr. Denise Faustman's proposed cure for type 1 diabetes is set to begin. Dr. Faustman's cure does not require any immunosuppression drugs. In my book - any cure that requires a continuum of drugs is not a cure, at all.

Neuropeptide regulating appetite may help in developing new diabetes treatments. The neuropeptide called melanin concentrating hormone (MCH) plays a role in the growth of insulin-producing beta cells and the secretion of insulin. MCH is found in the brain and regulates energy balance and appetite.

A previous study conducted at Joslin found an association between high levels of MCH and an increase in the number of beta cells in mice. When we eat food, our body needs more insulin. When MCH induces appetite, it simultaneously increased insulin secretion. This calls upon the beta cells and enhances their growth. If the proteins that mediate the growth mechanism can be identified, it could lead to the development of new drugs that would enhance beta cell growth to treat type 1 and type 2 diabetes.

Sounds great! However, this sounds similar to the function of SYMLIN, which is the synthetic form of amylin. Amylin is a hormone secreted by beta cells at the same time as insulin. If you've heard of Byetta - you've heard of Amylin Pharmaceuticals, the makers of SYMLIN. The researchers at Joslin and the guys at Amylin should get together and do lunch. They might have a lot to discuss between this research and the development of yet another biotechnological blockbuster drug.

In the summer iof 2004, research funded by JDRF revealed that a mutation of the SUMO-4 gene is a strong factor in the development of type 1 diabetes and the potential associated complications, such as kidney failure.

The gene called SUMO-4 is responsible for signaling the proteins that regulate the intensity and duration of the immune response. When the gene is mutated, it has an increased response to the stimulants of the immune system, that cause it to overreact. This overreaction results in a person's inability to distinguish between self and foreign cells, thus causing type 1 diabetes. The mutated SUMO-4 gene may exacerbate the inflammatory process, influencing the complications of diabetes.

The most influential genes in the development of type 1 diabetes are found in the HLA or human leukocyte antigen region. These genes help regulate the immune system by guiding it to differentiate between self and non-self. Variants of the DR and DQ genes in the HLA region are found in 95% of type 1 diabetics. Another gene that increases the chances of developing type 1 diabetes has been found in the region immediately preceding the insulin gene. This region contains a VNTR or variable number of tandem repeats. This refers to specific chemical bases that make up DNA. Inheritance of certain VNTR's increases the risk of developing type 1 diabetes.

Again I reiterate this research was unveiled in 2004. SUMO-4 was identified as a prime target to control the inflammatory process leading to the destruction of islets. As I search Google for, "sumo4, drugs, JDRF" I am terribly disappointed to see that my yearning for answers remains unrequited. Did SUMO-4 fall too hard too fast?

Like a dog chasing its own tail (but nowhere near as funny), type 1 diabetes is caused by a self-imposed attack on insulin producing cells. Here's your chance to chat live and learn about the latest discoveries to interfere with the automimmune confusion. Chat live with the head of the Immunogenetics Program at the Diabetes Research Institute, Alberto Pugliese, M.D.

The DRI program is specifically focused on understanding how genetic and immunological factors play a role in the development of type 1 diabetes and how certain genetic and immunological factors may actually afford protection from diabetes. The program is uncovering ways to interfere with the immune cells that attack the insulin producing cells in the pancreas resulting in diabetes.

In plain English, join Dr. Pugliese to enlighten yourself and ask any questions you may have regarding this impressive research. The chat begins at 9pm EST and those who miss it can catch the excitement in the transcript, to be posted shortly thereafter. I hope to see fellow IDDMs on the chat roster.

New research is revealing that cells passed from mother to child during pregnancy could be used to treat diabetes. Scientists found these cells can develop into functioning islet beta cells which produce insulin in the pancreas.

Scientists studied 172 individuals and took pancreatic tissue from four deceased males. They found small numbers of female islet beta cells able to produce insulin. There was no evidence the mother's cells were causing damage or becoming the target of an immune response. However, the team found more maternal DNA in the blood of children and young adults with type 1 diabetes than in healthy individuals. Researchers believe the maternal cells may be helping to regenerate tissue in the pancreas.

I heard about this study last year. It sounded quite promising and led me to wonder if I had a child - could the stem cells from the umbilical cord become healthy beta cells for me? Sure. However, the big question still remains - how can I stop the killer Ts from spanking my islets in the first place?

The Juvenile Diabetes Research Foundation announced that they have formed a partnership with MacroGenics. JDRF is providing up to $2 million to fund a clinical trial of a compound called anti-CD3 that has shown promise in slowing the progression of type 1 diabetes.

Anti-CD3 is capable of reducing the autoimmune attack that destroys insulin-producing beta cells. The treatment preserves beta cell function in newly diagnosed patients, and has the potential to decrease insulin requirements, leading to better glucose regulation, and decrease the complications of diabetes. Anti-CD3 blocks the function of CD3 cells - the T cells that destroy islets. The antibodies prevent "activation" of the T cells after they have identified their target, disarming them launching the attack on islets.

Let's hope the peace talks between JDRF, MacroGenics, anti-CD3 and killer Ts result in progressive measures to make the type 1 diabetic body a peaceful place, once and for all.

Japanese scientists have discovered an imbalance that leads to the development of type 2 diabetes in mice. A gene called GCK is responsible for sensing changes in blood glucose levels. Researchers found a molecule known as insulin receptor substrate 2 (IRS2) was shown to influence the beta cell mass increase after GCK sensed an increased in blood glucose levels.

The Journal of Clinical Investigation focused on mice with little increase in beta cell mass regardless of a rise in GCK. Researchers found, in healthy mice, the insulin receptor substrate 2 (IRS2) was shown to influence the beta cell mass increase after GCK first sensed an increased in blood glucose levels.

Before a person becomes diabetic, his or her body tries to compensate for the increasing resistance to insulin by upping the amount of insulin secreted and the mass of insulin-secreting cells (beta cells) in the pancreas. Researchers will look for new ways of increasing beta cell mass to prevent the onset of type 2 diabetes. Here's where I get a little confused - another study conducted a few years ago found evidence that a sucrose-rich diet (SRD) produces an increase in the pancreatic beta-cell mass in the rat. I'm neither a rat, nor a scientist - but I think a meeting of the minds behind these two discoveries might result in some forward-thinking treatments for type 2 diabetes. What compels the IRS2 to defy the command center of GCK? Perhaps another piece is missing from the balance of this equation.