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.

The Wall Street Journal posted an interesting story about a man who needed a drug to treat his ALS or Lou Gehrig's disease. He could not get the funding for a large scale trial to approve the drug. I empathize, completely! See that picture of the Hulk? That's me. I'm angry. You won't like me when I'm angry.

As a type 1 diabetic, my concern for improving the lives of people affected by diabetes involves preventing and reversing the complications associated with the disease. The American Diabetes Association states the same somewhere in their mission statement. Ok ADA, put MY money where YOUR 501(C)3 is!!

When I called the American Diabetes Association and shared my excitement for the C-peptide treatment in human trials (in Sweden) reversing type 1 diabetic complications - I was floored when I heard their response.

Allie B: Can the American Diabetes Association please encourage a big pharmaceutical company to sponsor these trials here in the United States? The results in Sweden have conclusively shown reversal of complications associated with type 1 diabetes.

Mat P at the American Diabetes Association: The topic of C-peptide is very sexy in scientific forums. BUT - we don't like to tell big pharmaceutical companies what to do with their money because we don't like them to tell us what to do with ours.

Allie B (in my head): WHAT THE F%^&*)(*&^%$F do you DO as an organization to improve the lives of people affected by diabetes if you are not going to push for trials to prevent and arrest complications associated with the disease?

I'm afraid the American Diabetes Association and I do not share the same goals any longer. It was a long marriage, over 21 years - but I want a divorce. The largest diabetic organization in the United States is not willing to assist in getting a trial underway to prevent and reverse complications that could affect 2 million type 1 diabetics and between 2 and 4 million type 2 diabetics injecting insulin (without C-Peptide).

I didn't feel this way until I realized how disconnected their perception of diabetes is from the reality of the disease. What do you think?

In 1996 a 41 year old male (a type 1 diabetic for 18 years) was injected with biocapsules containing pig islets to regulate his blood sugar level. The transplanted cells helped reduce the patient's insulin requirement by 34% for over a year, which provided better control. By 2005 the patient's glycated hemoglobin levels (HbA1c) remained lower than the pre-transplant levels.

Ten years later, the patent contacted Living Cell Technologies to inform them that he believed the transplanted pig islets were still alive and well. After tests were conducted, it was concluded that the pig cells were (as he reported) still functioning. This proved that the LCT patented technology for xenotransplantation was effective. It allows the islets to survive at least ten years in a micro-capsule coating and continue to release insulin into the patient's bloodstream without immune suppression. After tests we conducted on the type of insulin present in the patients blood - it was with 100% certainty that it was pig and not human insulin.

LCT has significantly advanced the encapsulation process since the 1996 clinical trial and there is an even greater understanding and control over the longevity and robustness of the encapsulation process, as well as the porcine islet cells. LCT will be trialing the DiabeCell pig islet cell transplant in patients in a phase I/IIa clinical trial, expected to begin in Quarter 2, 2007. In addition, LCT is awaiting approval to conduct an additional trial in New Zealand this year with a different treatment protocol. Subsequent trials in the US or Europe are intended following initial results from these studies.

If overseas trials are coming through with flying colors - why aren't we doing this yet? C'mon USA - where's your competitive spirit? All these pigs up in Spring Point might be put to good use, after all. Oink Oink.

Much like a roadblock, but with a fortuitous outcome -- an experimental heart drug didn't achieve the primary goal of a late-stage trial but it did dramatically reduce the risk patients would develop diabetes.

The anti-oxidant, anti-inflammatory drug, the first of its kind, reduced the risk of developing diabetes by 64% and demonstrated a small but statistically significant reduction in blood sugar after 12 months. The study included data from 6,144-patients. The company believes this finding to be a serendipitous outcome, despite the initial shortcomings of the trial objective. They need to confirm it in a large clinical trial. The impressive diabetes results may come as a surprise to investors who have abandoned AtheroGenics or who have been betting the drug will fail.

Heart patients in the study received either 300 milligrams of the drug or a placebo on top of a host of standard-of-care medicines they were already taking, such as aspirin, cholesterol-lowering statins, blood thinners and/or diabetes medicines.

The drug had an undesirable impact on blood fats, raising bad LDL cholesterol by about 12% and lowering good HDL cholesterol by roughly the same amount. There were also some potentially troubling safety signals with a trend toward more heart failure in those taking the drug. In spite of the undesirable affects on blood lipids, the drug has a profound effect on diabetes. Further research will be conducted on the efficacy of this drug in reducing the risk of developing diabetes.

When treating diabetes, today's doctors focus on establishing blood glucose control, but often overlook the need to protect against common diabetic complications such as blindness, kidney damage, and nerve damage. The DCCT, even with a comprehensive treatment program, had a complication rate of approximately 40% of participants.

People who do not have diabetes make insulin with C-peptide. Those of us diabetics who inject synthetic insulin do not get the C-peptide. When scientists began developing insulin - they weeded out the pieces of the amino acid chain they felt were insignificant in lowering blood glucose. Synthetic insulin was designed to reduce the dangerous buildup of excess sugar in the bloodstream. Uh oh - hindsight is surprisingly clear! The long-term complications were initially thought to be caused by lack of insulin - not lack of something that should've been in it. It would make sense if insulin came equipped with this critically important element, wouldn't it?

Tada! C-peptide is the connecting peptide found on the amino acid chain of naturally produced insulin, but left on the cutting room floor in the lab. Studies have shown that C-peptide prevents the development and progression of many diabetic complications and was shown to improve glucose metabolism up to 66%.

Regardless of the potential profit decay C-peptide might cause the production of insulin - the bottom line is the salvation it will provide every man, woman, and child injecting insulin. If you're taking insulin injections, chances are you won't stop taking insulin because you're adding C-peptide to your daily lineup. Chances are - you'll be around a lot longer, and a lot healthier because you do not have the complications most often associated with long-term diabetes.

Wouldn't that be reason enough for you to celebrate the company that brings C-peptide to the drugstore nearest you? Consumer loyalty goes a long way. For those companies who knew a long time ago how beneficial C-peptide would be but didn't do a thing about it - is it really the 33% loss in insulin sales you didn't want to encounter? C'mon. We can handle the truth.

Novartis SA reports the U.S. FDA has demanded additional data, including a clinical study in patients with kidney impairment, before giving Galvus its approval. Why the holdup?

The FDA wants more data studying Galvus in patients with impaired kidneys. It had been thought that Galvus might have an advantage because it is not processed by the kidneys, while Januvia is. But another molecule created when the body metabolizes Galvus does build up in the kidney.

In the Feb. 1 issue of The New England Journal of Medicine, David M. Nathan, a Harvard Medical School endocrinologist, noted that it was surprising that the FDA decided to clear Januvia at all, given the "paucity of published data from long-term clinical trials on its safety and efficacy." Nathan is a consultant for Novartis and other drug makers but not Merck.

There are several potential concerns about DPP-4 drugs, clear evidence has not turned up in clinical trials so far. The medicines could affect the immune system, because a receptor on immune cells is very similar to DPP-4. Merck says that Januvia was designed to bind only to the DPP-4 enzyme, reducing the chances of these side effects. Patients with impaired kidneys have more of the drug in their bloodstream and would be more likely to experience side effects.

A report published in Diabetes Care says C-peptide improves sensory nerve function in type 1 diabetic patients with early-stage diabetic neuropathy. Thanks to Scott Strumello's comment, earlier today, I couldn't help but query the world wide web for more information on this C-peptide revelation. If I forget to mention it - thanks a million, Scott!

C-peptide was shown to be a significant factor in the maintenance of microvascular function. In a 6 month study of type 1 diabetes patients receiving replacement C-peptide, their nerve functions improved remarkably. A randomized study of 139 patients received one of 3 daily treatments: 1.5 mg of C-peptide, 4.5 mg of C-peptide, or placebo. At the beginning of the study, the sensory and motor nerve conduction velocities were significantly reduced compared with normal. After 6 months of treatment, peak sensory nerve conduction velocities improved in the groups treated with low-dose or high-dose C-peptide, but not significantly compared with the control group. The study showed a significant advantage in nerve functions for those treated with C-peptide (37%) verses those in the control group (19%). Overall, there were no adverse drug reactions reported from treatment of C-peptide.

At this time, there is strong evidence supporting the belief that C-peptide may be beneficial not only for nerve function, but also for the treatment and prevention of other long-term complications caused by type 1 diabetes such as nephropathy and perhaps retinopathy. Phase II clinical studies are ongoing at this time to demonstrate the safety and efficacy of C-peptide replacement therapy for the treatment of diabetic peripheral neuropathy. I can hear the trumpets playing already. I'll be right there with pen-in-hand ready to sign the dotted line for such a study. Thank you, Scott and thank you, Creative Peptides.

Despite claims by zinc supplement manufacturers that the pills can help prevent type 2 diabetes, clinical trials do not support this hypothesis.

Laboratory research suggests that zinc helps promote the production and action of insulin. A four-week study of 56 obese women found that zinc did not have an effect on factors associated with the development of diabetes. This study was an example of one trial that treated 56 people with either zinc or a placebo for four weeks and found no effect. This single trial is too small and too short to tell us anything about the effectiveness of zinc in preventing the development of type 2 diabetes.

Research does support that zinc plays a key role in the regulation of insulin production and glucose utilization. Diabetics have shown a zinc deficiency, which impairs their ability to use glucose. However this fact does not confirm zinc as a supplement to prevent the development of diabetes. I apologize it's a nonevent insofar as news. But look at it this way – it's one trial. Nobody says you have to cross it off your list because 56 obese women didn't see a change in their risk factors for developing diabetes. One study is not gospel.

A small molecule has been identified that controls diabetes in mice and may pave the way to the development of easier treatment for adult-onset diabetes.

This key molecule, called Boc5, can stimulate insulin function and reduce body weight by 20%. The molecule stimulates the production of the glucagon-like peptide1 (GLP1), responsible for metabolizing glucose. The study intended to discover ways to sensitize insulin by stimulating production of GLP1. Boc5 is not powerful enough to become a diabetes or weight loss drug. But researchers suggest that similar compounds could join the latest generation of diabetes drugs, called "incretin mimetics." The first FDA-approved incretin mimetic was Byetta. A second such drug, with the generic name liraglutide, is in clinical trials.

The problem with the existing FDA approved incretin mimetic treatments is that they are large molecules that must be administered through injection. Boc5 is a small fry with big potential. Being a smaller molecule gives hope for a new generation in diabetes treatment in the form of a pill many of us would be happy to swallow.

Diamyd Medical's flagship drug, Diamyd, is showing promising results in reducing the need of insulin injections and preventing the destruction of beta cells.

Diamyd has demonstrated significant efficacy in preserving insulin production in 70 children and adolescents with type 1 diabetes. No serious adverse events associated with the therapy were observed. The results from the Diamyd study demonstrate that the group of 35 recently diagnosed type 1 diabetes patients that received Diamyd produced approximately twice as much meal stimulated insulin (as measured by C-peptide) 15 months after the first treatment as compared to the placebo group. Preserving insulin-production is crucial for delaying the complications associated with long-term diabetes which cost billions of dollars to treat. Furthermore, it may allow for regeneration of beta cells in a non-autoimmune environment, thus setting the stage for a cure of the disease.

"We look forward to opening the dialog with the FDA regarding the potential initiation of our clinical program for Diamyd in the US" says Anders Essen-Möller, CEO of Diamyd Medical. "We obviously cannot predict the outcome of any meeting with the regulatory authorities, but we hope we will gain some valuable guidance towards structuring a suitable US clinical program for the continued development of Diamyd as a therapy for type 1 diabetes." Anders-you let me know if the regulatory authorities give you any funny business. I'll see what the diabetic community has to say about it. The buck stops here!

Canadian researchers report that the drug, Avandia, approved for the treatment of type 2 diabetes, may help prevent the disease from developing in high-risk individuals.

In the Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medications (DREAM) trial, the Canadian team randomly assigned nearly 5,300 adults from clinics in 21 countries to get 8 milligrams of Avandia or a placebo daily for three years. All of the participants were at high risk of developing type 2 diabetes, having already shown signs of poor blood-sugar control. Over the course of the trial, 280 people (12 percent) taking Avandia went on to develop type 2 diabetes compared with 658 people (26 percent) who received the placebo, the researchers report.

The DREAM researchers announced their findings at a meeting of the European Association for the Study of Diabetes, in Copenhagen. The results of the Avandia arm of the study are also published in the Sept. 15 online edition of The Lancet. The results of the Altace arm of the study will appear in the Oct. 12 print edition of the New England Journal of Medicine; the findings were released Friday, to coincide with the presentation in Copenhagen.

The president for medicine and science of the American Diabetes Association, Dr. Larry C. Deeb is horrified by the diabetic explosion going on around us. He fears that diabetes prevention is becoming a pharmacological intervention. People would rather pop a pill than implement a healthier diet and exercising. Sadly, I must agree with you, Larr. The road to hell is paved with good intentions.