diabetes

Oramed Pharmaceuticals, Inc. (OTCBB ORMP.OB), a developer of oral drug delivery systems, announced that it has received approval from the Institutional Review Board (IRB) to commence human clinical trials of an oral GLP1 Analog. This approval was granted after successful preclinical results were reported. The trials will be conducted on healthy volunteers at Hadassah University Medical Center in Jerusalem.

Currently, all GLP1 Analogs are only available as injections. The oral administration of GLP1 Analogs may convey physiological advantages for diabetic patients, as the hormone mimics the physiological route of incretin absorption.

GLP1 analogs belong to the incretin family of drugs which have pleiotropic effects desirable in the management of diabetes. Among the most notable effects are its insulinotropic actions and resultant reduction in blood glucose levels, inhibition of glucagon secretion and restoration of β cell mass. GLP1 analogs are also associated with weight loss, an added benefit to diabetes control.

“The move from preclinical trials to human clinical trials of ORMD0901 marks a strategic milestone for the company. We have expanded our platform technology and will now have the opportunity to demonstrate its effectiveness in another important family of polypeptide drugs for diabetes, which is currently only available in injection form,” said Oramed CEO Nadav Kidron.

Oramed is currently conducting Phase 2b clinical trials of its flagship product, ORMD0801, an oral insulin capsule.

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In one of the longestterm randomized trials of its kind, researchers compared the effects of a Mediterraneanstyle diet versus a typical lowfat diet for diabetes management. The trial was designed to assess the effectiveness, durability, and safety of the two diets on the need for diabetes medications in overweight patients with newlydiagnosed type 2 diabetes.

Researchers randomly assigned 215 patients to follow either a low carbohydrate, Mediterraneanstyle diet or a lowfat diet for four years. Nutritionists and dietitians counseled both groups in monthly sessions for the first year and bimonthly sessions for the next three years. After four years, 44 percent of patients in the Mediterraneanstyle diet group required antihyperglycemic drug therapy compared to 70 percent in the lowfat diet group. Patients in the Mediterranean diet group also experienced greater weight loss and an improvement in some coronary risk factors.

Patients on a Mediterranean diet mainly consume fruits, vegetables, nuts, seeds, fish, and whole grains. The diet focuses on natural foods and healthy fats while eliminating processed foods.

UCSF researchers have identified the two key circuits that control a cells ability to adapt to changes in its environment, a finding that could have applications ranging from diabetes and autoimmune research to targeted drug development for complex diseases.

The new findings are featured as the cover story in the August 21, 2009 issue of the journal Cell and are available online at cell.com.

The limited number of circuits that can achieve adaptation represents a fundamental shift in our understanding of this important biological behavior, which previously had been thought to be affected by hundreds of different circuits, according to Chao Tang, PhD, who was cosenior author on the paper with Wendell Lim, PhD.

Both Lim and Tang are faculty members in the UCSF departments of Bioengineering and Therapeutic Sciences and of Biochemistry and Biophysics, and are affiliated with the California Institute for Quantitative Biosciences (QB3) at UCSF.

Adaptation is a fundamental property of many cellular sensing systems, allowing the cell to automatically reset itself after responding to a stimulus, Lim said. These adaptive circuits are what enable eyes to adjust to changes in light, white blood cells to move toward bacteria, or insulin levels to adjust to sugar loads. They are involved in heat adaptation, movement, sight and smell, among others. They also are often the mechanisms that go wrong at a molecular level in some of the most difficult diseases to treat.

“Many diseases are diseases of homeostasis,” explained Lim, who is also affiliated with the Howard Hughes Medical Institute. “Diabetes or autoimmune diseases, for example, are based on a disruption in the circuitry that prevents the body from readjusting itself.”

Until now, however, the millions of circuits involved in that adaptive response were impenetrably complex.

For this research, the team used a computational method to analyze 160 million circuits that come into play when a cell adapts to environmental stimuli and monitored them for the circuits sensitivity to a stimulus and the precision of its adaptation.

The result was an exhaustive circuitfunction map of enzymatic regulatory networks that identified two core structures that are common to every adaptive response, however simple or complex a negative feedback loop with a buffering node, and a feedforward loop that adjusts the proportion of response. Furthermore, the researchers said, they established that the most robust adaptive responses rely heavily on at least one of these two minimal motifs.

“This is a new way of looking at biology and disease,” Lim said. “Weve sequenced the genome, we know the genes involved and have started to understand how theyre connected together. But its like opening your computer and looking at the chips and circuits inside how do you begin to understand it?”

Unlike chemistry, in which the core elements were understood 100 years ago, there is no equivalent of the periodic table in the field of biology. The field of systems biology, in which both Lim and Tang focus, aims to create that same systematic approach to understanding how cells and biological systems work.

The goal is to break down the overwhelming amount of information that has been generated by advances over the last decade in genetic sequencing, into recognizable modules that can then be further studied, understood and ultimately used to create drug therapies for complex diseases such as cancer and diabetes that involve multiple genes.

Thus, beyond the specific advance in this particular research, the teams ability to reduce millions of cellular responses to two common circuits lays the groundwork for similar analyses in other biological systems. Despite the diversity of possible biochemical networks, the team said, it may be common to find that only a finite set of core structures can execute a particular function.

“From a scientific standpoint, this is about one thing Are there universal principles in biology, and if so, what are they,” Tang said.

The potential applications from these studies could be tremendous in medicine, an understanding of what causes a system to shift from one behavior to another could greatly aid in developing more targeted therapeutics for treatments of complex diseases like cancer, the researchers said.

Fundamentally, the complex network of homeostatic response is what makes these diseases so difficult to tackle therapeutically, according to the research team. If the entire network is out of balance, a drug that blocks a single receptor wont work. Identifying the core structures behind adaptive response, however, makes it possible to someday create a therapy that could readjust that network.

It also could have applications in the emerging field of synthetic biology, by serving as a manual for how to engineer robust biological circuits that carry out a target function.

The lead investigator on the paper was Wenzhe Ma, a visiting scholar in the Tang lab from the Center for Theoretical Biology, Peking University, Beijing, China. Coauthors were Ala Trusina, from the UCSF Department of Bioengineering and Therapeutic Sciences, and Hana ElSamad, with the UCSF Department of Biochemistry and Biophysics. Both Lim and Tang have joint appointments in the UCSF Department of Bioengineering and Therapeutic Sciences, in the School of Pharmacy, and in the School of Medicines Department of Biochemistry and Biophysics. Lim is also a member of the Department of Cellular and Molecular Pharmacology, and the Howard Hughes Medicial Institute. All coauthors on the paper are affiliated with the California Institute for Quantitative Biosciences (QB3) at UCSF.

Support for Tangs research came through grants from the Li Foundation, Sandler Family Supporting Foundation, National Science Foundation, Ministry of Science and Technology of China, and National Natural Science Foundation of China. Lim also received support from the Howard Hughes Medical Institute, the Packard Foundation and the NIH Nanomedicine Development Centers. The authors report no conflicts of interest on this research.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduatelevel education in the life sciences and health professions, and excellence in patient care.

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Kristen Bole

Richard Chapman, from Selsdon, near Croydon, stood on Trafalgar Squares Fourth Plinth yesterday from 9pm to 10pm to raise funds and awareness for Diabetes UK.

The Fourth Plinth in Trafalgar Square, London, is the central part of an art project by Antony Gormley. Called One and Other, the project sees a different person, selected randomly from a pool of thousands, stand on the plinth for an hour, every day, 24 hours a day, for 100 days.

Richard, 34, who has had Type 1 diabetes for 20 years, has been gathering sponsorship over the last few weeks for his onehour plinth stint.

He said “I have lived with Type 1 diabetes since I was 14 and want to support the great work that Diabetes UK does in funding research projects, providing information and support, and campaigning and lobbying for high quality healthcare for all people with diabetes.

“It was a great feeling to be on the plinth, getting a pigeons eye view of Londons most famous square. I originally set out to raise a fiver for each minute of my hour spent on the plinth, and thanks to peoples generosity have exceeded that target.

“Although Im now back on the ground people can still sponsor me and every penny will still go to Diabetes UK. I also hope that by going public about my diabetes for an hour on the Fourth Plinth, Ive made more people aware of diabetes.”

Holly de la Nougeréde, Fundraising Events Coordinator at Diabetes UK, said “Diabetes UK is delighted that Richard stood on the Fourth Plinth raising vital funds and awareness.

“Diabetes is a serious condition. If not managed effectively, it can lead to longterm complications such as heart disease, kidney failure and blindness. Fundraisers like Richard do a fantastic job in raising money to help Diabetes UK continue our work to improve the lives of people with diabetes.”

During his hour on the plinth, Richard raised awareness that one person is diagnosed with diabetes every three minutes by marking a whiteboard.

Richard has a Just Giving site set up, so to sponsor him, visit justgiving.com/richardontheplinth, until 14 August. Visit our Flickr page to see more pictures of Richards time on the Plinth.

Johnson & Johnson has announced that Axel Ullrich, Ph.D., director of the Department of Molecular Biology at the Max Planck Institute of Biochemistry in Germany, whose discoveries have led to novel cancer therapies including Herceptin® (trastuzumab) , is the winner of the 2009 Dr. Paul Janssen Award for Biomedical Research. An independent committee of worldrenowned scientists selected Dr. Ullrich, who on September 8 will receive a $100,000 prize during a ceremony in Beerse, Belgium.

“Dr. Ullrich was chosen for his pioneering work in applying molecular biology and molecular cloning to the discovery of protein therapeutics for the treatment of a wide range of diseases, including diabetes and cancer,” said Solomon Snyder, M.D., distinguished service professor of Neuroscience, Pharmacology and Psychiatry, Johns Hopkins School of Medicine and chairman of The Dr. Paul Janssen Award Selection Committee.

“He is one of few basic scientists whose work not only has influenced academic research, but also has helped millions of patients suffering from major chronic diseases,” Snyder continued. “We received a number of outstanding nominations for this years Award and are pleased to acknowledge Dr. Ullrich with this distinction. His work has had a remarkable impact on human health and truly embodies the efforts of the Awards namesake, Dr. Paul, who helped save millions of lives through his contribution to the discovery and development of more than 80 medicines.”

Ullrich has pioneered the translation of genomicsbased discoveries into novel approaches for the treatment of major diseases. Working at Genentech, Inc. in the early 1980s, he developed genetically engineered human insulin, the first therapeutic derived from gene cloning. In 1987, Ullrich and collaborators discovered that the neu/HER2 gene is amplified and overexpressed in more than 30 percent of invasive breast cancers. HER2 was chosen for the development of an entirely novel cancer therapy, culminating in the production of an antiHER2 monoclonal antibody that since 1998 has been used successfully to treat patients with metastatic breast cancer. This was the first targeted therapeutic agent developed on the basis of a newly discovered gene with an oncogenic function in human cancer.

In the early 1990s, Ullrich identified the signaling system involved in regulating tumor angiogenesis, the growth of blood vessels in tumors. He discovered that inhibiting a key player in the signaling system (called vascular endothelial growth factor receptor or VEGFR) suppresses the generation of blood vessels in tumors and slows down cancer cell growth. Years later, a small molecule inhibitor of the VEGFR2 kinase function was developed, from which a derivative was approved in 2006 for the treatment of kidney carcinoma and gastrointestinal stromal tumors.

“It is an honor to receive an award of this stature and to be recognized among so many outstanding scientists,” said Ullrich. “Dr. Paul is a legend whose work had a tremendous impact on combating some of the worlds most serious diseases. Four of the more than 80 medicines he developed are on the World Health Organizations list of essential medicines.”

“Johnson & Johnson is pleased the Selection Committee chose Dr. Ullrich as the recipient of the 2009 Dr. Paul Janssen Award, as we believe that his discoveries capture the spirit and legacy of Dr. Paul,” said Paul Stoffels, M.D., global head, Research & Development, Pharmaceuticals, Johnson & Johnson. “Dr. Pauls passion for his work and dedication to creating lifesaving therapies for the individuals most in need should continue to serve as an inspiration to the scientific community as we carry on with our quest to care for the world, one patient at a time.”

Nominations for the 2010 Dr. Paul Janssen Award will open in September and submission details will be announced at that time.

About The Dr. Paul Janssen Award

Established by Johnson & Johnson, The Dr. Paul Janssen Award salutes the most passionate and creative scientists in basic or clinical research whose scientific achievements have made, or have strong potential to make, a measurable impact on human health. The Dr. Paul Janssen Award is named for Dr. Paul Janssen, who founded Janssen Pharmaceutica, N.V. in 1953. Known to his colleagues as “Dr. Paul,” Janssen was one of the 20th centurys most gifted and passionate researchers, a physicianscientist who helped save millions of lives through his contribution to the discovery and development of more than 80 medicines, of which four are on the World Health Organizations list of essential medicines. In 1961, Janssen Pharmaceutica, N.V. joined the Johnson & Johnson Family of Companies. Janssens legacy continues to inspire Johnson & Johnson and its commitment to finding innovative cures for unmet medical needs.

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Seema Kumar, Johnson & Johnson Pharmaceutical Services, L.L.C

One of the worlds most respected medical journals, the New England Journal of Medicine, is publishing a landmark study this week that explores treatments for people with both Type 2 diabetes and coronary artery disease. The Lang Research and Education Center of New York Hospital Queens was one of the sites that conducted this study.

The study, known as BARI 2D, (Bypass Angioplasty Revascularization Investigation 2 Diabetes) was also presented yesterday in New Orleans at the American Diabetes Association 69th Scientific Sessions a national medical conference. The results demonstrated that there is no difference in mortality among patients with type 2 diabetes and stable heart disease who received prompt bypass surgery or angioplasty compared to drug therapy alone. The results also showed that while prompt bypass in patients with more severe heart disease did not lower mortality, it lowered their risk of subsequent major cardiac events.

Phyllis August, M.D., M.P.H., director, Lang Research Center for Research and Education, New York Hospital Queens, served as a coinvestigator and coauthor of the study. She called the results, “very exciting and good news.” “More than 20 million Americans suffer from type 2 diabetes and many of these people also have heart disease. This deadly disease duo is affecting more and more people at increasingly younger ages.”

According to Dr. August, the message to patients is a strong one; “you can modify this disease with careful attention to prevention, managing risk factors and by following your doctors instructions.”

“The studys results provide needed guidance about which approaches can best help these patients,” said August. They also indicate that when a patient with type 2 diabetes has more severe heart disease it may be better to do bypass surgery early than to wait and simply treat with medication. For patients with milder disease who are candidates for angioplasty, it is appropriate to treat with drug therapy first.”

Background

The BARI 2D study began recruiting patients in 2001. The results are based on 2,368 patients with both type 2 diabetes and stable heart disease who were under a physicians care to control their cholesterol and blood pressure. Patients were randomized to receive drug therapy plus undergo prompt revascularization to restore blood flow either angioplasty to open blocked arteries or bypass surger ?or to receive drug therapy alone. The investigators also looked at which of two diabetes drug treatment strategies resulted in better outcomes insulinproviding (increasing the amount of insulin) or insulinsensitizing (lowering the bodys resistance to its own insulin, such as metformin or rosiglitazone). The study was not a comparison between angioplasty and bypass surgery, but rather a comparison between a prompt procedure and medical therapy alone.

The results show that fiveyear survival rates did not differ significantly between the revascularization group (88.3 percent) and the drug therapy group (87.8 percent). In addition, there was no significant difference in survival between those who received insulinproviding drugs (87.9 percent) and those who received insulinsensitizing drugs (88.2 percent). However, in the group that received bypass surgery, the rate of all major cardiovascular events (heart attacks, strokes and death) was significantly lower (22.4 percent) compared to those who received drug therapy alone (30.5 percent). This benefit appeared to be greatest in those who underwent bypass and received insulinsensitizing drugs.

BARI 2D was coordinated by the Epidemiology Data Center at the University of Pittsburgh Graduate School of Public Health and involved 49 clinical sites in the United States and abroad, including The Lang Research and Education Center of New York Hospital Queens, Flushing Queens. Major funders of the study include the National Heart, Lung and Blood Institute, the National Institute of Diabetes and Digestive and Kidney Diseases and GlaxoSmithKline.

Health care supplier Johnson & Johnson will focus on new treatments and improved tests for cancer and other diseases for which company perceives unmet needs, like diabetes, hepatitis C, and HIV, as well as using new, Washingtonsupported research techniques to gauge their effectiveness, researchers and executives said at a briefing with analysts, BusinessWeek reports.

Even as several major products have been waiting for Food and Drug Administrations approval, analysts say the company has been making strides in its own clinical trials, according to Business Week. “In keeping with the Obama administrations priorities for healthcare reform, research directors for several disease areas at J&J said their teams have been doing larger patient studies of experimental drugs that compare them to widely used treatments rather than placebos, a new trend called comparative effectiveness research. And J&J is doing more studies seeking “hard endpoints” for example, how many heart attacks or strokes are prevented by a drug, rather than improvements in cholesterol or blood sugar.”

“Patients and payers increasingly demand such information,” BusinessWeek reports, and analysts add that providing it will allow J&J to corner an instant market for the products when new treatments do gain FDA approval (Johnson, 6/4).

This information was reprinted from kaiserhealthnews.org with kind permission from the Henry J. Kaiser Family Foundation. You can view the entire Kaiser Daily Health Policy Report, search the archives and sign up for email delivery at kaiserhealthnews.org.

© Henry J. Kaiser Family Foundation. All rights reserved.

Versartis, Inc., a new company developing novel biologics with enhanced properties for patients with metabolic diseases, published abstracts for preclinical data on its two product candidates, VRS859 (exenatiderPEG) and VRS808 (glucagonrPEG), at the American Diabetes Association Scientific Sessions annual meeting beginning today in New Orleans.

Versartis, through a unique licensing agreement with Amunix, Inc., uses the proprietary Amunix recombinant PEGylation (rPEG) technology to extend the half life of established biologics. The Versartis compounds in development have the potential for significantly less frequent dosing and fewer side effects than those products currently on the market or in development.

“With VRS859, we have a product candidate that may become a best in class GLP1 analog for the treatment of type 2 diabetes. This compound has similar preclinical efficacy to exenatide in animal models; and the pharmacokinetics in four species support monthly dosing in humans. VRS859 can also be administered in a small volume with a small gauge needle,” said Jeffrey L. Cleland, Ph.D., Founder and Chief Executive Officer of Versartis.

“VRS808 has the potential to prevent nocturnal hypoglycemia in type 1 diabetes, an unmet medical need,” Dr. Cleland continued. “VRS859 and VRS808 did not have significant toxicology at very high doses in preclinical studies, including a lack of immunogenicity in all studies. We look forward to moving these products rapidly into human clinical trials to benefit diabetes patients.”

ABSTRACTS
Exenatide 1994PO “An Extended Halflife Exenatide Construct for Weekly Administration in the Treatment of Diabetes Mellitus”

The current approved regimen of exenatide for the treatment of type 2 diabetes mellitus requires administration twice a day and is effective in reducing hemoglobin A1c and body weight. Common side effects of this treatment regimen for exenatide include nausea and hypoglycemia, possibly caused by the high peak levels (Cmax) of exenatide after each injection. The ideal dosage form of exenatide would maintain the exenatide blood level in the therapeutic window for at least one week without a high Cmax, which commonly occurs with depot dosage forms. We designed an extended halflife exenatide construct that contains a long unstructured tail of hydrophilic amino acids referred to as rPEG (ExenatiderPEG; VRS859). The rPEG tail both increases the serum halflife and provides a slower rate of absorption, thus reducing the peaktrough ratio significantly from the levels seen with twice daily injection of unmodified exenatide. Attachment of rPEG to a model protein (26.9 kDa) increased serum halflife to 75 hrs with a 99% absolute bioavailability following subcutaneous administration in cynomolgus monkeys. A similar halflife extension is expected with exenatide, enabling weekly or every two week dosing in humans. The preclinical efficacy, pharmacokinetics, and immunogenicity of VRS859 will be presented. The results of these studies will enable rapid progress of the construct into human clinical trials.

Glucagon 2001PO “An Extended Halflife Glucagon Construct for the Prevention of Nocturnal Hypoglycemia”

Nocturnal hypoglycemia is a common problem for type I diabetics, especially children, often leading to death. Glucagon is typically used to treat acute hypoglycemia, but the short halflife of glucagon ( < 17 minutes) prevents its use in nocturnal applications without complicated pump or depot system approaches. A novel glucagon construct that enables a single dose to maintain basal glucose levels during sleep while minimizing the chance for long term changes in hemoglobin A1c is the ideal approach to preventing hypoglycemia. We designed an extended halflife glucagon construct that contains a long unstructured tail of hydrophilic amino acids referred to as rPEG (GlucagonrPEG; VRS808) that increases the serum halflife. Following subcutaneous administration in cynomolgus monkeys, this construct maintains blood levels within the therapeutic window for 1012 hrs and is completely cleared within 24 hrs. The in vitro potency of the construct is ~20% of natural glucagon, possibly allowing a broader dosing range. A number of characterization experiments will be presented, demonstrating the efficacy and safety of this compound in preclinical models. The data presented will include the results of a dose finding study in fasting beagle dogs, and repeatadministration immunogenicity of the construct in normal mice. The results of these studies will serve as the foundation for moving this novel construct rapidly into human studies.

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US researchers found that a drug made from the root of the hydrangea plant, which has for centuries been used in Chinese medicine, showed promising results in treating autoimmune disorders such as rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, type 1 diabetes, eczema and psoriasis.

The study was the work of researchers from the Program in Cellular and Molecular Medicine and the Immune Disease Institute at Childrens Hospital Boston (PCMM/IDI), together with the Harvard School of Dental Medicine and is published in the 5 June issue of the journal Science.

An exciting new area in the field of autoimmune disease research is learning about the role of a particular immune system cell called the T helper 17 (Th17) which is genetically different from other types of CD4+ T cell like the Th1, Th2 and Tregulatory cells and appears to play a unique role in the part of the immune system that causes harm when it overreacts.

The immune system is a complex of delicately balanced “seek and destroy” systems that recognize when something is wrong in the body and then trigger a response to repair the damage or eliminate foreign agents. However, when this delicate balance is disturbed, the responses switch on when there is nothing wrong, causing the immune system essentially to “attack” healthy tissue.

This is what happens in rheumatoid arthritis, where the overactive inflammatory response eventually destroys cartilage in the joints and even healthy tissue in places like the lungs or under the skin. Exactly how and why this happens is still a mystery, but the more scientist look into it, the more they discover that immune cells like the Th17 are involved in unique ways.

In this study, the authors report how a small molecule called halofuginone (extracted from hydrangea root) selectively stops Th17 cells being made, without affecting the other CD4+ T cells, thus showing how it might be possible to stop the immune system from overproducing harmful Th17 cell responses.

They also showed that halofuginone reduced disease symptoms in mice bred with autoimmune disorders.

In the body, cytokines cause Th17 cells to differentiate from other CD4+ T cells, but when the researchers collected cultured mouse CD4+ T cells along with the cytokines, they found that adding halofuginone made levels of Th17 go down significantly but not Th1, Th2 or T regulatory cells.

They also found a similar effect in cultured human CD4+ Tcells halofuginone selectively stopped production of IL17, the principal cytokine made by Th17 cells.

The reason this discovery is important is because there are currently no good treatments for autoimmune disorders because you cant get in there and turn down just the inflammatory process without also turning down the protective processes that for instance protect patients from infections.

The main treatments currently rely on antibodies that neutralize cytokines, the chemical messengers that T cells use to control immune fuction and inflammatory responses.

But antibodies are expensive, have to be injected and/or infused, and dont actually solve the root cause of the problem, they just mop up cytokines rather than stop them being produced in the first place. So patients have to keep coming back for infusions to keep the inflammation under control.

As a last resort you can give patients drugs that completely suppress the immune system but for obvious reasons this is very risky.

In this study the researchers appear to have found a way, using halofuginone as the fine tuning tool, to selectively reduce production of Th17 cells and thereby only switching off the inflammatory response without altering the function of other parts of the immune system. The other good thing about this discovery is that halofuginone can be taken by mouth no injection necessary.

First author Dr Mark Sundrud, of the PCMM/IDI, said

“This is really the first description of a small molecule that interferes with autoimmune pathology but is not a general immune suppressant.”

“Halofuginone Inhibits TH17 Cell Differentiation by Activating the Amino Acid Starvation Response.”
Mark S. Sundrud, Sergei B. Koralov, Markus Feuerer, Dinis Pedro Calado, Aimee ElHed Kozhaya, Ava RhuleSmith, Rachel E. Lefebvre, Derya Unutmaz, Ralph Mazitschek, Hanspeter Waldner, Malcolm Whitman, Tracy Keller, and Anjana Rao.
Science, 324 (5932), 1334, 5 June 2009.
DOI 10.1126/science.1172638

Source Childrens Hospital Boston.

Written by Catharine Paddock, PhD

From 1 June 2009, HbA1c (long term blood glucose levels) in all people with diabetes will be measured in millimoles per mol as well as by percentage, the Department of Health said today.

The UK is responding to the International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) call for all countries to adopt the same measurement to make it easier to compare HbA1c results between laboratories throughout the UK and worldwide.

Both the old and the new measurements will be given for the first two years of the change, until 31 May 2011 when people with diabetes will receive their HbA1c measurement only in millimoles per mol.

Dr. Rowan Hillson MBE, National Clinical Director for Diabetes, said,

“It is really important that people with diabetes keep their blood glucose levels under good control. Controlling the glucose in a way that is safe and appropriate for each person reduces the risk of diabetic tissue damage. People with diabetes need HbA1c blood tests to check their glucose is under good control. This necessary change in the way that HbA1c is reported is being introduced in a way that allows plenty of time for us all to get used to it.”

Simon ONeill Director of Care and Policy at Diabetes UK said

“Diabetes UK welcomes this change to the way HbA1c results are reported and we believe that this will have the additional benefit of making comparing results from international laboratories and research trials easier, as the new system will be adopted worldwide.

“For a period of 2 years people with diabetes will get their results in both percentage and millimoles per mol which will help them get used to the new system. In addition, Diabetes UK has designed a convenient online HbA1c converter tool for people with diabetes to help them through the transition. To use the calculator and for more general information on the changes and what they mean, people can visit diabetes.org.uk/HbA1c.”