DexCom Receives FDA Approval for STS(TM) Continuous Glucose Monitoring System

SAN DIEGO, March 27, 2006, (BUSINESS WIRE) -DexCom, Inc. (NASDAQ:DXCM) today announced that it has received Food and Drug Administration (FDA) approval for its STS(TM) Continuous Glucose Monitoring System, a first generation device designed to help people with diabetes more conveniently and effectively manage their blood sugar levels. Widely recognized as one of the leading causes of death and disability in the United States, diabetes is a chronic disease with no known cure that afflicts approximately 20 million people in the U.S., according to the Center for Disease Control (CDC). In the U.S., diabetes is the leading cause of adult blindness, end stage kidney failure and lower limb amputations. People suffering from diabetes are also more significantly at risk for cardiovascular disease and stroke.

"We are very pleased the FDA has approved the DexCom STS Continuous Glucose Monitoring Product and are hopeful this novel technology will improve the quality of life for people living with diabetes," said Andrew P. Rasdal, DexCom President and Chief Executive Officer.

The DexCom STS consists of a tiny wire-like sensor that is inserted by the patient just under the skin. The sensor continuously measures glucose levels which are transmitted wirelessly to the cell phone-like STS Receiver. With the push of a button, the handheld Receiver conveniently provides the patient with real-time glucose measurements and trends, as well as providing alerts to warn of high and low glucose levels. The results of a study on the DexCom STS published in the January 2006 edition of Diabetes Care, a publication of the American Diabetes Association, demonstrated patients could achieve better control of glucose levels when using the information from the DexCom STS.

"We are appreciative of the efforts by the FDA and FCC to help make this technology available to people with diabetes," said Rasdal. "Further, we are especially thankful for the support of the patients, physicians, nurses, and diabetes educators who have participated in our clinical studies supporting this approval."

DexCom management will hold a conference call starting at 4:30 PM (Eastern Time) on Monday, March 27, 2006 to discuss this important development. The conference call will be concurrently webcast. The link to the webcast will be available on the DexCom Inc. website www.dexcom.com under the investor webcast section and will be archived for future reference. To listen to the conference call, please dial (800) 811-0667 (U.S./Canada) or (913) 981-4901 (International) and use the participant code "6796471" approximately five minutes prior to the start time.

We have not sold any of our products to date. Successful commercialization of our products is subject to various risks and uncertainties, including possible delays in our development program, the inability of patients to receive reimbursements from third-party payers, a lack of acceptance in the marketplace by physicians and patients, inadequate financial and other resources, and the inability to manufacture products in commercial quantities at an acceptable cost.

Posted by dlife at 10:42 AM | Comments (0)

Infused Spleen Cells Found Not To Impact Islet Recovery and Reversal of Type 1 Diabetes in Mice

BOSTON, March 24, 2006 (Joslin) - Researchers from Joslin Diabetes Center have published in the March 24, 2006, issue of the journal Science a significant study about islet cell recovery and reversal of type 1 diabetes in mice.

It is generally believed that an effective cure for type 1 diabetes will require two substantial scientific advances. First, in order to restore the pancreas' ability to produce insulin, new islet beta cells must be provided, either by transplanting cells from a healthy donor or by encouraging the growth and/or function of the diabetic patient's own cells. Second, to protect the new beta cells, no matter what their origin, it is necessary to repair the breakdown in immunological tolerance that precipitated the anti-islet attack in the first place.

In a widely discussed paper that appeared in Science in 2003, Dr. Denise Faustman and her colleagues reported successful achievement of both of these advances, resulting in the "cure" of a substantial fraction of severely diabetic NOD mice, the most popular animal model of human type 1 diabetes. Their method entailed giving diabetic mice a
temporary islet transplant from a genetically identical mouse, administering a single injection of an immuno-stimulatory compound called Complete Freund's Adjuvant (CFA), and repeatedly injecting a large number of spleen cells taken from genetically different mice. It was thought that the islets served to keep the animals with diabetes healthy long enough for the other treatments to have their effects, that the CFA eliminated the autoimmune attack on the islets, and that the spleen cells somehow gave rise to insulin-producing cells, presumably beta-cells, ultimately leading to islet regeneration.

"The compound CFA has been used to modulate diabetes in NOD mice for a number of years in a variety of experimental contexts, so its effect was not very surprising. However, the notion that adult spleen cells from one mouse could give rise to new islets in the pancreas of another mouse was a novel and exciting one," said Diane Mathis, Ph.D., who led the Joslin study along with Christophe Benoist, M.D., Ph.D. Drs. Benoist and Mathis head Joslin's Section on Immunology and Immunogenetics, hold the William T. Young Chair in Diabetes Research, and are Professors of Medicine at Harvard Medical School.

Therefore, many research teams were interested in extending the potentially important findings of Dr. Faustman and her colleagues by defining the precise cellular and molecular mechanisms involved. As a necessary first step, the researchers needed to reproduce the results published in the 2003 Science paper. Unfortunately, this did not prove possible, as reported in three papers appearing in the March 24, 2006, issue of Science from groups based at Joslin Diabetes Center in Boston, Washington University in St. Louis and the University of Chicago, working entirely independently. For example, the Joslin team was not able to replicate the original findings even though it strove to match as closely as possible the published methods, and also incorporated supplementary details from more extensive protocols provided by the authors. In short, like the study of Dr. Faustman and colleagues, the three new studies resulted in a substantial fraction of severely diabetic NOD mice being "cured" of their hyperglycemia as well as their autoimmunity against beta cells. However, none of the teams found any evidence that new islet cells emanating from donor spleen cells were the source of the insulin responsible for the reversal of diabetes. Rather, even though severely diabetic, the host mice kept a substantial number of residual beta cells, and the recovered islets were all of host, rather than donor spleen cell, origin.

"Given recent reports from several groups that beta cells in adult mice can undergo active cell division, the most likely explanation for islet recovery in the 'cured' mice is that when the autoimmunity was suppressed, beta-cell growth was permitted -- or even promoted -- exceeding death of the beta cells," said Dr. Benoist. "An additional possibility is that eliminating the inflammation improved the function of the residual beta cells."

"The obvious implication from these new results, given that CFA is a reagent that can potentially alter the immune system, is that the donor spleen cells might not be an essential element of the Faustman protocol," Dr. Mathis said. "The original study did not report a control group in which spleen cells were left out of the treatment protocol. Both the Joslin and Washington University groups did include this important control, and found that CFA alone (plus the temporary islets) was as effective as the full protocol with its multiple injections of spleen cells. This finding again argues that the 'cure' of diabetes afforded by the Faustman protocol did not involve donor spleen cells giving rise to host islet beta cells."

Should the effectiveness of CFA alone demonstrated in these new studies prompt a reconsideration of the analogous reagent Bacille Calmette-Guerin (BCG), in isolation, to treat people with diabetes? BCG is a component of some human vaccines, like the vaccine agent used against tuberculosis, and the Faustman group has proposed using it as a treatment for type 1 diabetes. Three BCG trials large enough to be informative have previously been performed and failed to show any positive effect. "A likely explanation for the difference in results is that the injection of CFA into the footpad of mice and the injection of BCG under the skin of humans are actually radically different interventions, the former provoking a massive inflammatory response throughout the body, a procedure that is difficult to contemplate in a patient context," Dr. Benoist explained. "It should also be kept in mind that the mice were also treated with an islet transplant, the precise role of which has not really been explored. Lastly, it might be relevant that BCG has been reported to increase the incidence or accentuate the course of diabetes in humans in certain contexts."

Posted by dlife at 10:49 AM | Comments (0)

Abbott Receives FDA Clearance to Market New Blood Glucose Monitor

New Glucose Meter Requires Tiny Blood Sample, Provides Results in Just Five Seconds

ALAMEDA, Calif., March 13 (PRNewswire-FirstCall) - Abbott Diabetes Care announced today it has received 510(k) clearance from the U.S. Food and Drug Administration (FDA) to market its FreeStyle(R) Freedom(TM) blood glucose monitoring system for consumer use.

FreeStyle Freedom offers virtually pain-free testing because it measures glucose levels using a very small blood sample size (0.3 micro liter), the smallest sample size required of any blood glucose monitoring product on the market. FreeStyle Freedom provides results in just five seconds and features a large, high contrast display, making it easy to read, and easy to hold. The new meter also allows people with diabetes to test on less sensitive parts of the body such as the forearm, thigh and palm. FreeStyle blood glucose meters offer the most approved alternative testing sites of any glucose monitoring system available.

"To successfully manage diabetes, patients must monitor their blood glucose levels frequently," said Sherwyn L. Schwartz, M.D., founder and chief executive officer of the Diabetes & Glandular Disease Clinic in San Antonio, TX. "In clinical trials, we found FreeStyle Freedom to be very accurate, and the small sample size and rapid test time associated with this new blood glucose meter may make testing less painful and could ultimately encourage those with diabetes to test more often," Dr. Schwartz added.

FreeStyle Freedom uses a technology exclusive to all FreeStyle meters based on coulometric measurement. This unique, patented, electrochemical technology measures virtually all of the available glucose in the blood sample, making it ideal for measuring a small sample size. Coulometric technology has already been used by people with diabetes worldwide in more than 2 billion blood glucose tests using FreeStyle blood glucose strips.

"FreeStyle Freedom expands Abbott's product line of innovative, easy-to- use and less painful blood glucose testing devices to meet the diverse needs of people with diabetes," said Ed Fiorentino, president of Abbott Diabetes
Care.

FreeStyle Freedom blood glucose monitoring systems will be available in April, 2006.

Posted by dlife at 11:04 AM | Comments (0)

Smiths Medical Find Cinnamon Lowers Blood Glucose Levels

Cinnamon is not just a means for spicing up your food anymore. According to a recent study published in the journal, Diabetes Care, cinnamon helps lower blood glucose, cholesterol and triglyceride levels.

St. Paul, MN, March 23, 2006, (Open Press) - The report, the first of its kind, was published in Diabetes Care, illustrated cinnamon’s positive effects on lowering triglycerides, total cholesterol and LDL (bad) cholesterol. The study found that 3 grams of cinnamon a day produced the best results but no recommended dosage was named.

Cinnamon is believed to have properties that can often help people with and prone to type 2 diabetes. Studies show that cinnamon may decrease insulin resistance and allow the body to make better use of the insulin that is made in the pancreas. According to these results, cinnamon improves insulin sensitivity which in turn lowers blood glucose levels.

Although these first findings are positive more research must be done in order to determine in cinnamon can in fact help those with type 2 diabetes. With this being said, because an increase in cinnamon intake is not harmful those with type 2 diabetes are encouraged to follow the findings of the report.

Posted by dlife at 10:55 AM | Comments (0)

Procedure Cures Some Diabetic Mice, but not in the Way Previously Reported

March 23, 2006 (Washington University School) - Researchers attempting to reproduce a controversial 2003 mouse experiment suggestive of a cure for type 1 diabetes have found evidence that the experimental procedure does eliminate diabetic symptoms in a small fraction of the mice exposed to it.

However, scientists from Washington University School of Medicine in St. Louis found no signs that the procedure was working in the manner reported by the group of scientists at Harvard University who originated it.

The Washington University group is one of three labs reporting in the March 24 issue of Science on attempts to reproduce the earlier experiment. All three groups independently found no evidence of a key claim of the earlier study: that cells injected from the spleens of healthy mice had formed new insulin-producing beta cells in the diabetic mice, a finding that created hope that the approach might be used to cure diabetes in humans.

"We showed that various immunological processes had rejected the injected cells," says senior author Emil R. Unanue, M.D., Mallinckrodt Professor of Pathology and Immunology. "In the mice who were cured, we found no evidence linking restoration of beta cell function to the spleen cell injections."

Researchers are following up on the study with new experiments designed to determine how the mice were cured.

"It's a positive thing that 4 of 22 mice recovered beta cell function, and we're investigating where that recovery of beta cell function came from," says lead author Anish Suri, Ph.D., a research assistant professor of pathology and immunology in Unanue's lab. "Conceivably, controlling the autoimmune response in patients with early diabetes may allow for recovery of some beta cell function and a degree of reversion of the diabetic process."

As in the 2003 experiment, researchers performed their studies in female mice from the NOD mouse strain, which develops diabetes in a manner very similar to human type 1 diabetes mellitus. Between the age of 20 and 30 weeks, immune system cells in the mice begin attacking beta cells in the pancreas, leading to death of the cells and onset of diabetic symptoms such as hyperglycemia, or abnormally high blood sugar levels.

Following the procedures developed for the prior study by Harvard researcher Denise L. Faustman, Washington University scientists gave the mice injections of a solution called complete Freunds adjuvant (CFA) that contains water, oil and portions of dead bacteria. Scientists had previously established that such injections stop immune attacks on beta cells.

Researchers also gave the mice repeated large injections of spleen cells from healthy male mice. Faustman's group has hypothesized that the spleen is erroneously promoting the survival and reproduction of immune cells that attack beta cells; they theorize that injections of spleen cells from healthy mice will help reset this dysfunctional selection mechanism.

Finally, scientists took islets, structures in the pancreas containing insulin-producing beta cells, from healthy mice and transplanted them into one of the diabetic mice's kidneys.

The experimental procedures began when the mice first became hyperglycemic, indicating that a substantial portion of their beta cells had died off as a result of immune assault. In 22 of 53 mice, the injections and the transplant restored normal blood sugar levels. Scientists followed these mice for at least 120 days, continuing to give them spleen cell injections. Then they removed the kidney with the transplanted islets.

This caused 18 of the 22 mice to revert to hyperglycemia and diabetes. Studies of the four mice that continued to have normal blood-sugar levels revealed signs that the pancreas was regaining beta cell mass and function.

In the 2003 study, scientists looked in the pancreas of cured mice for indications of the presence of the Y chromosome, the male sex chromosome. When they found it, they interpreted this as proof that stem cells from the spleen cell injections, which all came from male mice, had developed into new beta cells in the diabetic mice, which were all female.

Washington University scientists did not see this same indicator or any other signs that the male spleen cells had survived in cured mice.

"This idea that spleen cell injections not matched for immune compatibility could lead to new beta cells was very controversial," Unanue says. "Everything we know in immunology suggests that such injections should be rejected by the immune system."

In a second test performed after they repeated the earlier experiment, researchers gave the mice the CFA injection and the islet transplants but did not give spleen cell injections. For periods of more than 100 days, this temporarily cured diabetes in 69 percent of the mice that received it (20 of 29). The procedure that included the spleen injection had a temporary cure rate of 42 percent.

Laboratories at the Joslin Clinic in Boston, a hospital affiliated with Harvard Medical School, and the University of Chicago also found they could not reproduce the 2003 results. The three laboratories had no contact prior to acceptance of their manuscripts for publication by Science.

Posted by dlife at 10:53 AM | Comments (0)

Efforts to Replicate Controversial Diabetes Therapy Bring Partial Success

Researchers have been able to confirm most but not all of the results of a high-profile study that brought new hope to diabetes patients. This study provides a boost for efforts to reverse type-1 diabetes in recently diagnosed patients but not for efforts to grow new islets from spleens.

March 23, 2006 (Newswise) — An effort by researchers at the University of Chicago to confirm the results of a high-profile study that brought extraordinary hope to diabetes researchers and patients worldwide has met with considerable, but not complete, success. The researchers were able to reverse type-1 diabetes in one-third of mice but were unable to find any evidence of insulin-producing beta cells derived from donated spleen cells, initially thought to be a crucial component of the therapy.

Two other research teams, one from Harvard University and one from Washington University in St. Louis, found similar results. All three papers are published in the March 24, 2006, issue of Science.

"Using a protocol that was identical to the original study, we were able essentially to cure 32 percent of treated mice, which was quite encouraging, even though it was less than the 67- to 92-percent cure rates previously reported," said transplant immunologist Anita Chong, Ph.D., associate professor of surgery at the University of Chicago and lead author of the study. "We saw no evidence, however, of spleen-derived beta cells in the pancreas, despite using very sensitive tests."

While the results provide a boost for efforts to reverse type-1 diabetes in recently diagnosed patients by manipulating the immune system, they come as a disappointment for those who hoped to cure established diabetes by using stem cells from donor spleens to help patients grow new pancreatic islets.

In type 1 diabetes, the body's immune cells mistakenly attack the insulin-producing beta cells found in the pancreatic islets. As the islets die, insulin production ceases and blood sugar levels rise, damaging organs throughout the body.

One of the most promising treatments is islet transplantation, in which islets are extracted from a donated pancreas and injected into the patient's liver, where they take up residence and begin making insulin, restoring control of blood sugar levels. Widespread use of islet transplantation is constrained, however, by the challenges of preventing the recipient's immune system from attacking the transplanted islets, and by the extreme shortage of pancreas donors.

A paper published by Denise Faustman and colleagues at Harvard Medical School in Science on November 14, 2003, on "Islet Regeneration During the Reversal of Autoimmune Diabetes in NOD Mice," appeared to provide a way around both hurdles. In that paper, Faustman argued that her team had been able to cure diabetic mice by disrupting the immune system's attack on the insulin-producing beta cells and injecting the mice with cells from the spleens of other mice, which would "rapidly differentiate into islet and ductal epithelial cells within the pancreas."

"It was immediately clear that this could be extremely important," said diabetes specialist Louis Philipson, M.D., Ph.D., professor of medicine at the University of Chicago and senior author of the paper. "Patients wait years for pancreatic islets. We have hundreds of people on our waiting list, yet we perform only a few islet transplants a year. Having a plentiful source of potential islet cells is our dream, so the news was almost too good, which is why the diabetes community wanted to see this replicated before it moved into human trials."

The three papers in the current issue of Science attempt to replicate that work. With funding from the Juvenile Diabetes Research Foundation, the Chester Foundation and the National Institutes of Health, Chong, Philipson and colleagues set out to copy the Faustman protocol exactly -- with one slight twist.

They worked with non-obese diabetic (NOD) mice, a common model for studies. When the mice developed severe diabetes, they injected one foot pad of each mouse with Freund's complete adjuvant, a potent mixture that can over-stimulate the immune cells that cause diabetes. To protect the mice from the ravages of their diabetes during the study, they temporarily transplanted 400-500 islets per mouse under one kidney capsule. And they injected the mice with spleen cells.

In the original study, the treated mice were all female and the spleen cells came from male donors. The presence of a Y chromosome served as a marker for donated cells, a technique that, according to Philipson, can be "fraught with technical artifacts." Instead, Chong and Philipson used spleen cells from mice that expressed the transgene for green fluorescent protein (GFP) driven by the insulin promoter. So if any of these spleen cells begin to produce insulin, they would glow bright green, making then easy to detect.

They treated 22 mice. Seven of those mice (32%) maintained normal blood sugar levels for the duration of the study, 90 to 100 days. Although one died from unrelated causes, the kidney containing the transplanted islets was removed from the remaining six mice. All six continued to maintain normal blood sugar levels for an additional 29 to 42 days. This suggested that the 'cured' diabetic mice now had enough beta cells to maintain normal blood glucose without the transplanted islets.

In none of those mice, however, was the pancreas normal. Mice of this age would ordinarily have about 2,000 small islets, scattered throughout the organ. These mice had about a dozen extremely large islets, five times normal size, composed almost entirely of beta cells and surrounded by white blood cells. Total beta-cell volume in treated mice was about 22 percent of normal for mice of that age, but it was enough to maintain normal blood sugar levels.

However, no beta cells expressing GFP were detected in any of the islets examined or in the organs outside the pancreas. "Our data," the authors note, "do not support a conclusion of beta-cell regeneration from spleen-derived stem calls."

"The question we are now addressing is the source of these beta cells," Philipson said. "They could be beta cells that survived the initial immune onslaught, recovered and replicated. Or they could be pancreatic stem cells, which had matured into beta cells once autoimmunity was controlled."

Despite the inability of any of the three teams to replicate that aspect of the study, the authors were encouraged by their other successes. "Our studies confirm that autoimmune diabetes can be reversed," they conclude, "and that sufficient beta-cell mass can be restored to cure diabetic NOD mice with the treatment protocol developed by Faustman and colleagues."

Posted by dlife at 10:51 AM | Comments (0)

Reduced Insulin in the Brain Triggers Alzheimer's Degeneration

Providence, RI, March 23, 2006 (EurekAlert) – By depleting insulin and its related proteins in the brain, researchers at Rhode Island Hospital and Brown Medical School have replicated the progression of Alzheimer's disease – including plaque deposits, neurofibrillary tangles, impaired cognitive functioning, cell loss and overall brain deterioration – in an experimental animal model. The study demonstrates that Alzheimer's is a brain-specific neuroendocrine disorder, distinct from other types of diabetes.

In the study, brain deterioration was not related to the pancreas, which regulates insulin for the body. When pancreatic insulin is deficient or the body fails to respond to it, the result is type 1 or type 2 diabetes. Previous work by the researchers with postmortem brain tissue of Alzheimer's patients showed a strong link between insulin depletion in the brain and Alzheimer's disease, raising the possibility that Alzheimer's is a neuroendocrine disorder, or a type 3 diabetes.

"We have demonstrated that a loss of insulin in the brain triggers the onset of Alzheimer's, probably because as the brain loses insulin, the cells that require insulin to function and survive also eventually die. The consequences are increased oxidative stress, brain deterioration, loss of cognitive function, and a buildup of plaques and tangles in the brain – all hallmarks of Alzheimer's, says senior author Suzanne M. de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital and a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI.

"We now know that if you specifically target insulin and its actions in the brain, you could develop new treatments for this disease," de la Monte says.

The study is published in the current issue (Volume 9, Issue 1) of the Journal of Alzheimer's Disease (http://www.j-alz.com).

Researchers injected the brains of rats with Streptozotocin (STZ), a compound that when metabolized, destroys beta cells in pancreatic islets and produces diabetes. When injected directly into the brain, the treatment caused neurodegeneration, while the pancreatic islet cells remained intact. That is because insulin depletion produced by STZ was confined to the brain, just like what occurs in most cases of Alzheimer's.

"This study provides definitive evidence that impairments in insulin/IGF signaling and deficiencies in the corresponding growth factors can occur in the central nervous system (CNS) independent of type 1 or type 2 diabetes," the authors write.

As a result of the treatment, insulin and its IGF-I receptors were significantly reduced in the brain, triggering a cascade of neurodegeneration. Both insulin and IGF-I activate complex signaling pathways downstream, prompting energy metabolism and growth required for learning and memory, and inhibition of oxidative stress, which unchecked could trigger neurodegeneration. As insulin was depleted, neurons died and the brain dropped to half its size, a result of atrophy which is a prominent feature of Alzheimer's. At the same time, there was an increase in astrocytes and microglial cells, which are responsible for neuroinflammation, another critical and consistent feature of Alzheimer's and probably related to the increased amyloid deposition in the brain, the researchers say.

Also, there was increased activation of a kinase called GSK-3 beta. This kinase is overactive in Alzheimer's and triggers tau phosphorylation, which is known to be at the core of neurofibrillary tangles. The researchers had previously shown that tau is regulated by insulin and insulin-like growth factor (IGF-I). In the current research, they found that as insulin and IGF-I were depleted in the brain, the expression of GSK-3 beta increased, leading to oxidative stress and cell death.

While the link between insulin and tau had been established, researchers also looked at the connection between insulin and amyloid precursor protein gene expression, as increased levels could account for amyloid accumulation, or the buildup of plaques in the brain. They found that amyloid beta deposits in vessels and plaques did build up in the brain, and they suggest that these abnormalities occurred due to increased oxidative stress.

Another feature of Alzheimer's affected by impaired insulin signaling, acetylcholine deficiency, is linked to dementia and has long recognized as an early abnormality in Alzheimer's. The enzyme that makes acetylcholine, choline acetyltransferase (ChAT), was previously found to be regulated by insulin and IGF-1. In brains with Alzheimer's, impairment of insulin and IGF-I signaling mechanisms correlate with deficits in acetylcholine production. In this study, ChAT was markedly reduced in the experimental Alzheimer's model.

"Our previous work has shown that many of the important features of Alzheimer's – such as the accumulation of phosphorylated tau and the death of neurons – were somehow linked to insulin deficiency in the brain. This study shows that insulin is the controlling factor in all of these features of Alzheimer's disease," de la Monte says.

"The evidence suggests that impaired insulin and IGF signaling must be addressed in order to make significant progress in the treatment and prevention of Alzheimer's disease," she says.

Posted by dlife at 10:46 AM | Comments (1)

Diabetes Research Yielding Breakthrough Success

University of Calgary bioengineering team successfully growing insulin-producing cells in lab

March 16, 2006 (Eurekalert) - Freedom from insulin injections and the myriad of health problems related to type 1 diabetes is closer to becoming reality, thanks to University of Calgary researchers who are developing the first bioreactor procedures to grow pancreatic cells in their laboratory. This opens the door to the possibility of providing a steady supply of insulin-producing cells that can be transplanted into patients affected by this serious disease.

"This is a significant milestone on the path to effectively producing human tissue that may be used to treat type 1 diabetes," said Dr. Leo Behie, professor of chemical engineering in the Schulich School of Engineering and holder of a Canada Research Chair in BioMedical Engineering. "The precursor cell type we are using appears to be a good candidate and brings us much closer to clinical trials," Behie said. "There is a huge international push to find a human pancreatic cell source-- a 'holy grail' of sorts-- that could be used for transplantation. Once it is found, our lab will be ready to grow these cells in a clinically acceptable manner."

In a study funded by the New York-based Juvenile Diabetes Research Foundation (JDRF) to appear shortly in the journal Biotechnology Progress, Behie's team developed bioreactor protocols to produce large quantities of pig pancreatic insulin-producing cells that has set the stage for the large-scale production of islet-like structures containing insulin-producing cells. This work was conducted at the Pharmaceutical Production Research Facility (PPRF) and included U of C colleagues Meera Chawla, Cheryl Bodnar, Michael Kallos and Arindom Sen.

In a second paper available online for the journal Biotechnology and Bioengineering, Behie and colleagues report that they have cultured human cells that are believed to be good candidates for generating islet cells that can make insulin. The study sponsored, by the Canadian Stem Cell Network, included Cheryl Bodnar, Michael Kallos and Arindom Sen, in collaboration with Maria Petropavlovskaia and Lawrence Rosenberg from McGill University's Faculty of Medicine. The successful growth and characterization of these functional islet cells in the lab led to the conclusion that they may be suitable for treating individuals with type 1 diabetes, formerly known as juvenile diabetes, which requires patients to receive multiple daily insulin injections in order to survive.

"This is very encouraging news for people with type 1 diabetes who look forward to a future without this serious condition," said Donna Lillie, Vice President, Research and Professional Education, Canadian Diabetes Association. "Dr. Behie's all-Canadian team has brought us one more step towards potentially securing a large supply of insulin-producing pancreatic cells for transplantation into individuals with type 1 diabetes."

Scientists at the University of Alberta were the first to successfully transplant islet cells into people with diabetes in 2000, freeing them from insulin injections. Follow-up studies have shown that the transplanted cells continued to function in many of these so-called Edmonton Protocol patients for up to five years. However, a significant bottleneck to treating large numbers of people with type 1 diabetes using this approach is that it takes pancreas cells from as many as three donor cadavers to supply enough for one patient transplant.

"Injecting islet cells into people with diabetes has gotten people off insulin. The problem is there aren't enough cells available to treat everyone," Behie said. "If we can expand cell populations in our bioreactors, we'll be able to supply everyone who needs them and dramatically improve their quality of life."

About 10 per cent of Edmonton Protocol transplant recipients have been able to stay off insulin after five years, and patients are required to take anti-rejection drugs after receiving the new cells. By producing a reliable supply of cells, Behie said he hopes people with type 1 diabetes will one day be able to receive booster shots of islet cells, as required, and that producing cloned cells from individual patients could result in the elimination of transplant rejection issues.

Behie is the only Canadian member of a "dream team" of researchers established by the New York-based Juvenile Diabetes Research Foundation International (JDRF) last year in hopes of accelerating the development of new therapies and possible cures for type 1 diabetes. The 16 researchers from 13 universities around the world are trying to uncover the cause of type 1 diabetes that affects more than 19-million people worldwide, and investigating various potential cures including new drug therapies and islet cell regeneration techniques. Type 1 diabetes affects about 19 million people worldwide, while type 1 and 2 diabetes affects approximately 194 million.

Posted by dlife at 10:57 AM | Comments (0)

Biotech Firm Announces Additional Preliminary Results in Type 1 Diabetes Trial

TORONTO, 03/15/2006 (MARKET WIRE) - Generex Biotechnology Corporation (NASDAQ: GNBT), a leader in the area of buccal drug delivery, announced today additional preliminary results (10 weeks) of a long-term (six month) clinical trial of Generex Oral-lyn, the Company's proprietary oral insulin spray product, in adolescent and young adult patients with type-1 diabetes mellitus. This data, which complements the positive data announced by the Company on March 8, 2006, shows the variations of glycosylated hemoglobin (HbA1c), a very well-known marker for monitoring diabetes, during the first 10 weeks of the study.

Glycosylated hemoglobin (HbA1c) is considered by regulatory agencies and endocrinologists as the best long-term measure of metabolic control of diabetes. "HbA1c correlates with the level of risk for diabetes complications," said Dr. Gerald Bernstein, the Company's Vice-President for Medical Affairs. "The continuous and dramatic reduction seen in these preliminary results bode well for patients with diabetes, and society generally, in reducing the burdens of diabetes and its complications."

The investigators concluded that, during the first 10 weeks of this ongoing six-month trial, replacement of subcutaneous injections of regular insulin by Generex Oral-lyn at lunchtime in adolescent and young adult patients with Type-1 diabetes was associated with overall adequate glycemic control and similar glycosylated hemoglobin (HbA1c) concentrations.

About Generex

Generex is engaged in the research and development of drug delivery systems and technologies. Generex has developed a proprietary platform technology for the delivery of drugs into the human body through the oral cavity (with no deposit in the lungs). The Company's proprietary liquid formulations allow drugs typically administered by injection to be absorbed into the body by the lining of the inner mouth using the Company's proprietary RapidMist™ device. The Company's flagship product, oral insulin (Oral-lyn™), which has been approved for commercial sale in Ecuador for the treatment of patients with Type-1 and Type-2 diabetes, is in various stages of clinical trials around the world.

For more information, visit the Generex Web site at www.generex.com.

Safe Harbor Statement: This release and oral statements made from time to time by Generex representatives concerning the same subject matter may contain "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. These statements can be identified by introductory words such as "expects," "plans," "intends," "believes," "will," "estimates," "forecasts," "projects" or words of similar meaning, and by the fact that they do not relate strictly to historical or current facts. Forward-looking statements frequently are used in discussing potential product applications, potential collaborations, product development activities, clinical studies, regulatory submissions and approvals, and similar operating matters. Many factors may cause actual results to differ from forward-looking statements, including inaccurate assumptions and a broad variety of risks and uncertainties, some of which are known and others of which are not. Known risks and uncertainties include those identified from time to time in the reports filed by Generex with the Securities and Exchange Commission, which should be considered together with any forward-looking statement. No forward-looking statement is a guarantee of future results or events, and one should avoid placing undue reliance on such statements. Generex cannot be sure when or if it will be permitted by regulatory agencies to undertake additional clinical trials or to commence any particular phase of clinical trials. Because of this, statements regarding the expected timing of clinical trials cannot be regarded as actual predictions of when Generex will obtain regulatory approval for any "phase" of clinical trials. Generex claims the protection of the safe harbor for forward-looking statements that is contained in the Private Securities Litigation Reform Act.

Posted by dlife at 10:59 AM | Comments (0)

Cleveland Clinic Research Finds Intensive Statin Therapy Can Reverse Coronary Artery Disease

Study Notes Several Groundbreaking Firsts in Research of Cholesterol-Lowering Drugs

ATLANTA, March 13, 2006 (PRNewswire) - A Cleveland Clinic-led study has found that intensive use of statins, the most commonly prescribed cholesterol- lowering drugs, can reverse the build-up of plaque in coronary arteries. Previous studies have shown only a slowing or halting of the progression of coronary disease, but never regression or reversal.

Atherosclerosis, the most common cause of heart disease and death, involves the build-up of fat, calcium and other deposits in the coronary arteries. Removing these deposits has been a difficult challenge for drug- therapy in patients with heart disease.

"These findings suggest that maximizing the use of statins to lower cholesterol levels in patients with heart disease can substantially reduce plaque burden, an outcome previously thought unattainable," said Steven Nissen, M.D., the study's lead author and interim Chairman of the Cleveland Clinic Department of Cardiovascular Medicine. "These results also imply that the goal of statin treatment in coronary disease patients should be the maximum cholesterol reduction that can be achieved safely, rather than an arbitrary target level."

Complete results for ASTEROID (A Study to Evaluate the Effect of Rosuvastatin On Intravascular Ultrasound-Derived Coronary Atheroma Burden) will be presented at the 55th Annual Scientific Session of the American College of Cardiology (ACC) in Atlanta on March 13 and simultaneously published online in the Journal of the American Medical Association.

In their work, researchers found that high doses of rosuvastatin, trade name Crestor(R), reduced LDL-C (bad cholesterol) by 53 percent from baseline measurements to 60.8mg/dL, the lowest level ever achieved in a statin outcomes trial. Researchers likewise noted a statistically significant increase in HDL- C (good cholesterol) of 14 percent, also groundbreaking in a statin trial. The study's combined results led to a highly significant and unprecedented reversal of coronary artery disease in all patient groups and the drug was well tolerated, Dr. Nissen said.

At its onset ASTEROID aimed to determine if very intensive statin therapy could reverse coronary atherosclerosis as determined by intravascular ultrasound (IVUS) imaging. IVUS imaging is a technique in which a small probe is placed in the coronary artery to obtain images that can be analyzed to determine the amount of plaque in arteries.

ASTEROID involved 507 patients enrolled between November 2002 and October 2003. The patients received a baseline IVUS examination and were treated with (40mg) of rosuvastatin for 24 months. After completion, 349 patients received follow-up IVUS examinations. Study endpoints included several different measurements of the volume of plaque in the coronary arteries.

Further studies are needed to verify the results and determine clinical consequences of the findings.

"It is important to understand that our study measured the amount of plaque in the coronary arteries, not the rate of occurrence of adverse events, such as heart attack or stroke," Dr. Nissen said. Therefore, these findings need to be confirmed in a larger study that assesses the effects of very intensive cholesterol lowering on clinical outcome."

Funding for the ASTEROID trial was provided by AstraZeneca. Dr. Nissen does not accept any company honoraria, donating any money that comes to him to a charity run by the American College of Cardiology.

Cleveland Clinic Heart & Vascular Institute is the recognized world leader in diagnosis and treatment of cardiovascular disease. Cleveland Clinic has been ranked No. 1 in the nation for cardiac care by U.S. News & World Report every year since 1995. Cleveland Clinic has been ranked among America's Ten Best Hospitals every year since 1990 by U.S. News & World Report.

The Cleveland Clinic Foundation, located in Cleveland, Ohio, is a not-for- profit multispecialty academic medical center that integrates clinical and hospital care with research and education. The Cleveland Clinic was founded in 1921 by four renowned physicians with a vision of providing outstanding patient care based upon the principles of cooperation, compassion and innovation. U.S. News & World Report consistently names The Cleveland Clinic as one of the nation's best hospitals in its annual "America's Best Hospitals" survey. Approximately 1,500 full-time salaried physicians at The Cleveland Clinic and Cleveland Clinic Florida represent more than 100 medical specialties and subspecialties. In 2004, patients came for treatment from every state and 100 countries. The Cleveland Clinic website address is http://www.clevelandclinic.org/.

Posted by dlife at 11:01 AM | Comments (0)

Cleveland Clinic Research Explores Value of Two Blood Thinners Versus Just One

Certain Subgroups May Benefit From Dual Therapy, Others Should Avoid It

ATLANTA, March 12 (PRNewswire) - A Cleveland Clinic-led international study has found that long-term therapy with low-dose aspirin plus another antiplatelet agent, clopidogrel (Plavix(R)), is not more effective than aspirin alone in preventing heart attack, stroke, and cardiovascular death in a broad patient population.

Results from the study will be presented at the 55th Annual Scientific Session of the American College of Cardiology (ACC) in Atlanta on March 12 and simultaneously published online in the New England Journal of Medicine.

The majority of patients in the study, those who had already experienced a heart attack or stroke or who had symptomatic blockages in their legs (Peripheral Arterial Disease or PAD), did benefit from the dual therapy, demonstrating a significant 12.5% reduction in their risk of heart attack and stroke. Unexpectedly, researchers also found that the subgroup of patients with multiple risk factors for heart attack or stroke but who did not have established cardiovascular disease may have experienced some harm, including higher rates of severe bleeding.

"There are several important findings from this study," says Deepak L. Bhatt, M.D., lead author and director of the Cardiovascular Trials Unit and associate director of the Cleveland Clinic Cardiovascular Coordinating Center. "Although the study found that clopidogrel plus aspirin was not effective in patients with multiple risk factors only, it may be effective in secondary prevention, or preventing a second heart attack or stroke in people who have already experienced one of these events or who have PAD. This is a large population that is in need of improved therapies."

CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance) was a prospective, multicenter, randomized, double-blind, placebo controlled study of the safety and efficacy of clopidogrel plus aspirin compared to aspirin alone in stable patients at high risk for a cardiovascular event. Prior studies had established the efficacy of clopidogrel plus aspirin in patients with acute coronary syndromes, but long-term dual therapy had not been evaluated in a broad population of stable patients.

The CHARISMA study included 15,603 patients with either diagnosed cardiovascular disease (~80% of the study population) or multiple risk factors for cardiovascular disease (~20% of study population). Patients were randomly assigned to receive clopidogrel (75 mg per day) plus low-dose aspirin (75 to 162 mg per day) or placebo plus low-dose aspirin for a median of 28 months. The primary endpoint was measured as a combination of heart attack, stroke, or death from cardiovascular causes.

Dr. Bhatt says further investigation is needed to better understand how dual antiplatelet therapy may be optimally utilized in appropriate populations. "Our findings from the CHARISMA trial suggest a significant benefit of dual antiplatelet therapy in patients with established cardiovascular disease, while demonstrating a lack of benefit and increased bleeding in patients only having multiple risk factors. Future research will help determine exactly which patients need more aggressive antiplatelet therapy than just an aspirin a day to prevent heart attacks and strokes."

Funding for the CHARISMA trial was provided by Sanofi-Aventis and Bristol- Myers Squibb. Dr. Bhatt has been paid honoraria from both companies in the past, though he currently donates such honoraria to a not-for-profit organization.

Cleveland Clinic Heart & Vascular Institute is the recognized world leader in diagnosis and treatment of cardiovascular disease. Cleveland Clinic has been ranked No. 1 in the nation for cardiac care by U.S. News & World Report every year since 1995. Cleveland Clinic has been ranked among America's Ten Best Hospitals every year since 1990 by U.S. News & World Report.

Cleveland Clinic, located in Cleveland, Ohio, is a not-for-profit multispecialty academic medical center that integrates clinical and hospital care with research and education. Cleveland Clinic was founded in 1921 by four renowned physicians with a vision of providing outstanding patient care based upon the principles of cooperation, compassion and innovation. U.S. News & World Report consistently names Cleveland Clinic as one of the nation's best hospitals in its annual "America's Best Hospitals" survey. Approximately 1,500 full-time salaried physicians at Cleveland Clinic and Cleveland Clinic Florida represent more than 100 medical specialties and subspecialties. In 2004, patients came for treatment from every state and 100 countries. Cleveland Clinic website address is http://www.clevelandclinic.org/.

See All March 2006 dLife News Items

Posted by dlife at 11:08 AM | Comments (1)

Joslin Researchers Reveal Mechanisms Behind A Class of Oral Agents Used to Treat Type 2 Diabetes

BOSTON, March 9, 2006 (Joslin) - Thiazolidinediones (TZD's) are drugs commonly prescribed to patients with type 2 diabetes, the most common form of diabetes. Current U.S. Food and Drug Administration-approved agents are known as Actos (pioglitazone) and Avandia (rosiglitazone). These oral agents improve blood glucose levels in people with diabetes by improving insulin action in the body. While it is known that these drugs work primarily by binding to a receptor in the nucleus of cells called Peroxisome Proliferator Activated Receptor-gamma (PPARg), all of the molecular signaling events important for the drugs to work are not completely understood.

A new study by researchers at Joslin Diabetes Center in Boston helps to explain how these drugs work. The manuscript appears in the March edition of the American Diabetes Association's journal Diabetes.

In a clinical research study, Joslin researchers Allison B. Goldfine, M.D., Sarah Crunkhorn, Ph.D., and Mary-Elizabeth Patti, M.D., examined muscle and fat tissue from patients with type 2 diabetes before and after they took the drug rosiglitazone. The researchers found that levels of two proteins called Necdin and E2F4, which are important in regulating cell replication, are altered in muscle and fat after patients took the drug for two months. Dr. Goldfine is an Investigator in Joslin's Section on Cellular and Molecular Physiology, Assistant Director of Clinical Research at Joslin and Assistant Professor of Medicine at Harvard Medical School. Dr. Patti is Director of Joslin's Genomics Core Lab and also an Investigator in Cellular and Molecular Physiology and Assistant Professor of Medicine, Harvard Medical School. Dr. Crunkhorn is a postdoctoral fellow in Dr. Patti's laboratory.

"Because the proteins are important in regulating the cell cycle, the findings suggest that the thiazolidinediones may work, in part, by altering the cell differentiation state, or level of cell maturity. Additionally, the two proteins Necdin and E2F4 may represent new drug targets that may be useful in the future for treatment of patients with diabetes," says Dr. Goldfine.

Others who participated in the study include Maura Costello, Hiral Gami, Edwin J. Landaker, and Jose Jimenez-Chillaron, Ph.D., of Joslin; Michio Niinobe, Ph.D., and Kazuaki Yoshikawa, M.D., Ph.D., of Osaka University, Japan; David Lo, M.D., Ph.D., of the La Jolla Institute for Allergy and Immunology, La Jolla, CA; and Amy Warren, Ph.D., of Digital Gene Technologies/Neurome of La Jolla.

Funding for the study was provided by the National Institutes of Health and generous support from the Iacocca Foundation.

Posted by dlife at 11:14 AM | Comments (0)

People with Diabetes Who Control Blood Sugar Today are More Likely to Have Healthy Feet and Nerves Tomorrow

Effects of tight glucose control seen years later in diabetic neuropathy study

ANN ARBOR, Mich., March 9, 2006 (EurekAlert) - People with diabetes who keep their blood sugar in check today will probably have a far lower chance of developing foot pain or other nerve damage tomorrow, according to new research results from a national study.

In fact, the study shows that the positive effects of tight blood glucose control can be seen more than a decade later. At the end of the study period, patients who had controlled their blood sugar tightly ever since the start of the study were 51 percent less likely to have nerve problems than patients who started the study at the same time but did not have the initial 5 year period of intensive blood sugar control.

The study, published in the February issue of the journal Diabetes Care, involved 1,441 people with Type 1 diabetes, also known as juvenile diabetes. Although patients with the more common Type 2 form of diabetes were not involved, the results may have implications for the 18 million Americans with type 2 diabetes.

Two-thirds of all people with diabetes have some degree of nerve problems, or neuropathy, related to their diabetes. The most common sign is numbness or pain in the feet and legs, which can progress over time to cause disability. Neuropathy plays a major role in 80,000 foot and leg amputations in American diabetics each year.

"This is an exciting finding that adds credence to the idea of metabolic memory, or the concept that there can be a durable effect from early and sustained efforts to keep blood sugar low," says senior author Eva Feldman, M.D., Ph.D., the DeJong Professor of Neurology at the University of Michigan Medical School and director of the U-M Neuropathy Center. "It suggests that good glucose control clearly protects patients over the long term."

The new study marks the first time that tight blood sugar control has been shown to have a long-term effect on the chance that a person with diabetes will develop neuropathy. Similar findings have been made for two other frequent complications of diabetes, retinopathy (eye disease) and nephropathy (kidney disease).

The new findings come from the Epidemiology of Diabetes Intervention and Complications (EDIC) study that grew out of the national Diabetes Control and Complications Trial (DCCT). Funded by the National Institute of Diabetes and Digestive & Kidney Diseases, the DCCT began in the 1980s by randomly assigning people with type 1 diabetes to either tight blood-sugar control using three insulin injections per day or an insulin pump, or to more typical blood sugar control for the time, using one to two insulin injections a day. The latter group was later encouraged to adopt tight blood sugar control, and the EDIC study tracked all patients' health.

The new paper reports results from eight years of neuropathy assessments under the EDIC study, among 1,441 DCCT participants who had no symptoms or signs of neuropathy at the end of the DCCT.

The symptoms and signs were assessed using a standardized questionnaire developed and validated by U-M researchers from the Michigan Diabetes Research and Training Center. Called the Michigan Neuropathy Screening Instrument, the questionnaire is completed by both patients -- who report symptoms such as tingling, pain, numbness, and sensitivity -- and by physicians, who complete a physical examination of the patients' feet, including sensitivity to touch and vibration, and the presence of calluses and sores that the patients might not be able to feel because of nerve damage.

Such foot problems can become infected and lead to open wounds that can be hard to heal because of other aspects of diabetes. Unhealed infections, if bad enough, can lead to decisions to amputate toes, feet and legs. This "domino effect" starting with neuropathy and leading to infection and amputation is the reason that current guidelines call for people with diabetes to have annual foot exams.

Feldman, who led the analysis along with research nurse Catherine Martin, M.S., notes that the study looked at the percentage of participants who had any positive sign of neuropathy on their questionnaire or their foot examination each year of the EDIC study, and then separated them according to which DCCT group (tight glucose control or regular control) they had been in.

This allowed them to track the impact of prior tight glucose control, even though all the participants were encouraged to control their blood sugar tightly once they entered the EDIC phase of the project. Test results taken each year show that the two groups achieved very similar blood-sugar control in the later years of the EDIC study, with levels of a measure called A1C around 8 percent for both groups.

After the first year, 28 percent of the regular-control patients showed signs of neuropathy on their physical exam, though only 4.7 percent reported symptoms on their questionnaires. By contrast, 17.8 percent of the tight-control patients had neuropathy signs on their foot exams, and 1.8 percent reported symptoms. The difference between the two groups was highly statistically significant.

Over time, the difference between the two groups continued to be significant, although the percentage of both groups that showed signs or reported symptoms of neuropathy increased over time. By the end of the eighth year of follow-up, almost 7 percent of the participants who had been in the regular-control group reported feeling symptoms of neuropathy, compared with about 3.5 percent of the tight-control patients. And at the end of eight years, more than 26 percent of regular-control participants had signs of neuropathy on their physical exam, compared with just over 20 percent of tight-control participants.

The researchers calculated statistical likelihoods for these measures. In all, participants who had begun with tight blood-sugar control and stuck with it were 51 percent less likely to report symptoms of neuropathy, and 43 percent less likely to show signs of it, than those who had started out with regular blood-sugar control and then gone to tight control. There were also differences between the two groups in the incidence of open sores requiring medical or surgical treatment, and in incidence of amputation.

In all, says Feldman, the results reinforce a key message for all of today's diabetes patients, though type 2 diabetics tend to have other health problems that can interfere with the protective effects of tight sugar control. That message: Check your blood sugar levels regularly, and take steps to keep them under tight control, with few extremes of low or high sugar.

Posted by dlife at 11:10 AM | Comments (0)

Effect of Diabetes on Heart May Differ by Ethnicity, Study Finds

March 8, 2006 (EurekAlert) - Diabetes strongly increases the risk of heart failure in all ethnic groups, but early effects of diabetes on the heart may differ depending on whether the subjects are white, African-American, Hispanic or Chinese. These results emerged from the Multi-Ethnic Study of Atherosclerosis (MESA) when the investigators focused on heart mass – the weight of the heart muscle as measured by MRI, according to Alain Bertoni, M.D., M.P.H., at Wake Forest University School of Medicine.

"People with diabetes are recognized as having an increased risk of heart failure," Bertoni said. "We sought to better understand why.

We were especially interested in the role atherosclerosis may play."

In a report in the March issue of Diabetes Care, the researchers compared people with diabetes or impaired fasting glucose (which means their blood sugar levels were too high) with those who had normal blood sugar levels.

The investigators particularly looked at the muscle mass of the left ventricle, the part of the heart that pumps the blood through the aorta and out into the circulatory system. They measured the left ventricle itself, not the blood in it.

They also measured the volume of the ventricle when filled with blood just before it pumps the blood out. A lower volume indicates less blood is able to enter the ventricle, and suggests increased heart stiffness, said Bertoni.

"Increased left ventricular muscle mass suggests the future possibility of developing heart failure," he said. "We also think that if you have a stiffer heart, that could be an early indication that you have a propensity for developing heart failure."

MESA measured "subclinical" atherosclerosis – atherosclerosis that has yet to produce symptoms – through CT scans measuring the amount of calcium in the coronary arteries and ultrasound measuring the wall thickness of the carotid artery in the neck. Both are indications of atherosclerosis.

"Every ethnic group seems to have a set of abnormalities related to diabetes. While we think those with diabetes from all ethnic groups are at increased risk for heart failure, perhaps there is a different mechanism in play in each of the ethnic groups," Bertoni said.

"We found evidence that in whites, African-Americans, and Hispanics with diabetes there was increased heart muscle mass over those without diabetes," he said. In whites, the increased left ventricular mass was completely explained by subclinical atherosclerosis and high blood pressure, he said. With partial blockage of the coronary arteries, some areas of the heart muscle are getting less blood flow and are weakened, which means the rest of the heart muscle has to bulk up, he said.

In African-Americans and Hispanics, the increased mass was not fully explained by these factors. Among Chinese participants no differences in mass were observed.

In contrast, lower volumes, suggestive of increased stiffness, were seen in whites, blacks, and Chinese participants with diabetes, but not Hispanics.

Bertoni stressed that none of the MESA participants actually had heart failure. "We did not see any significant difference in the function of the heart, the squeeze of the heart."

"Other studies have in fact suggested that the incidence of heart failure is similar between whites and African-Americans with diabetes, but somewhat lower among Hispanics and Asians with diabetes."

The MESA investigators intend to follow the participants at least until 2008, with some participants in a sub-study called MESA Air being followed at least until 2012. If the measurements do predict heart failure, "they would help us target preventive therapies," Bertoni said.

"Further investigation will be required to determine whether there are differences in the incidence of heart failure by ethnicity in this [group], and if so, whether the observed differences at baseline will be predictive of the future risk of heart failure," the researchers said in Diabetes Care.

Posted by dlife at 11:12 AM | Comments (0)