November 7, 2007, 7:49 PM CT

Gene's Role in Type 1 Diabetes

Scientists at the University of Virginia Health System have identified an enzyme believed to be an important instigator of the inner-body conflict that causes Type 1 diabetes. A chronic condition that affects nearly three million American children and adults, Type 1 diabetes is more severe than Type 2. Type 1 diabetes, also called autoimmune diabetes, arises when the body's infection-fighting white blood cells start destroying the beta-cells that produce insulin in the pancreas.

To shed light on how this conflict begins, UVa scientists focused on a single gene, 12/15-lipoxygenase (12/15-LO). This gene leads to the production of the enzyme, which appears to have an important role in the activation of white blood cells in the pancreas.

Scientists developed non-obese diabetic female mice to serve as a model of Type 1 diabetes. After turning off the 12/15-LO gene in study mice, they discovered that these mice without the enzyme were 97 percent less likely to develop diabetes than mice that had normal levels of it, as per the study, published online in the journal Diabetes (would be published in print in February 2008).

"This research is exciting because it advances our knowledge of a new gene that is involved in causing Type 1 diabetes and could pave the way for new therapys to prevent or reverse this increasingly prevalent disease," said Dr. Jerry L. Nadler, who is chief of the UVa Division of Endocrinology and Metabolism......... Posted by: Josly2006      Read more         Source

November 5, 2007, 8:20 PM CT

Diabetic drugs does not impair ability to survive heart attack

Mayo Clinic scientists helped clarify a growing concern about the link between diabetes mellitus therapys and heart attack with the first large, population-based study showing that a group of common medications does not reduce diabetic patients heart attack survival rates. These results were presented today at the American Heart Associations Scientific Sessions 2007 in Orlando, Fla.

The drugs studied are called sulfonylureas and include several usually used pills to increase insulin release to lower blood sugar. Second-generation sulfonylureas -- known collectively as SU2 -- include glimepiride (Amaryl), glipizide (Glucotrol, Glucotrol XL), and glyburide (DiaBeta, Micronase, Glynase).(1).



Significance of the Mayo Clinic Study

The prevalence of diabetes mellitus is growing rapidly, and physicians need evidence for their therapy recommendations. Worldwide, the number of diabetics is projected to more than double in three decades, from 171 million in 2000 to 366 million in 2030.(2) A number of patients with diabetes are at increased risk for heart failure. This complicates their therapy, and has raised concern in recent years among some physicians that SU2s may impair the hearts ability to withstand stress, thus reducing patients ability to survive heart attacks, says Veronique Roger, M.D., M.P.H., the Mayo heart specialist and epidemiologist who led the study......... Posted by: Josly2006      Read more         Source

October 31, 2007, 7:19 PM CT

High Blood Pressure Heart Disease And Diabetes

High-blood-pressure patients treated for enlarged heart (left ventricular hypertrophy, LVH) who have regression or prevention of LVH may also have a better chance of preventing diabetes. Led by physician-researchers at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, the research is reported in the November Hypertension, a journal of the American Heart Association (AHA).

An estimated 20 percent of all high-blood-pressure patients, or 12 million Americans, have LVH and are at increased risk of developing diabetes.

The study reports a 38-percent reduced risk of developing diabetes for high-blood-pressure patients who demonstrated regression of LVH during therapy for high blood pressure, with a 26-percent reduced risk after adjusting for other risk factors for diabetes. The reduction in risk of diabetes was independent of therapy type and of the degree of blood pressure change in this population.

"A healthy heart is a prerequisite for the health of the body as a whole. Our prior research has shown that treating enlarged heart in high-blood-pressure patients reduces the risk for a variety of cardiovascular conditions. This new study finds an important new benefit-namely a better chance of avoiding diabetes among patients who exhibit a reduction of their hypertrophy during therapy," says the study's principal investigator, Dr. Peter Okin, director of clinical affairs and professor of medicine in the Greenberg Division of Cardiology at Weill Cornell Medical College and attending doctor at NewYork-Presbyterian/Weill Cornell......... Posted by: Josly2006      Read more         Source

October 26, 2007, 5:11 AM CT

The new source of islet cells

The shortage of islet cells limits the development of islet transplantation. One new approach was published in the October 21 issue of the World Journal of Gastroenterology because of its great significance in enhancing the output of islet cells. This article will undoubtedly bring benefit to diabetic patients.

The article describes the differentiation of rat pancreatic ductal epithelial cells into insulin-producing cells by the transfection of PDX-1. In recent years, though great efforts have been made to differentiate embryonic stem cells, pancreatic ductal epithelial multipotent progenitor cells and bone marrow stem cells into islet cells, the process of cell differentiation and growth is long. Moreover, the amount of islet cells of differentiation, and the insulin released by islets, is not enough to meet the clinical needs.

To shorten the process of differentiation and enhance the output of insulin-producing cells and increase the amount of insulin-releasing, Dr Liu et al. transfected PDX-1 into primary pancreatic ductal epithelial cells and then differentiated the transfected cells into insulin-producing cells. In contrast, the expression of PDX-1 and insulin mRNA and protein were detectable in the transfected cells. Endogenous PDX-1 might play an important role during differentiation and the transfected cells can produce more insulin-releasing cells and release more insulin after induction......... Posted by: Josly2006      Read more         Source

October 19, 2007, 5:02 AM CT

Cross-species transplant toward diabetes cure

With an eye on curing diabetes, researchers at Washington University School of Medicine in St. Louis have successfully transplanted embryonic pig pancreatic cells destined to produce insulin into diabetic macaque monkeys all without the need for risky immune suppression drugs that prevent rejection.

The transplanted cells, known as primordia, are in the earliest stages of developing into pancreatic tissues. Within several weeks of the transplants, the cells became engrafted, or established, within the three rhesus macaque monkeys that received them. The cells also released pig insulin in response to rising blood glucose levels, as would be expected in healthy animals and humans.

"The approach reduced the animals' need for insulin injections and has promise for curing diabetes in humans," says senior investigator Marc Hammerman, M.D., the Chromalloy Professor of Renal Diseases in Medicine. "The transplants worked without a need for immune suppression and that is a major obstacle we have overcome."

The researchers' results appear online and would be reported in the journal Xenotransplantation in November.

Eventhough the transplants fell short of producing sufficient insulin to cure the macaques' diabetes, Hammerman predicts that with additional research, including the transplantation of additional embryonic pig cells into the animals, he will be able to reduce their need for insulin injections entirely......... Posted by: Josly2006      Read more         Source

October 1, 2007, 9:09 PM CT

Potential role of leptin in diabetes

A new Joslin-led study has shown that leptin, a hormone known mainly for regulating appetite control and energy metabolism, plays a major role in islet cell growth and insulin secretion. This finding opens up new avenues for studying leptin and its role in islet cell biology, which may lead to new therapys for diabetes. This study appears in the October 2007 issue of The Journal of Clinical Investigation.

Prior in vitro studies suggested that leptin receptors, which are found in tissues throughout the body including the pancreas as well as the brain, mediate leptin-induced inhibition of insulin secretion in islet cells, also known as beta cells. We wanted to further our understanding of leptin and its role in beta cells independent of its effects in the brain, said Rohit N. Kulkarni, M.D., Ph.D., principal investigator at Joslin Diabetes Center and Assistant Professor of Medicine at Harvard Medical School, who led this study. It is currently not known why obese individuals exhibit a high occurence rate of diabetes despite high levels of both insulin and leptin circulating in the bloodstream.

To understand the role of leptin in the islets, scientists developed a mouse model (known as a knock out or KO mouse) genetically engineered not to produce leptin receptors in the pancreas, while maintaining the receptors in the brain and the rest of the body. Scientists observed that the mice lacking leptin receptors in the pancreas showed improved glucose tolerance and greater insulin secretion and beta cell growth. Since the normal function of leptin is to keep insulin levels from getting too high, the lack of leptin enhances insulin action in the beta cells and promotes insulin secretion, which was the result we expected, said Dr. Kulkarni......... Posted by: Josly2006      Read more         Source

September 26, 2007, 8:35 PM CT

Alzheimer's disease as form of diabetes

Insulin, it turns out, may be as important for the mind as it is for the body. Research in the last few years has raised the possibility that Alzheimers memory loss could be due to a novel third form of diabetes.

Now researchers at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimers disease. They have shown that a toxic protein found in the brains of individuals with Alzheimers removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for amyloid -derived diffusible ligand.).

With other research showing that levels of brain insulin and its related receptors are lower in individuals with Alzheimers disease, the Northwestern study sheds light on the emerging idea of Alzheimers being a type 3 diabetes.

The new findings, published online by the FASEB Journal, could help scientists determine which aspects of existing drugs now used to treat diabetic patients may protect neurons from ADDLs and improve insulin signaling in individuals with Alzheimers. (The FASEB Journal is a publication of the Federation of American Societies for Experimental Biology.)

In the brain, insulin and insulin receptors are vital to learning and memory. When insulin binds to a receptor at a synapse, it turns on a mechanism necessary for nerve cells to survive and memories to form. That Alzheimers disease may in part be caused by insulin resistance in the brain has researchers asking how that process gets initiated......... Posted by: Josly2006      Read more         Source

September 21, 2007, 5:34 AM CT

Smart Insulin Nanostructures Pass Feasibility Test

Biomedical engineers at The University of Texas School of Health Information Sciences at Houston have announced pre-clinical test results in the recent issue of the International Journal of Nanomedicine demonstrating the feasibility of a smart particle insulin release system that detects spikes in glucose or blood sugar levels and releases insulin to counteract them.

Designed to mimic functions of the pancreas which produces the blood-sugar regulating hormone insulin, the smart particle system stabilized blood sugar levels in animal models with suppressed pancreatic functions for up to six hours, scientists reported. It is an inhalable system.

The study, "Glucose-sensing pulmonary delivery of human insulin to the systemic circulation of rats," was conducted in the laboratory of Ananth V. Annapragada, Ph.D., an associate professor at the UT School of Health Information Sciences. Research assistant Efstathios Karathanasis was lead author and postdoctoral fellow Rohan C. Bhavane was a contributor on the article.

The smart particle system consists of a blood sugar sensing protein named concanavalin A (Con A) and bundles of tiny fat bubbles called liposomes that are loaded with insulin. "Con A binds insulin-containing liposomes that are coated with sugars, to each other, to form the inhaled particles," Annapragada said. "When blood sugar becomes present, the Con A releases the particles to bind independently to the sugars. The released particles then release their insulin"......... Posted by: Josly2006      Read more         Source

September 14, 2007, 5:21 AM CT

Metabolic syndrome and uric-acid kidney stones

Scientists at UT Southwestern Medical Center have observed that patients suffering from the metabolic syndrome - a cluster of conditions that increases the risk for heart disease, stroke and diabetes - also have a propensity to develop highly acidic urine, which increases the risk of developing kidney stones.

The first study, to demonstrate this relationship independent of age and renal function, appears in the recent issue of the Clinical Journal of the American Society of Nephrology.

Typically the metabolic syndrome is characterized by a group of risk factors that include obesity, high blood pressure, diabetes and high cholesterol. The American Heart Association estimates that more than 50 million Americans suffer from the syndrome.

"Our findings suggest that the presence of an increasing number of metabolic syndrome features augments the propensity for uric-acid stone formation," said Dr. Naim Maalouf, assistant professor of internal medicine and the study's lead author.

In prior studies, UT Southwestern scientists have observed that people who were overweight or suffered from diabetes had highly acidic urine, which often leads to the development of uric-acid kidney stones.

The current findings indicate that people with the other components leading to the metabolic syndrome also have highly acidic urine......... Posted by: Josly2006      Read more         Source

September 12, 2007, 7:58 PM CT

How Cells From Pigs May Cure Diabetes

Within three years, insulin-producing islet cells from pigs may be used in clinical trials on a path to finally cure insulin dependant diabetes.

This key finding was the discovery of Dr. Bernhard Hering, Scientific Director of the Diabetes Institute for Immunology & Transplantation at the University of Minnesota and his team, who documented their medical breakthrough in the prestigious scientific journal Nature Medicine in March of 2006.

On Thursday, September 20, at 10:00 a.m. CDT, Hering will present the latest research on pig islet xenotransplantation at the Diabetes Research and Wellness Foundation Symposium at the Hyatt Regency Minneapolis in Minneapolis, MN.

The symposium will be part of The Transplantation Societys 2007 Joint Conference (www.cts-ipita-ixa-2007.org), an international event that will unite the greatest innovators from three sections of the Transplantation Society the Cell Transplant Society (CTS), the International Pancreas and Islet Transplant Association (IPITA) and the International Xenotransplantation Association (IXA) for the first time in history. Hering also serves as the Joint Conference president.

Research has shown that the transplantation of islet cells, harvested from the pancreas of a pig, yields a long-term reversal of diabetes in monkeys, opening the path to unprecedented new opportunities for human patients with the disease. To oversee immunosuppression issues, scientists are now working to transplant porcine islets in an engineered pre-vascularized, cytoprotective and immune-privileged implantation site. This procedure has many advantages including:........ Posted by: Josly2006      Read more         Source