January 10, 2007, 9:11 PM CT

Diabetes Drug Prevents Brain Injury

Scientists at Wake Forest University School of Medicine are the first to report that in animal studies, a common diabetes drug prevents the memory and learning problems that cancer patients often experience after whole-brain radiation therapys.

"These findings offer the promise of improving the quality of life of these patients," said Mike Robbins, Ph.D., senior researcher. "The drug is already prescribed for diabetes and we know the doses that patients can safely take".

Whole-brain radiation is widely used to treat recurrent brain tumors as well as to prevent breast cancer, lung cancer and cancerous melanoma from spreading to the brain. About 200,000 people receive the therapy annually, and beginning about a year later, up to one-half develop progressive cognitive impairments that can affect memory, language and abstract reasoning.

In the current issue of the International Journal of Radiation Oncology - Biology -Physics, Robbins and his colleagues report that rats receiving the diabetes drug piolitazone (sold under the trade name Actos®) before, during and after radiation therapys did not experience cognitive impairment.

The researchers compared whether therapy with Actos for four weeks or for 54 weeks after radiation would be more effective, and found there was not a significant difference.........

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January 9, 2007, 5:06 AM CT

Antibody therapy prevents type 1 diabetes in mice

University of Pittsburgh researchers have successfully prevented the onset of type 1 diabetes in mice prone to developing the disease using an antibody against a receptor on the surface of immune T-cells. As per the investigators, these findings, which are being reported in the recent issue of the journal Diabetes, have significant implications for the prevention of type 1 diabetes.

More than 700,000 Americans have type 1 diabetes, an autoimmune disorder in which the body errantly attacks the insulin-producing cells of the pancreas, causing chronically elevated levels of sugar in the blood, leading to blindness, kidney failure, heart disease and nerve damage. Previously known as juvenile diabetes, type 1 diabetes is commonly diagnosed at a very early age, but in some cases it can be diagnosed in adulthood.

In this study, the Pitt scientists treated non-obese diabetic (NOD) mice with an antibody -- a type of protein produced by the immune system that recognizes and helps fight infections and other foreign substances in the body -- directed against a receptor known as CD137 on the surface of a type of immune cell called T-cells. Treating NOD mice with the anti-CD137 antibodies significantly suppressed the development of diabetes, whereas most of the control mice developed diabetes by the time they were six months old.........

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December 28, 2006, 9:05 PM CT

Glucose 'Sensor' That Plays Dual Role

In the study, glucose is shown to stimulate the activity of the Liver X Receptors (LXR) a and b, The LXRs act as sensors of dietary components, orchestrating the body's response to nutrients such as oxysterols (short-lived derivatives of cholesterol) and controlling gene expression associated with cholesterol and fat metabolism.

"When you eat, glucose pours into the gut and is recognized by LXR in the liver, which then activates expression of the enzymes that turn excess glucose into triglycerides that are stored as fat," said Enrique Saez, a Scripps Research scientist who led the study. "The fact that our study demonstrates that LXR does both-it binds to glucose and it induces fatty acid synthesis-is significant and makes LXR a potential target for diabetes and obesity therapys".

In some recent animal studies, Saez pointed out, activation of LXRs using synthetic molecules also induced regression of atherosclerosis, the clogging, narrowing, and hardening of the body's large arteries and blood vessels that can lead to stroke, heart attack, and eye and kidney problems. Elevated levels of pathogenic cholesterols, also known to bind LXR, are a primary risk for development of atherosclerosis.

"The integration of glucose sensing and control of lipogenesis by LXR may explain why low-fat/high-carbohydrate diets induce hypertriglyceridemia [an elevated level of triglycerides in the blood]," Saez said. "LXR can sense surplus glucose, induce fatty acid synthesis, and prompt the liver's export of triglycerides into the bloodstream. Since LXR acts as the body's sensor of a buildup of pathogenic cholesterol, its ability to bind both glucose and oxysterols suggests that LXR may be a link between hyperglycemia and atherosclerosis."........

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December 20, 2006, 10:06 PM CT

Pharmacists Might Play Direct Diabetes Management

Ever wondered about the role your pharmacist in you diabetes management? I think a number of times our pharmacists are more familiar with our unique diabetic situation rather than our physicians. After all how often do we see our pharmacists as in comparison to our physicians? It seems that pharmacists are going to have a more direct role in the management of your diabetes in future. Read the story below:

Community pharmacists could soon be playing a more direct role in diabetes management according to findings of a new study. The aim of the study was to help people with Type 2 Diabetes gain better control over their blood glucose levels to reduce their need for visits to the doctor or hospital admissions.

Wesley Research Institute Director, Professor Julie Campbell, said that patients in the study would use hi-tech glucose meters to measure their blood glucose levels at varying times during the day. The metres are attached to their computers and a special software program is used to chart changes in glucose levels.

"Half the study participants will take this information to their pharmacists who can advise on changes in lifestyle to help moderate their blood glucose levels and prevent them becoming unwell," said Professor Campbell. "The other half will continue to manage their blood glucose levels themselves".........

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December 18, 2006, 5:09 AM CT

Nervous System And Type 1 Diabetes

It has long been believed in the scientific community hat Type 1 diabetes occurs after a prolonged miscue by the immune system causes insulin-producing cells in the pancreas to be destroyed. Now a group of scientists have observed that immune cells aren't the only culprits in developing the disease - the nervous system also plays a pivotal role.

With Type 1 diabetes, the destruction of the islet cells in the pancreas leaves the body without insulin to regulate the metabolism of blood glucose, or sugar. The disease, which affects about 200,000 Canadians, can lead to severe complications even with daily insulin injections, including blindness, limb amputation and kidney failure.

In studies of laboratory mice specially bred to make them susceptible to Type 1 diabetes, scientists at the Hospital for Sick Children and the University of Calgary discovered that a control circuit exists between insulin-producing cells and their associated sensory, or pain-related, nerves.

It turns out that this control circuit is necessary to retain the health and normal function of islet cells, said principal investigator Dr. Michael Dosch, an immunologist at Sick Kids Hospital.

"What we really have discovered is that the immune system is under much closer control by the nervous system than we thought, that this control to a large extent involves sensory nerves," said Dosch, explaining that such nerves are the same kind that signal the brain to send out pain messages when an ankle is broken or a finger is burned on a hot stove.........

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December 16, 2006, 1:02 PM CT

New Drugs For Diabetes

Scientists from the new interdisciplinary LIMES (Life & Medical Sciences) Centre at the University of Bonn have identified a new gene which could play an important role in the development of diabetes. Flies in which this hereditary factor is defective are also significantly smaller than other members of their species and live appreciably longer. The gene seems to have such a crucial function that it has hardly changed in just under a billion years: it is found in flies, but in a similar form it is also found in mice and humans. In the current issue of the prestigious journal Nature the Bonn researchers have published two articles on this topic.

Sometimes science resembles a relay race: in 1996 the biochemist Professor Waldemar Kolanus discovered a group of cellular proteins, the cytohesins, and described their function in the immune system. Two of his colleagues at the LIMES Centre in Bonn have now found a totally new and completely unexpected function of these proteins which is very relevant to medicine. 'We wanted to know whether there were also cytohesins in the fruit fly drosophila and what functions they have there,' the evolutionary biologist Professor Michael Hoch reminisces. He and his team were in fact successful. They discovered a protein which is very similar to the cytohesins in mammals. Even more interestingly, fruit flies in which the genetic blueprint for this gene is defective are smaller in size. So the researchers nicknamed cytohesin 'Titch'. 'The effect on the insect's growth showed us that 'Titch' could play a key role in the metabolism of insulin - a completely new role for cytohesins,' Professor Hoch says.........

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December 16, 2006, 9:06 AM CT

Managing Sugar To Managing Healing

Insulin is a hormone known primarily for regulating sugar levels in the blood, yet scientists at the University of California, Riverside, recently observed that applying insulin directly to skin wounds significantly enhanced the healing process.

Skin wounds in rats treated topically with insulin healed faster"surface cells in the epidermis covered the wound more quickly and cells in the dermis, the deeper part of the skin, were faster in rebuilding blood vessels.

In follow-up studies of human skin cells in culture, Manuela Martins-Green and his colleagues explored the molecular impact of topical insulin on keratinocytes, the cells that regenerate the epidermis after wounding, and on microvascular endothelial cells, the cells that restore blood flow.

Using various cell and molecular techniques, the scientists discovered that insulin stimulates human keratinocytes in culture to proliferate and migrate. In cultured human microvascular endothelial cells, the insulin stimulates only migration into the wound tissue. The insulin works by switching on cellular signaling proteins called kinases (specifically Src, PI3K, and Akt) and a protein (SREBP) that binds elements in DNA that regulate the production of cholesterol and its relatives.

Chronic or nonhealing wounds take an immense toll on American health and on health care systems. It especially affects millions of patients with impaired mobility, as well as those with diabetes. Because diabetes is a disease caused by impaired production or utilization of insulin, this work may help explain the correlation between diabetes and poor healing.........

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December 16, 2006, 9:02 AM CT

New Insights Into The Cause Of Diabetes

The cause of insulin-dependent, permanent, diabetes in newborn babies may be a deficiency in the enzyme Pancreatic Endoplasmic Reticulum Kinase (PERK) during a critical period of development before birth, as per a new hypothesis put forward by a team of scientists from Penn State University. In this most severe type of diabetes, individuals are unable to regulate glucose normally because they have few insulin-producing beta cells in their pancreas and the remaining cells do not produce enough insulin. Using special strains of mice bred to be PERK-deficient, the scientists demonstrated that the lack of this enzyme blocked the proliferation of beta cells, hampered the normal functioning of beta cells, and also kept beta cells from clustering into islets. "What happens during fetal development predisposes people either to be able to maintain glucose levels normally or to have diabetes," says team leader Douglas Cavener, professor and head of the Department of Biology. The research results would be reported in the journal Cell Metabolism on 6 December 2006.

The team, consisting of graduate students Wei Zhang, Yulin Li and Kaori Iida, Postdoctoral Fellow Daorong Feng, and Research Assistant Professor Barbara McGrath, made use of the lab's earlier discovery that mice deficient in PERK show a number of parallels to human sufferers of Walcott-Rallison Syndrome (WRS), in which diabetes is combined with skeletal and growth abnormalities. The research provided an experimental model for investigating the cause of permanent neonatal diabetes that was more revealing than cell culture studies.........

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December 16, 2006, 8:56 AM CT

Can we prevent type 1 diabetes?

Within the next 10 years the EU-funded Diabetes Prevention study, part of an international study called TRIGR (Trial to Reduce IDDM in the Genetically at Risk), coordinated at the University of Helsinki, Finland, will generate a definite answer to the question whether early nutritional modification may prevent type 1 diabetes later in childhood.

Type 1 diabetes is a growing health problem among European children. European data indicate that the disease incidence has increased five-six-fold among children under the age of 15 years after World War II, and there are no signs that the increase in incidence is levelling off. The most conspicuous increase has been seen among children under the age of 5 years.

The TRIGR study is the first study ever aimed at primary prevention of type 1 diabetes. The study is designed to answer to the question whether excluding cow's milk protein from the infant's diet decreases the risk of fu-ture diabetes. All subjects are followed for 10 years to get information on whether the dietary recommendations for infants at increased genetic risk of type 1 diabetes should be revised.

Starting in May 2002, 76 study centres from 15 countries (Australia, Canada, the Czech Republic, Estonia, Finland, Gera number of, Hungary, Italy, Luxembourg, the Netherlands, Poland, Spain, Sweden, Switzerland and USA) have been recruiting families for the study. To be eligible the newborn infant has to have at least one family member (mother, father and/or sib) affected by type 1 diabetes and carry a HLA genotype conferring increased risk for type 1 diabetes. The initial recruitment target of 2032 eligible infants was reached at the be-ginning of September 2006, but the Study Group has decided to continue recruitment till the end of December 2006 (when the EU contribution will finish) to make the study even more powerful statistically.........

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December 16, 2006, 8:42 AM CT

Holiday Gluttony Dangerous For Undiagnosed Diabetics

Hearty feasts and couch-potato marathons are holiday traditions, but UT Southwestern Medical Center experts warn that packing on pounds and not exercising could be deadly for the 6 million Americans who have diabetes and don't even know it.

Diabetes, a metabolic disorder linked with obesity, can be a silent killer because its symptoms aren't sudden, but build up over time and lead to heart disease or other maladies.

That's bad news for those with undiagnosed diabetes.

"The obesity epidemic is surging and people don't realize they're setting themselves up to develop diabetes. They're like ticking time bombs," said Dr. Manisha Chandalia, an endocrinologist at UT Southwestern. "Without therapy, high levels of blood sugars in the body can damage blood vessels and nerves over time, leading to high cholesterol, hypertension, stroke, kidney disease and amputations".

If you are age 40 or older, obese, lack physical activity or have a family history of diabetes, Dr. Chandalia recommends making time during the holidays to visit a doctor for a diabetes test. Symptoms include excessive thirst or hunger, dramatic weight loss, fatigue, frequent urination or blurry vision.

The holidays also are a perfect time to start getting healthy, she said, offering these tips:........

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