Taking a brisk walk several times a week for exercise appears to reduce black women’s risk of developing type 2 diabetes, according to a study published this month in the American Journal of Epidemiology, Reuters Health reports. Few studies have been conducted on the benefits of exercise among black women, according to Reuters. For the study, Julie Palmer of Boston University and colleagues used data from the ongoing Black Women’s Health Study that followed 45,000 black women from 1995 to 2005.

Researchers found that those who said they walked for a minimum of five hours weekly for exercise were one-third less likely to develop type 2 diabetes than those who did not walk. The risk of being diagnosed with the disease was significantly lower among women who said they regularly took a brisk walk even when taking into account possible contributing factors such as age, income and diet. The study included a large number of obese women and they too appeared to have a lower risk for developing diabetes if they exercised regularly.

Palmer said, “This is important, because it suggests a way to reduce diabetes risk even among the women who are at highest risk of the disease,” adding, “The finding that brisk walking for a few hours a week or longer reduces diabetes risk may be the most important finding of all. This is something almost all women can do in the course of their daily lives.”

Researchers also found that women who watched television for five or more hours a day were 86% more likely to develop diabetes than those who watched less than one hour per day

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A biological tit for tat may hold clues to improving the success of islet cell transplants intended to cure type 1 diabetes, according to a Medical College of Georgia scientist.

In type 1, the immune system attacks insulin-producing cells causing high blood glucose levels that may temporarily reduce the attack, said Dr. Rafal Pacholczyk, an immunologist in the MCG Center for Biotechnology and Genomic Medicine.

He just received a three-year, $495,000 grant from Juvenile Diabetes Research Foundation to find out whether this counteraction offers insight for transplants.

High blood glucose, or hyperglycemia, causes all sorts of dysregulation throughout the body. “It throws off metabolism, hormonal interplay and increases the risk of severe infections,” Dr. Pacholczyk said. A shot of insulin or an islet cell transplant normalizes blood glucose levels, enabling, among other things, restoration of the usual balance between effector T cells which mount an immune or autoimmune response and regulatory T cells which suppress attacks.

He’s obviously not saying hyperglycemia is good; in fact if diabetics were to get a transplant while their blood glucose was high the procedure alone could be lethal. But Dr. Pacholczyk hypothesizes it causes a temporary shift in the immune playing field that gives advantage to regulatory T-cells long enough for the body to accept the transplanted cells. One reason may be that suppressive regulatory cells recover differently or are less influenced by hyperglycemia.

Researchers at Canada’s University of Alberta were the ones to find high blood glucose causes a short-lived suppression of the attack mode of the immune system followed by a slow return of homeostasis. The result: Islet cell transplants done in mice immediately after a blood glucose spike were dramatically more successful than those done days later, according to the research published in 2007 in the Scandinavian Journal of Immunology. In fact, the early recipients did not require immunosuppression, which transplants patients receive to reduce the risk that their new insulin-producing cells also will become targets for their immune system. However, this generalized immune suppression puts patients at increased risk for infections, cancer and other diseases. “Basically, your guard is down,” Dr. Pacholczyk said.

Seventy percent of mice that got transplants two days after they became hyperglycemic did not need immunosuppression, the Canadian researchers found; after nine days, the acceptance rate was reduced to about 10 percent. “The question is why?” Dr. Pacholczyk said.

Typically the path isn’t easy for transplanted cells. Many die from the stress of transplantation or immune system attack either because they are rejected as invaders or because the same autoreactive mechanism that led to destruction of the patient’s own cells is resurrected. “Cells that survive are the ones being counted on. Over time, they should increase in mass to a level that should produce sufficient amounts of insulin,” the researcher said.

Type 1 diabetes results from the wrong mix of genes and environmental triggers. For example, early exposure of a genetically predisposed child to cow’s milk and a viral infection could trigger an immune response to bovine insulin which, in turn, leads to islet cell destruction.

The researcher’s animal model reflects the human condition fairly well; it’s inbred to have diabetes but Dr. Pacholczyk developed a system to chemically induce the disease when he wants so he’ll know exactly when islet cells are destroyed by the immune system. He’ll document hyperglycemia’s impact on all immune cells with the long term goals of identifying the magic that enables acceptance of islet cells and finding a safer, more direct way to replicate it.

In 2007, he and colleague Dr. Leszek Ignatowicz caused a stir in the scientific community when they found that regulatory T cells, which always suppress the immune response, can recognize invaders as well as body tissue. That means they could technically keep the immune system from attacking a foreign substance, such as transplanted islet cell. But researchers cautioned then that manipulating T-cell levels to treat autoimmune diseases, such as type 1 diabetes and lupus, must be done cautiously and selectively to ensure patients are not put at the same risk as those on traditional immunosuppressive therapy. MCG news categories related to this story:

Diabetes and Obesity
School of Medicine

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ALR Technologies Inc. (OTCBB: ALRT) announces the initial results from the ECHO Healthcare Education Foundation of Alabama comprehensive diabetes intervention program. The program, sponsored by ALRT, shows significant reduction in A1c values.

Participants in the program for three months showed statistically significant changes in:

– Rates of self-monitoring of blood glucose
– Hemoglobin A1c value
– Frequency of exercise sessions
– Adherence to medication protocols
– Participation in weight management programs
– Self-evaluation of level of adherence in: self-monitoring of blood glucose, exercise and diet

Average A1c score for the participants dropped from 7.6 to 6.7. A level below 7.0 is recommended by the American Diabetes Association and shown to reduce microvascular and neuropathic complications of diabetes. Equally encouraging were the findings of the out of range group (those with A1c over 7.0). Their A1c dropped from an average of 9.0 to 7.4. Prior to the pilot program, none of the participants had blood sugar score below the critical 7.0 level and after 3 months, 47% reached that important target.

The average frequency of self-testing for blood sugar increased from 1.4 times per day to 3.1 per day. Testing of the out of range group increased from 1.5 times per day to 3.5 per day.

The pilot was implemented by ECHO Healthcare Education Foundation of Alabama with an ECHO member company. The program was conducted with 33 Type 2 Diabetics, 2 Type 1 Diabetics and 11 Pre-Diabetics.

The program is ongoing and data will be reported on a quarterly basis.

ECHO

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Children with diabetes are at an increased risk for developing eating disorders and researchers want to know if it’s their disease or treatment that’s to blame.

“Diabetes treatment prescribes obsessive food behavior, such as carbohydrate restriction,” said Dr. Deborah Young-Hyman, pediatric psychologist in the Medical College of Georgia’s Georgia Prevention Institute. “We want to know if those prescribed behaviors contribute to disordered eating and/or whether there are physiological mechanisms which prevent children with diabetes from controlling their eating behavior. For example, treatment with insulin makes you hungry and can cause you to gain weight.”

There is some unfortunate synergy: diabetes makes it difficult to control blood glucose and disordered eating behavior does as well, Dr. Young-Hyman said.

Over the next three years, with funding from the American Diabetes Association, she and researchers at Emory and Harvard universities will study 90 children age 10-17 newly-diagnosed with diabetes or transitioning to an insulin pump. They will monitor treatment patterns, weight, psychological adjustment and attitudes about weight and eating. They’ll also look at changes in eating patterns and blood sugar levels in response to insulin.

Children and their parents will answer computer-based questionnaires about eating behaviors and psychological adjustment - in the context of their disease and its treatment.

These include questions about parental attitudes, family factors, personality of the child and parents and perceived societal attitudes.

“As they are diagnosed and are adjusting to diabetes treatment, children are already dealing with all sorts of issues that put them at an increased risk for eating disorders. The psychological issues that come with the diagnosis can add to that risk,” she said. “There is also the existing drive for thinness that exists in our society, dealing with the diagnosis and management of a long-term illness and the psychological adjustment that comes with that.”

Even the insulin the children must take may be a factor. “Large doses can lead to uncontrolled hunger, which can be mislabeled as disordered eating behavior. Patients with type 1 diabetes also lose amylin production - a hormone responsible for gastric emptying and associated with feelings of fullness - that can also lead to increased feelings of hunger,” Dr. Young-Hyman said.

Study findings could support a different treatment approach.

“We might come to understand that putting a child or adolescent on an insulin pump sooner rather than later and providing them with a more flexible nutrition regimen could decrease their insulin needs and prevent excess hunger,” she said. “If we don’t approach weight control as dieting, place less emphasis on food restriction and focus on healthy nutrition and usual eating patterns, we can help patients gain more control over their eating behaviors and their treatment without adoption of maladaptive weight management strategies. Studies indicate that feeling in control of your illness is one of the keys to successful treatment and good psychological adjustment.”

Jennifer Hilliard
Medical College of Georgia

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A new University of Illinois study suggests that we may pay a price for ingesting too much fructose. According to lead author Manabu Nakamura, dietary fructose affects a wide range of genes in the liver that had not previously been identified.

Chances are you consume quite a bit of fructose. Most Americans do - in refined sugars such as sucrose or table sugar (which is half fructose) and in high-fructose corn syrup, used in products as diverse as soft drinks, protein bars, and fruit juice.

But many scientists believe that high dietary fructose contributes to the development of metabolic syndrome, a group of risk factors that predict heart disease and Type 2 diabetes.

“For this reason, it’s important for scientists to understand exactly how consuming high amounts of fructose affects human health,” said Nakamura, a U of I associate professor of food science and human nutrition.

Nakamura’s lab is continuing to study the metabolism of fructose with an eye to making recommendations about its dietary use.

His study shows that the metabolism of fructose is more complex than the data had indicated. “Our gene-expression analysis showed that both insulin-responsive and insulin-repressive genes are induced during this process. Our bodies can do this, but it’s complicated, and we may pay a price for it,” he said.

According to the scientist, most carbohydrates are handled fairly simply by our bodies. They are converted quickly to glucose and used for energy or stored as fat. “When we are eating, blood sugar–and insulin production–goes up. When we sleep or fast, it goes down,” he said.

The process is not so simple with fructose, he noted. “In order for fructose to be metabolized, the body has to create both fasted and fed conditions. The liver is really busy when you eat a lot of fructose.”

Because, unlike glucose, fructose metabolism occurs mainly in the liver, Nakamura wanted to gain a complete picture of gene expression in the liver during fructose metabolism.

In Nakamura’s study, 24 rats were fed either a 63 percent glucose or fructose diet four hours a day for two weeks; at the end of this period, half the animals fasted for 24 hours before the scientists performed a gene expression analysis; the other half were examined at the end of a four-hour feeding.

Fructose feeding not only induced a broader range of genes than had previously been identified, there were simultaneous increases in glycogen (stored glucose) and triglycerides in the liver.

“To our surprise, a key regulatory enzyme involved in the breakdown of glucose was about two times higher in the fructose-fed group than in the glucose-fed group,” Nakamura said.

The study also suggests that a protein called carbohydrate response element binding protein is responsible for the fructose effect on certain genes that trigger the production of fat, he said.

“We’re continuing to assess the risk of fructose insulin resistance and the consequent risk for development of diabetes,” he said.

Phyllis Picklesimer
University of Illinois at Urbana-Champaign

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