Reversal of type 1 diabetes in mice may eventually help humans, says new research. Investigators at the University of Cincinnati (UC) have found a therapy that reverses new onset Type 1 diabetes in mouse models and may advance efforts in combating the disease among humans. Can a new pathway of targeting the immune system be tested in humans? The study, led by William Ridgway, MD, was presented Saturday, June 14, 2014, at the American Diabetes Association’s 74th Scientific Sessions – American Diabetes Association in San Francisco.
Type 1 diabetes is usually diagnosed in children and young adults and affects about 5 percent of all people with diabetes, according to the American Diabetes Association. In Type 1 diabetes, the body does not produce sufficient insulin, which is central to glucose metabolism: without insulin, blood glucose rises.
There is no cure for Type 1 diabetes though it can be controlled with insulin therapy. Symptoms of the disease include frequent urination, excessive thirst and weight loss even though you are eating more
Researchers say the incidence of Type 1 diabetes and autoimmunity in general has risen rapidly since the mid-20th century, possibly the result of under-stimulation of innate immune systems which trigger autoimmunity in children and young adults. In Type 1 diabetes, autoimmunity causes the body’s T-cells to attack its insulin-producing beta cells.
Previously, it has been reported that non-obese diabetic mice have defects in innate immune cells and that TLR4, a toll-like receptor, plays a protective role in preventing Type 1 diabetes.
Ridgway, Alice W. and Mark A. Brown Professor and Director of the division of immunology, allergy and rheumatology at UC, says his team of researchers used an agonistic monoclonal antibody, UT18, to boost the activity of TLR4 and reverse new onset diabetes in a high percentage of newly diabetic non-obese mice.
“We have shown that by using an antibody to stimulate a specific molecule in the innate immune system we can reverse—with a high rate of success—new onset diabetes in mice that have already developed the symptoms of diabetes,” says Ridgway, according to the June 14, 2014 news release, Reversal of type 1 diabetes in mice may eventually help humans. “The cause of this reversal is a preservation of the endocrine pancreatic beta cells that produce insulin. These cells are preserved from the autoimmune attack which is the hallmark of Type 1 diabetes.”
The key to reversing Type 1 diabetes in mice, says Ridgway, is catching the disease at its onset, which is typically within a very short time window
The time frame would be longer in humans. But it’s still a relatively short time from new onset to end-stage Type 1 diabetes, says Ridgway. A different part of the immune system has to be targeted, since there are two ‘arms’ of the immune system.
Ridgway says this approach differs from most in combating Type 1 diabetes because his team’s therapies in mice do not directly interact with T-cells. He says treatment of autoimmunity has often been directed at suppressing an over-zealous adaptive immune response by eliminating auto-reactive T-cells.
The difference between the adaptive immune system and the innate immune system
“We are targeting a different part of the immune system,” says Ridgway, according to the news release. “There are two arms of the immune system. One is called the adaptive immune system and the other is the innate immune system. Basically the T-cells and B-cells are in your adaptive immune system and they respond to many different antigens. The innate system tends to have a stereotypical response. We are targeting a receptor that is found mostly on the innate immune cells, such as dendritic cells.
“This same molecular TLR4 pathway operates in humans in many similar ways; though there are some differences, it’s possible this new pathway of targeting the immune system could be tested in humans,” says Ridgway, according to the news release.
Additional study will be required, but the therapy may hold promise because one agonistic anti-TLR4 agent is already FDA approved and others are under development, says Ridgway, according to the news release.
Are grandparents feeding visiting grandchildren healthier diets higher in vegetables and fruits, traditional diets from previous generations, or lower-cost fast-foods and sodas?
Obese children on unhealthy diets start to have not only more but also larger fat cells (called adipocytes), at a very young age that’s associated with increased inflammation and is linked to impaired metabolic function. But parents and others choosing foods for kids and teenagers can introduce more vegetables and fruits and fewer meals of red meat, fried starchy vegetables, rich desserts like cake and sodas at an early age. A lot of parents don’t even know what vegetables to choose or even what some vegetables or fruits look like. What parents may not realize is that kids’ bodies are processing unhealthy food, including excess sugar differently than adults’ systems.
Some parents can’t afford healthier foods. If you take a parent shopping at the produce counter, the parent may not know what unfamiliar healthier vegetables look like or have never seen them in their homes as children. So the same unhealthy foods may get passed from parents to kids, such as eating lots of fast-foods because they’re cheaper than buying fresh produce on a tight food budget. One example are diets of take-out fast foods because there’s little time to cook and prepare food for the next day or the week ahead of time.
You can help your child or teenager improve nutrition before it leads to type 2 diabetes or pre-diabetes. Improving diet quality reduces risk for type 2 diabetes. A new study finds healthier eating pattern provides benefit independent of other lifestyle changes. Improving the overall quality of one’s diet helps to prevent type 2 diabetes, independent of other lifestyle changes, according to a study presented at the American Diabetes Association’s 74th Scientific Sessions®.
The study, by researchers at the Harvard School of Public Health, found that those who improved their diet quality index scores by 10 percent over four years – by eating more whole grains, fruits and vegetables, and less sweetened beverages and saturated fats, for example – reduced their risk for type 2 diabetes by about 20 percent, compared to those who made no changes to their diets. Dietary quality was measured using the 110-point Alternate Healthy Eating Index 2010.
The study also examined whether improved diet was a marker of other lifestyle changes, such as weight loss or increased physical activity, or if it could independently reduce a person’s risk for developing type 2 diabetes
“We found that diet was indeed associated with diabetes independent of weight loss and increased physical activity,” says lead researcher Sylvia Ley, PhD, according to the June 14, 2014 news release, “Improving diet quality reduces risk for type 2 diabetes.” Ley is a post-doctoral fellow at the Harvard School of Public Health.
“If you improve other lifestyle factors you reduce your risk for type 2 diabetes even more, but improving diet quality alone has significant benefits. This is important because it is often difficult for people to maintain a calorie-restricted diet for a long time. We want them to know if they can improve the overall quality of what they eat – consume less red meat and sugar-sweetened beverages, and more fruits, vegetables and whole grains – they are going to improve their health and reduce their risk for diabetes.”
The study also showed that it didn’t matter how good or poor a person’s diet was when they started out, she explains, according to the news release. “Regardless of where participants started, improving diet quality was beneficial for all.”
Funding for this research was provided by the National Institute of Diabetes and Digestive and Kidney Diseases, part of the National Institutes of Health, under grant number DK058845.
Kids process sugar in a different way than adults
Understanding the unique nature of children’s bodies and brains is explained in a new study that shows adolescent brains process sugar differently than adult brains. Another study finds evidence changes in adipose tissue begin at very young age for obese children. If you’re in San Francisco this week, perhaps you’ve heard that the American Diabetes Association is having their 74th Scientific Session there this week of June 15, 2014.
With the increase in childhood obesity and the associated increase in type 2 diabetes among children and adolescents, there is growing interest in how children’s bodies process the foods they eat and how obesity and diabetes begin to develop at early ages. Two studies presented at the American Diabetes Association’s 74th Scientific Sessions® help to shed light on this topic.
One study, by researchers at the Yale School of Medicine, compared how the brains of adolescents and adults differed in their response to ingestion of a glucose drink. It found that in adolescents, glucose increased the blood flow in the regions of the brain implicated in reward-motivation and decision-making, whereas in adults, it decreased the blood flow in these regions.
“While we cannot speculate directly about how glucose ingestion may influence behavior, certainly we have shown that there are differences in how adults and adolescents respond to glucose,” says lead researcher Ania Jastreboff, MD, PhD, according to the June 15, 2014 news release, “Understanding the unique nature of children’s bodies and brains.” Jastreboff is an Assistant Professor of Medicine and Pediatrics at the Yale School of Medicine.
“This is important because adolescents are the highest consumers of dietary added sugars. This is just the first step in understanding what is happening in the adolescent brain in response to consumption of sugary drinks. Ultimately, it will be important to investigate whether such exposure to sugar during adolescence impacts food and drink consumption, and whether it relates to the development of obesity.”
Comparing fat cell composition and biology in lean and obese children and teenagers
Another study, by researchers in Germany at the University Children’s Hospital in Leipzig, compared fat cell composition and biology in lean and obese children and adolescents. They found that when children become obese, beginning as early as age six, there was an increase in the number of adipose cells, and that they are larger in size than the cells found in the bodies of lean children. The researchers also found evidence of dysfunction of the fat cells of obese children, including signs of inflammation, which can lead to insulin resistance, diabetes and other problems, such as high blood pressure.
“Our research shows that obese children start to have not only more but also larger adipocytes, or fat cells, at a very young age and that this is associated with increased inflammation and is linked to impaired metabolic function,” says lead researcher Antje Körner, MD, according to the news release. Körner is a Professor of Pediatrics and Pediatric Researcher at the Pediatric Research Center, University Children’s Hospital, Leipzig. “What we were interested in was seeing whether something was already going on with the adipose tissue itself if the children become obese at an early age, and it appears that there is. It’s important because this can contribute to the development of comorbidities of obesity in children, such as diabetes.”
For more information, you may wish to check out the website of the 74th Scientific Sessions – American Diabetes Association. Or you may be interested in another website, “Dietary Sugar and Body Weight: Have We Reached a Crisis in the Epidemic of Obesity and Diabetes?: Health Be Damned! Pour on the Sugar.” There’s the website, “ADA Cardio Disease Review #4 – American Diabetes Association.” And there’s also a noteworthy PDF article, “So Many Nutrition Recommendations–Contradictory or Compatible? Also, you may wish to check out the website of the American Diabetes Association.