New Pill Could be Better than Byetta
Filed under: Type 2, Adult Onset, Drugs, Research
A small molecule has been identified that controls diabetes in mice and may pave the way to the development of easier treatment for adult-onset diabetes.This key molecule, called Boc5, can stimulate insulin function and reduce body weight by 20%. The molecule stimulates the production of the glucagon-like peptide1 (GLP1), responsible for metabolizing glucose. The study intended to discover ways to sensitize insulin by stimulating production of GLP1. Boc5 is not powerful enough to become a diabetes or weight loss drug. But researchers suggest that similar compounds could join the latest generation of diabetes drugs, called "incretin mimetics." The first FDA-approved incretin mimetic was Byetta. A second such drug, with the generic name liraglutide, is in clinical trials.
The problem with the existing FDA approved incretin mimetic treatments is that they are large molecules that must be administered through injection. Boc5 is a small fry with big potential. Being a smaller molecule gives hope for a new generation in diabetes treatment in the form of a pill many of us would be happy to swallow.
Protein in the Brain Regulates Obesity
Filed under: Type 2, Adult Onset, Research
Scientists have found that mice lacking a protein known as SH2B1 throughout their body are obese and ultimately develop diabetes. Researchers replaced SH2B1 in the brain of obese mice and it seemed to deter the onset of obesity. The study reveals that targeting SH2B1 in the brain might be a new avenue of treatments for obesity and type 2 diabetes.
SH2B1 is expressed in tissues related to obesity, including the brain, liver, pancreas, and fat tissue. Replacing SH2B1 in the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content.
This study implies that SH2B1 in the brain is a practical target for the development of new drugs to treat obesity and type 2 diabetes.
Zinc Does Not Prevent Diabetes
Filed under: Type 2, Adult Onset, Research, Products
Despite claims by zinc supplement manufacturers that the pills can help prevent type 2 diabetes, clinical trials do not support this hypothesis.
Laboratory research suggests that zinc helps promote the production and action of insulin. A four-week study of 56 obese women found that zinc did not have an effect on factors associated with the development of diabetes. This study was an example of one trial that treated 56 people with either zinc or a placebo for four weeks and found no effect. This single trial is too small and too short to tell us anything about the effectiveness of zinc in preventing the development of type 2 diabetes.
Research does support that zinc plays a key role in the regulation of insulin production and glucose utilization. Diabetics have shown a zinc deficiency, which impairs their ability to use glucose. However this fact does not confirm zinc as a supplement to prevent the development of diabetes. I apologize it's a nonevent insofar as news. But look at it this way - it's one trial. Nobody says you have to cross it off your list because 56 obese women didn't see a change in their risk factors for developing diabetes. One study is not gospel.
12/15-LO gene implicated in diabetes inflammation
Filed under: Type 1, Type 2, Childhood, Adult Onset, Research
Type 1 is considered an autoimmune disease, and in the last few years, the immune system has been implicated in type 2 diabetes. Imbalances of the immune system's cytokines cause inflammation linked to both forms of diabetes.
The gene 12/15-LO (12/15-lipoxygenase) produces two proteins which convert fatty acids into cytokines. Mice research by Dr. Jerry Nadler and team has determined obesity in and of itself is not the cause of type 2 diabetes. (Many obese people are not type 2s). Studies done on knockout mice -- mice with inoperative genes -- have shown activation of the 12/15-LO gene is the problem. Knockout mice fed an extremely high-fat diet do not develop diabetes.
12/15-LO lies within insulin-producing cells of the pancreas, and its activation causes the cells to malfunction. The gene is also activated by white blood cells called macrophages. Now here is the link to obesity -- macrophages appear in high concentrations in fatty tissues, and imbalances in cytokines become especially pronounced as people become obese. Dr. Nadler's work has identified how large numbers of fat cells stimulate macrophages to activate 12/15-LO, and documented the inflammatory fallout.
Dr. Nadler stated 12/15-LO under normal conditions is likely involved in cell development. But it is only in pathologic conditions that the gene is activated in adults. Dr. Nadler believes blocking 12/15-LO activation could be a new therapy to protect inflammation in the pancreatic beta cells. 12/15-LO is also involved in heart and blood vessel disease and nerve cell death seen in Alzheimer's.
In terms of type 1, Dr. Nadler has found eliminating 12/15-LO in a mouse model results in over 90 percent protection from developing the disease. He is working on identifying the role of the gene in type 1. Read more in Science Daily.
Mapping Diabetes
Filed under: Type 2, Adult Onset, Diet, Lifestyle, Research, Daily News
Scientists have mapped the genes responsible for causing type 2 diabetes. This new research is giving hope to new tests that can predict an individuals risk for developing the disease and future treatments.
The study compared the genetic make-up of 700 people with type 2 diabetes and a family history of the condition, with 700 diabetes-free people. Four points on the gene map linked to a person's diabetes risk and were confirmed with another group of 5,000 type 2 diabetics. The findings of this research could explain up to 70% of the genetics related to developing diabetes. A particular zinc transporter, known as SLC30A8, which regulates insulin secretion, was shown to have a mutation. Researchers feel they may be able to treat some cases of diabetes by correcting this mutation.
These findings will allow for the creation of a genetic test to predict people's risk of developing type 2 diabetes, as well as better treatments for the presiding cause of their diabetes. Nary a day passes that I am not motivated for the future of all diabetics. This is the type of research that strengthens my faith in the coming of a cure. Identify the nature of the problem and nip it in the bud.
Diabetes Doubles in the Last 10 Years
Filed under: Type 1, Type 2, Childhood, Adult Onset, Diet, Lifestyle, Research, Exercise, Daily News
An area in Seattle, WA is reporting a two-fold increase in the number of diabetics, up from ten years ago. In addition to this -- type 1 diabetes is on the rise.
The numbers show that 84,000 adults (nearly 6% of the adult population of the county) were diagnosed with diabetes in 2006, compared with 2.8% in 1996. Even more are unaware they have the condition. Type 1 diabetes, for which there is no known prevention, is showing a dramatic increase in the area, as well.
A researcher involved in the study explains "this is not a question of raising awareness of diabetes anymore -- we're beyond that. We need to understand why people aren't listening." The comment pertains to type 2 diabetics and why they have not altered unhealthy lifestyles choices such as high-fat foods and not enough exercise. Both contribute to skyrocketing obesity rates. And obesity is a major risk factor for Type 2 diabetes, by far the most common form.
Seattle has one of the highest rates of type 1 diabetes in children under 5, and they don't know why. But early research shows that oral insulin in family members of those already diagnosed showed a 4 1/2-year delay in the onset of the disease.
What does the Vagas Nerve have to do with Diabetes?
Filed under: Type 2, Adult Onset, Research, Daily News
According to scientists at Washington University School of Medicine in St. Louis, interrupting nerve signals to the liver can prevent diabetes and hypertension in mice.
Mice were treated to become diabetic with glucocorticoids, a class of steroid hormones characterized by an ability to bind with the cortisol receptor. Once diabetes was established, the researchers surgically removed the vagus nerve. The vagus nerve is the only nerve that starts in the brainstem and extends all the way down to the abdomen. More impressive is the fact that once the nerve was removed from the diabetic mice, insulin resistance and high blood pressure was prevented or reversed. This is an interesting discovery because people with asthma, arthritis, and organ transplants often rely on steroid treatments. It just so happens that many of them go on to develop insulin resistance.
Don't go ripping your vagus nerve out just yet. A fun fact about the vagus nerve is that it's name is taken from the Latin word meaning "wanderer". The vagal nerve pathway can influence seizures, depression and other disorders. Although the research is thoroughly enlightening, it is still very green. Hang on to your vagus nerve while the research continues.
Top rated diabetes books - what's yours?
Filed under: Type 1, Type 2, Childhood, Adult Onset, Books, Support
TuDiabetes.com is a site for people touched by diabetes. The creator of the site, Manny Hernandez, got the ball rolling on a topic of interest we all take to heart - diabetes book recommendations.
When you ask diabetics to brainstorm on a terribly intrinsic topic you get some pretty good responses. One suggested read was The Diabetes Improvement Program. This book helped a diabetic overcome depression, when the talented team of healthcare professionals could not. Other honorable mentions include: Psyching Out Diabetes, Dr. Bernstein's' Diabetes Solution, Diabesity, and Diabetes for Dummies.
Somebody actually asked something very interesting - where is the book on the evolution of diabetes treatment? Often a topic of discussion, and yet so rarely documented is the sequential events of diabetes treatment, starting with the discovery of insulin. A lull ensued from about 1930 till the boom of genetically modified human insulin, in the early 80s. Any investigative journalist willing to take a stab at it? I guarantee the book will make my must read. And Eli Lilly might actually pay you not to write it.
P.S. One reader pointed out - a chapter of Brent Hoadley's book, Too Profitable to Cure presented a chronology of the evolution of diabetes treatment.
Chiropractors adjusting Diabetes Control
Filed under: Type 2, Adult Onset, Lifestyle, Research, Support
Researchers are finding evidence that chiropractic adjustments could enhance diabetes control.
The study focused on the positive response chiropractic adjustments contributed in the care of a patient with adult onset diabetes. The chiropractic care was directed toward correcting misalignments in the spine, called vertebral subluxations. Vertebral subluxation is a chiropractic term to describe a myriad of symptoms thought to occur as a result of a misaligned spinal segment. However, specifically for this patient, it was the vertebral relationship governing his nervous system and endocrine organs. After one month of being on the program, the patient's glucose levels had normalized in both the blood and urine. His medical doctor, who monitored his progress, said the patient would not need insulin if the condition remained stable.
The study was one of several projects exploring the impact of vertebral subluxations on human health and well-being. For more than 100 years, chiropractors have maintained that what they do affects organ system function and general health. Case studies like this demonstrate the urgency for more research on chiropractic and its effects beyond neck and back pain.
Does Diabetes Boost Parkinson's Risk?
Filed under: Type 2, Adult Onset, Lifestyle, Research
Acording to a Finnish study, diabetes may increase the risk of developing Parkinson's disease.
Researchers have found that people with type 2 diabetes were more than 80% more likely to be later diagnosed with Parkinson's disease than people without diabetes. This is the first study to suggest that diabetes may be a risk factor of Parkinson's disease, a progressive disease that causes muscle rigidity and tremors.
The study followed a group of more than 50,000 men and women over a period of 18 years. During that time, 324 men and 309 women developed Parkinson's disease. People who had type 2 diabetes at the start of the study were far more likely to be later diagnosed with Parkinson's disease. Overall, after adjusting for other possible risk factors for Parkinson's disease, men and women with type 2 diabetes were 83% more likely to develop Parkinson's disease than those without it.
Although the exact nature of the relationship between diabetes and Parkinson's disease is unclear, researchers say several lifestyle factors may be associated with both disorders. Among these factors are: obesity, cigarette smoking, and lack of physical activity.
Perhaps further research between the association of diabetes and Parkinson's disease could help researchers better understand an avenue to a cure. . Pioglitazone is a drug used to treat diabetes. It may also help fight the onset of Parkinson's. Thanks to funding from The Michael J. Fox Foundation we may be closer to clinical trials and an answer.