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.
Protein Coat might Cure Diabetes
Filed under: Type 2, Adult Onset, Research, Daily News
Researchers found a protein that coats the liver is directly correlated with visceral-fat induced diabetes, or type 2 diabetesWhen visceral fat accumulates, the amount of a hormone called adiponectin, decreases. Adiponectin is found in fat cells, and plays a role in glucose regulation and fatty acid metabolism. Researchers found two types of protein on the surface of mouse liver cells. When the proteins and adiponectin interact, blood sugar and neutral fat levels fall, boosting fat-burning functions. However, obese mice with accumulated visceral fat have fewer of these proteins on the surface of their liver cells. When these proteins increased in number, blood sugar levels would decline. The study hypothesizes that if the quantity of adiponectin decreases in obese people, a potential cure for type 2 diabetes may be found by increasing the proteins found on the surface of the liver.
Talk about the power of protein! We've all heard about the leaders in the pack when it comes to dropping pounds - eggs, fish, chicken, soy and whey protein. But this discovery reveals a new way to combat the bulge and reduce your chances of developing type 2 diabetes. Although these new proteins won't find accommodations in your local grocery store - perhaps Big Pharma will have a designer label to sport in the near future. You'd buy it, wouldn't you?
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.
History underway in type 1 diabetes cure
Filed under: Type 1, Childhood, Research, Events, Support
Dr. Faustman's lab is currently collecting blood samples from individuals with established Type 1 diabetes. These samples are being used to quantify the number of autoreactive T-cells and develop the adequate dosage for Phase 1 of human trials to cure Type 1 diabetes.
The research has been presented and the NIH confirmed it. By reeducating the confused T-cells and instructing them not to attack healthy islets, an apparent cure of established type 1 diabetes in non-obese diabetic mice is possible. Now, Dr. Faustman is collecting human samples to bestow the same cure for diabetes in humans.
If you wish to be a part of this revolutionary event for curing Type 1 diabetes, please contact the Clinical Coordinator or call Dr. Faustman's lab at (617) 726-4084. Each participant is asked to bring a control person along with them - an unrelated person without Type 1 diabetes or another autoimmune disease. Diabetic or not - you can be a part of history in curing Type 1 diabetes!
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.
Vagus nerve inerference may prevent diabetes and hypertension
Who knew that all it took was removing the vagus nerve to prevent or reverse the development of insulin resistance. Wait -- what the hell is the vagus nerve? Turns out that it is a rather important nerve communicates with with just about everything in your body. It's truly no wonder that the terms 'vagus' itself is derived from the Latin word meaning "wanderer." And, thanks to researchers from Washington University School of Medicine in St. Louis, it has been found to play a very important role in preventing both diabetes and hypertension.
The scientists published their findings in the February issue of the journal Cell Metabolism, first pointing to a nuclear receptor they had previously highlighted called PPAR-Alpha (Ppara). This receptor had been shown to be necessary for the induction of both hypertension and diabetes when lab mice were treated with steroids. Considering that steroids are commonly prescribed for people who ave asthma, arthritis, and organ transplants, it has been suggested that this treatment has lead to insulin resistance and, in some cases, result in diabetes.
However, in the research team's most recent study, they found that both the Ppara and the vagus nerve play a significant role in the development of diabetes and hypertension. It appears as though by removing the vagus nerve, the risk of developing these disorders in response to steroid treatment, even if they have Ppara.
While the research on the interruption of nerve signals to the liver has only been performed on mice thus far, scientists are hopeful that their results will also hold true for humans.
Less insulin longer life
Filed under: Type 1, Type 2, Childhood, Adult Onset, Diet, Research
Howard Hughs Medical Experts have discovered the key to a longer life is lower insulin levels. Less insulin helps cells fend off diseases that lead to early death like heart disease, cancer and diabetes. So how does one lower their insulin levels? Caloric restriction by way of eating less carbohydrates.
Caloric restriction postpones the onset of life-threatening conditions like cancer, diabetes, and heart disease. It may still happen, but at a later age. Scientists manipulated genes in mice to produce 50% less insulin and saw the mice live 18% longer. While lowering insulin throughout the body can lead to a diabetic state, scientists found that allowing insulin levels to be high throughout most of the body, and lowering the insulin signaling only in the brain through genetic manipulation, extended the life of mice.
Although the mice were overweight, they lived longer and seemed active and youthful. Scientists believe that this research explains why some people who live past 100 may have a natural genetic tendency for lower insulin signaling in the brain. They eat a normal amount of calories and may even be a bit overweight, but still enjoy the benefit of life extension. This begs the question: if all diabetes oral meds multiply the effect of insulin -- doesn't this increase the chances of heart disease and cancer? New Rule: Black box warning on ALL prescription diabetes drugs!!
Health, longevity linked to insulin in the brain
Filed under: Type 2, Diet, Lifestyle, Research, Exercise
What makes for a long and healthy life? Why, you say, how about a healthy diet and liberal quantities of exercise? True! A healthy lifestyle keeps you in shape and is one factor that promotes longevity. But have you ever wondered exactly how this works on a physiological level? How does the brain understand you skipped the gym all summer and had French fries for lunch yesterday? The answer, according to the results of a new study published in Science (July 2007), could relate to insulin levels in the brain. Researchers induced lab mice to overeat until they became obese and some exhibited symptoms of diabetes. Yet some of those same mice actually lived eighteen percent longer than their slender mice buddies. The researchers attributed that longevity to a gene that affects insulin. Put simply: the longevity gene (called Irs2) effectively "tricked" the brains of those mice into thinking they were slim and fit, when in fact the opposite was true.
For diabetics, the study raises an additional question: if raising insulin levels decreases the body's sensitivity to it, is it really desirable to treat type 2 diabetics with insulin over the long-term? Lead author of the study, Morris White of Children's Hospital in Boston, says it's highly preferable (when possible) to get type 2 diabetes under control through old-fashioned diet and exercise, rather than through insulin or other meds.Permalink | Email this | Linking Blogs | Comments
Type 1 vaccination successfully tested on mice
I do not like vaccinations. I wonder if they are connected to the autism and diabetes epidemics, even attention-deficit disorders. I do vaccinate my children, just begrudgingly. Yet if there ever was a vaccination against type 1 diabetes, I would be first in line.
Researchers in France and Germany have demonstrated you can treat a type 1 diabetic mouse with a vaccination. Type 1 diabetes is an autoimmune disease in which the immune system's T cells cannot distinguish between "non-self" and "self", attacking cells of the pancreas that produce insulin.
Previously, Drs. Falk and Rotzschke of the Max Delbruck Center for Molecular Medicine (MDC), blocked the misdirected immune system by vaccinating mice with modified structures of the same organ targeted by the defective T cell immune response. Antigens are structures which activate a body's immune system, and the mice were protected from type 1 diabetes through the body's own antigens linked together in a repetive chain of identical copies. But the researchers did not understand how this protective string of antigens worked.
In a new study, Drs. Liblau, Falk and Rotzschke have proven this protective effect is due to the activation of an immune system's suppressor cells, the very cells that block those misguided T cells. Suppressor cells only inhibit T cells that attack a body's own tissue, allowing T cells to continue to attack foreign viruses and bacteria.
Dr. Rotzschke believes suppressor cells are a promising research focus in immunology. Even better, he is confident suppressing a haywired immune system through a specific vaccination with one's own antigens opens up a whole new treatment approach.
New trial uses small doses of oral insulin to prevent type 1
Filed under: Type 1, Childhood, Research
Nine-year-old Devin Linendoll was diagnosed with type 1 diabetes at the tender age of two. He's gone from a toddler criss-crossed with comforting Band-Aids after a day of shots, to a whiz with his insulin pump. Now Devin's parents, Amy and Lawrence, just found out their youngest son, Trevor, has at least a 50 percent chance of developing type 1 within the next five years. After a lengthy set of complex blood tests, Dr. Bill Russell, Devin's pediatric endocrinologist, determined Trevor's six-year-old body is attacking its insulin. He makes plenty now, but his body thinks insulin is an invader. If Trevor follows in Devin's footsteps, his immune system will continue to attack insulin-generating cells, slowly destroying insulin capacity.
The Linendoll's decided to enter Trevor in a study examining a new treatment to possibly block the development of type 1. In this trial, patients orally ingest small doses of insulin for several years to allow the body to develop tolerance. Dr. Russell stated the digestive system is better at accepting new exposures than the bloodstream. The hope for those prone to diabetes is repeated exposure can train a body to react to insulin more normally -- to develop tolerance for something it would normally reject.
Trevor is the first child to participate in this seven-year study. But since it is a blind trial, he'll either be receiving oral insulin or swallowing a placebo. Read more in the Tennessean.