However, new research coming out of Emory University in Atlanta, Georgia in the United States, suggests that, especially for people in India, there might be an altogether different cause for Type II diabetes.
The study, published online April 17 in Diabetes Care shows is that impaired pancreatic beta-cell function seems to play a larger role than insulin resistance in the very early stages of type 2 diabetes in Asian Indians, according to a new study, published online April 17 in Diabetes Care. Dysglycemia is a generic term for abnormal blood sugar levels from any cause which results in disease. An Ecosystem of Health provides general information on health and wellness as well as advances in a range of medical fields. If you want health and wellness information specific to your conditions and interests, please SIGN UP TODAY and create your own health profile. In this study, an international team of researchers investigated how genetic variation controls the development of diabetes. Current treatments for T2D rely on improving the metabolic response of the liver to insulin. Dr Lydia Makaroff (International Diabetes Federation, not an author of the current study): "The health cost for diabetes currently exceeds US$600 billion, 12% of the global health budget, and will only increase as diabetes becomes more common. Researchers at the University of Massachusetts Medical School have discovered a new pathway that triggers regeneration of beta cells in the pancreas, a key development that may aid in the development of diabetes treatments.
Diabetes researchers at Sweden's Karolinska Institutet have developed a novel technique that makes it possible to monitor insulin resistance in a non-invasive manner over time in mice. Researchers at Lund University in Sweden have made two new discoveries with regard to the beta cells' ability to release insulin. I? cells in pancreatic islets are responsible for producing insulin, which is essential to regulate blood glucose homeostasis.
Patients with a rare, genetic form of diabetes often are misdiagnosed as having type 2 diabetes because the two share symptoms. Alcohol-craving rats have provided researchers with a detailed look into the complicated genetic underpinnings of alcoholism. New research has identified how cells protect themselves against 'protein clumps' known to be the cause of neurodegenerative diseases including Alzheimer's, Parkinson's and Huntington's disease.
In one of the largest international genetic studies of congenital heart disease (CHD), researchers have discovered gene mutations linked to three new rare congenital heart disorders. Scientists have discovered 15 genome sites - the first ever - linked to depression in people of European ancestry. Researchers are closer to finding a better way to treat children with a rare metabolic disorder called MPS I.
Why can't they use stem cell technology and create a new pancreas and liver and transplant them, that would rid the patient of diabetes for the rest of his life.
Excess fat in the diabetic pancreas is specific to Type-2 diabetes and important in preventing insulin being made as normal. LONDON – Researchers have shown that Type-2 diabetes is caused by fat accumulating in the pancreas and that losing less than one gram of that fat through weight loss reverses the condition.
In a trial, 18 people with Type-2 diabetes and nine people who did not have diabetes were measured for weight, fat levels in the pancreas and insulin response before and after bariatric surgery. The participants in the study had all been selected to have gastric bypass surgery for obesity and were measured before the operation then again eight weeks later. Critically, the pool of fat in the pancreas did not change in the non-diabetics but decreased to a normal level in those with Type-2 diabetes. LMC is looking for individuals with Type 1 Diabetes to participate in a research study involving an experimental insulin medication that may help lower meal-time glucose levels. We have over 40 years of combined & trusted experience conducting clinical research studies to thoroughly test new medications or medical devices for safety and efficacy. Diabetes mellitus occurs throughout the world, but is more common (especially Type 2) in the more developed countries.
What this means is that there is a defective response of body tissues to insulin due to problems with the insulin receptors in those body tissues. Usually the more specific terms hyperglycemia, hypoglycemia, or others are used instead, and dysglycemia is used only when a firm diagnosis has not yet been made. Patients with diabetes mostly fall into one of two categories, type 1 diabetics, triggered by autoimmunity at a young age, and type 2 diabetics, caused by metabolic dysfunction of the liver.
Thanks to our genetic make-up, some of us have beta cells that are tough and robust, while others have beta cells that are fragile and can't handle stress. One out of every 11 adults is suffering from the disease, yet half of them have not even been diagnosed.
While most previous work has focused on the effect of genetics in altering the immune system (in T1D) and metabolic dysfunction of the liver (in T2D), this research found that genetics also affected the beta cells that produce insulin. These antidiabetic drugs, in conjunction with lifestyle interventions, can control the early stages of T2D by allowing insulin to function on the liver again. Much of this health care burden is caused by late-stage type 2 diabetes, where we do not have effective treatments, so we desperately need new research into novel therapeutic approaches. Previously, animal models were all based on the early stage of metabolic dysfunction in the liver, which has allowed the development of good drugs for treating early-stage T2D. It is caused by a deficiency of the key enzyme IDUA needed to break down complex sugars in cells. After the operation, those with Type-2 diabetes were immediately taken off their medication. This shows that the excess fat in the diabetic pancreas is specific to Type-2 diabetes and important in preventing insulin being made as normal.
We are one of the largest networks of fully-owned and integrated outpatient clinical research sites in North America. However, the greatest increase in prevalence is expected to occur in Asia and Africa, where most patients will probably be found by 2030. These abnormalities cannot be attributed to differences in age, adiposity, insulin sensitivity, or family history.
Diabetes is caused by the inability of the body to lower blood glucose, a process normally driven by insulin. Mice with fragile beta cells that were poor at repairing DNA damage would rapidly develop diabetes when those beta cells were challenged by cellular stress. However during the late stages of T2D, the death of beta cells means that there is no longer any insulin being produced in the pancreas. This discovery dramatically improves our understanding of type 2 diabetes, which will enable the design of better strategies and medications for diabetes in the future". This new mouse model will allow us, for the first time, to test new antidiabetic drugs that focus on preserving beta cells. At present the only way we have to achieve this is by calorie restriction by any means — whether by diet or an operation,” Taylor noted. The people with Type-2 diabetes were found to have increased levels of fat in the pancreas. In patients with type 1 diabetes (T1D), this is caused by the immune system killing off the beta cells that produce insulin. Other mice, with robust beta cells that were good at repairing DNA damage, were able to stay non-diabetic for life, even when those islets were placed under severe cellular stress. At this stage, antidiabetic drugs and lifestyle interventions have poor efficacy, and medical complications arise. There are many promising drugs under development at life sciences companies that have just been waiting for a usable animal model.
In patients with type 2 diabetes (T2D), a metabolic dysfunction prevents insulin from working on the liver. The same pathways for beta cell survival and DNA damage repair were also found to be altered in diabetic patient samples, indicating that a genetic predisposition for fragile beta cells may underlie who develops diabetes. Who knows, there may even be useful compounds hidden away in alternative or traditional medicines that could be found through a good testing program.
In both cases, left untreated, the extra glucose in the blood can cause blindness, cardiovascular disease, diabetic nephropathy, diabetic neuropathy and death.
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