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Landmark study highlights complex genetic risk factors behind type 2 diabetes
04-26-2007 · EurekAlert!A UK collaboration of scientists has identified three new genes that predispose individuals to develop type 2 diabetes, bringing scientists a step closer towards understanding what causes this complex disease. The findings bring the total number of genes known to be involved in type 2 diabetes to nine.
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08-10-2007 · EurekAlert!
Researchers report for the first time that genetic variants in mitochondria -- energy-producing structures harboring DNA that are inherited only from the mother -- are directly linked to metabolic markers for type 2 diabetes. The study, which highlights the role of mitochondrial genome variation in the pathogenesis of common diseases, is published online in Genome Research.
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- MUHC-led research identifies risk-factor genes for type 2 diabetes
02-19-2007 · EurekAlert!
A new study led by researchers at the McGill University Health Centre has identified four genes that increase the risk of developing type 2 diabetes. This form of diabetes is the most common worldwide and affects nearly 2 million Canadians. In recent years, the prevalence of Type 2 diabetes has increased rapidly. This genetic discovery may help stem this rise.
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- Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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- Genome-wide search unearths surprising clues for diabetes and triglycerides
04-26-2007 · EurekAlert!
Scientists from the Broad Institute of Harvard and MIT, Lund University and Novartis today announced the discovery of three unsuspected regions of human DNA that contain clear genetic risk factors for type 2 diabetes, and another that is associated with elevated blood triglycerides. The study is among the first to apply a suite of genomic resources to clinical research, including the Human Genome Project, the SNP and HapMap Projects, and genome-scale laboratory and analytical tools.
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- U of M-led study identifies new genetic risk factors for type 2 diabetes
04-26-2007 · EurekAlert!
Ten genetic variants associated with type 2 diabetes, a disease which impacts more than 170 million people worldwide, have been identified or confirmed by a US-Finnish team led by scientists at the University of Michigan School of Public Health.
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- Study of diabetes and race reveals the imperfect science of defining ethnic groups
02-14-2007 · EurekAlert!
While previous biomedical research studies have found that genetics and race increase risk for some diseases, a new look into how researchers study genetic triggers of type 2 diabetes suggests that defining race remains an inexact science, with social and historic facts mixing with biology throughout the research process.
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01-18-2007 · EurekAlert!
Obesity is one of the main risk factors for developing type II diabetes. Previous studies have shown that mice lacking a protein known as SH2B1 throughout their body are obese and develop diabetes. However, a new study now shows that replacing SH2B1 only in the brain of these mice rescues them from obesity, indicating that SH2B1 in the brain might be a new target for the development of treatments for obesity and type II diabetes.
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- Breakthrough in understanding type-2 diabetes as key genes identified
02-14-2007 · EurekAlert!
The most important genes associated with a risk of developing type-2 diabetes have been identified, scientists report today in a new study. The research, published online in Nature, is the first time the genetic makeup of any disease has been mapped in such detail. It should enable scientists to develop a genetic test to show an individual their likelihood of developing diabetes mellitus type 2, commonly known as type-2 diabetes.
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- Identifying the mechanism behind a genetic susceptibility to type 2 diabetes
08-01-2007 · EurekAlert!
Type 2 diabetes is reaching epidemic proportions in the developed world. Determining if and how certain genes predispose individuals to type 2 diabetes is likely to lead to the development of new treatment strategies for individuals with the disease. A new study now shows that certain variants of the gene TCF7L2 make individuals more susceptible to type 2 diabetes and provides a mechanism by which these genetic variants might cause susceptibility to the disease.
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- Researchers identify new genetic risk factors for type 2 diabetes
04-26-2007 · EurekAlert!
New research, published in the online edition of the journal Science, provides most comprehensive look yet at genetic variants associated with increased risk for type 2 diabetes.
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