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Despite overeating, morbidly obese mice gain protection against diabetes

The "world's fattest mice" can overeat without developing insulin resistance or diabetes thanks to a glut of a key hormone, a dichotomy that helps explain why not all obese people are diabetic, a UT Southwestern Medical Center researcher has found.

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Keywords: despite, overeating, morbidly, obese, mice, gain, protection, diabetes, diabete

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1. JCI table of contents: Sept. 6, 2007
   09-06-2007 · EurekAlert!
   This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published online, Sept. 6, 2007, in the JCI, including: Hunger hormone fights aging in the thymus; Drug's potential adverse side effect explained; To kill or not kill that is the questions for IFN-alpha; When does being obese not lead to diabetes" When mice lack osteopontin; Understanding why infection with HIV-2 is not as bad as HIV-1; and others.
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2. Single molecule extends fat mice lives by reversing gene pathways associated with disease in obese
   11-01-2006 · EurekAlert!
   Researchers have used a single compound to increase the lifespan of obese mice, and found that the drug reversed nearly all of the changes in gene expression patterns found in mice on high calorie diets -- some of which are associated with diabetes, heart disease and other significant diseases related to obesity. The research is the first time that the small molecule resveratrol has been shown to offer survival benefits in a mammal.
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3. Gene deficiency is a protective barrier to obesity
   06-26-2007 · EurekAlert!
   A search for the molecular clues of longevity has taken Mayo Clinic researchers down another path that could explain why some people who consume excessive calories don't gain weight. The study, which was done in laboratory mouse models, points to the absence of a gene called CD38. When absent, the gene prevented mice on high-fat diets from gaining weight, but when present, the mice became obese.
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4. Mind over matter: SH2B1 in the brain regulates obesity
   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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5. Drug could improve pregnancy outcomes in wider range of women with insulin resistance
   09-06-2007 · EurekAlert!
   Women who are obese, have type 2 diabetes or a family history of type 2 diabetes could one day have more successful pregnancies because of a study at Washington University School of Medicine in St. Louis. This study, performed in mice, suggests that Metformin, the most commonly prescribed anti-diabetes drug, could potentially improve pregnancy outcomes in women with insulin resistance.
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6. A relative of anti-aging gene Klotho also influences metabolic activity, obesity
   04-23-2007 · UT Southwestern Medical Center
   A relative of the anti-aging gene Klotho helps activate a hormone that can lower blood glucose levels in fat cells of mice, making it a novel target for developing drugs to treat human obesity and diabetes, UT Southwestern Medical Center researchers have found.
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7. New survey ranks the nation's most and least sun-smart cities
   05-07-2007 · EurekAlert!
   Most Americans are familiar with the popular city rankings of the fattest cities, the fittest cities, the most livable cities and the most expensive cities. Now, in the first-of-its-kind survey, the American Academy of Dermatology (Academy) has identified the cities that take sun protection seriously and those that fail to make the grade despite repeated health warnings.
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8. 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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9. Collaborative Cross attracting diverse genetics experiments
   08-29-2007 · Oak Ridge National Laboratory (ORNL)
   Mice that are part of the Collaborative Cross project at Oak Ridge National Laboratory are helping scientists around the world learn more about possible causes of drug abuse, diabetes, sleep disorders, stress and pain, kidney disease and a number of other conditions that affect millions of people.
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10. Cancer and arthritis therapy may be promising treatment for diabetes
    12-18-2007 · EurekAlert!
    An antibody used to treat certain cancers and arthritis also greatly delays type 1 diabetes in mice.
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