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Body-weight regulation scientists give perspective on obesity-related research

The health effects of obesity involve complex interactions between many body organs that can obscure insight into underlying mechanisms. A more complete understanding of the common underlying defects that occur at the cellular level might prove productive in uncovering the causes and consequences of obesity.

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Keywords: body-weight, regulation, scientists, perspective, obesity-related, research, body, weight, scientist, obesity, related

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1. AGA Institute takes leadership role in exploring obesity and its complications
   05-14-2007 · EurekAlert!
   Due to the gastrointestinal tract's role in body weight regulation, gastroenterologists should work closely with other medical disciplines to oversee and coordinate the care of obese individuals, according to an American Gastroenterological Association Institute Obesity Task Force Report. The report was published in a special 13th issue of Gastroenterology, the official journal of the AGA Institute, that focuses on the growing problems related to obesity and nutrition.
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2. 'Knocking out' cell receptor may help block fat deposits in tissues, prevent weight gain
   10-25-2007 · EurekAlert!
   University of Cincinnati pathologists have identified a new molecular target that one day may help scientists develop drugs to reduce fat transport to adipocytes in the body and prevent obesity and related disorders, like diabetes.
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3. Researchers show how obesity causes breakdown in system which regulates appetite and weight
   03-06-2007 · EurekAlert!
   Research led by scientists at the Oregon National Primate Research Center demonstrates how obesity causes the breakdown of a brain system that regulates appetite. Specifically, the scientists determined that leptin resistance prevented a portion of the brain called the arcuate nucleus from taking part in an important signaling function that regulates appetite and body weight.
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4. Major link in brain-obesity puzzle found
   01-29-2007 · EurekAlert!
   A single protein in brain cells may act as a linchpin in the body's weight-regulating system, playing a key role in the flurry of signals that govern fat storage, sugar use, energy balance and weight, researchers report. And although it's far too early to say how this protein could be useful in fighting obesity, the finding gives scientists an important system to target in future research and the development of anti-obesity medications.
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5. Clock gene plays role in weight gain, study finds
   05-17-2007 · EurekAlert!
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6. Scripps research team discovers a chemical pathway that causes mice to overeat and gain weight
   02-12-2007 · EurekAlert!
   Researchers from the Scripps Research Institute who are studying how body temperature and energy metabolism are regulated have discovered a pathway that appears to play a critical role in the onset of obesity. Further study of the pathway could lead to better understanding of the physiological foundation of obesity in humans and even the discovery of new treatments for the condition.
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7. New role for protein in fat cells may improve understanding of obesity and diabetes
   07-19-2007 · EurekAlert!
   Scientists have shown for the first time that a protein involved in the transfer of fat in the blood may also influence how fat cells store fat. Richard E. Morton and Lahoucine Izem, research scientists at the Cleveland Clinic Foundation, have shown that the protein, called cholesteryl ester transfer protein, is involved in the cellular storage and regulation of cholesterol and other fats and, as a result, probably has unexpected contributions to obesity and diabetes.
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8. Alzheimer's prevention role discovered for prions
   07-03-2007 · EurekAlert!
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9. Mouse genome will help identify causes of environmental disease
   07-29-2007 · EurekAlert!
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10. 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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