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Modest gain in visceral fat causes dysfunction of blood vessel lining in lean, healthy humans

11-05-2007 · EurekAlert!

When lean, healthy young adults gained about nine pounds, the functioning of their blood vessel lining became impaired -- but shedding the weight restored proper functioning, according to a Mayo Clinic research report.

Keywords: modest, gain, visceral, fat, causes, dysfunction, blood, vessel, lining, lean, healthy, humans, cause, human

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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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Prehistoric origins of stomach ulcers uncovered
02-07-2007 · EurekAlert!
Scientists have discovered that the ubiquitous bacteria that causes most painful stomach ulcers has been present in the human digestive system since modern man migrated from Africa over 60,000 years ago. They compared DNA sequence patterns of humans and the Helicobacter pylori bacteria now known to cause most stomach ulcers and found that the genetic differences between human populations that arose as they dispersed from Eastern Africa over thousands of years are mirrored in H.pylori.
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Common virus may contribute to obesity in some people, new study shows
08-20-2007 · EurekAlert!
A common virus may cause obesity in some people, according to new evidence in a controlled laboratory study. Scientists showed that infection with human adenovirus-36, long recognized as a cause of respiratory and eye infections in humans, transforms adult stem cells obtained from fat tissue into fat cells. The study, which might lead to new treatments for obesity, will be reported in August at the American Chemical Society national meeting in Boston.
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Study of malaria parasites reveals new parasitic states
11-28-2007 · EurekAlert!
Although malaria parasites have undergone extensive laboratory study, relatively little is known about how they behave in humans to cause disease. Newly published data from a study of malaria-infected human blood reveal two biological states of the parasite Plasmodium falciparum not observed under laboratory conditions. This information may help scientists develop new strategies for treating malaria.
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Dragonfly's metabolic disease provides clues about human obesity
11-20-2006 · EurekAlert!
Parasite-infected dragonflies suffer the same metabolic disorders that have led to an epidemic of obesity and type 2 diabetes in humans, according to research to be published in the Proceedings of the National Academy of Science. The discovery expands the known taxonomic breadth of metabolic disease and suggests that the study of microbes found in human intestines may provide a greater understanding of the root causes of human metabolic dysfunction.
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Find yields further insight into causes of Parkinson's disease
02-01-2007 · EurekAlert!
In the fruit fly Drosophila, the mutated parkin gene causes motor dysfunction and may be key to understanding the cause of familial Parkinson's in humans.
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New blood test might offer early warning of deep belly fat
07-10-2007 · EurekAlert!
Measuring levels of a chemical found in blood offers the best indicator yet of the amount of fat surrounding abdominal organs, according to a new study of lean and obese individuals reported in the July issue of Cell Metabolism, a publication of Cell Press. The buildup of such "visceral fat" is of particular health concern as it has been linked to insulin resistance, type 2 diabetes, and heart disease risk.
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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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Modulating fat levels essential for successful pregnancy
09-20-2007 · EurekAlert!
A new mouse study has provided a potential reason for early pregnancy loss in humans. Female mice lacking a protein known as sphingosine kinase 1 (Sphk1) and expressing reduced levels of Sphk2 were found to experience early pregnancy loss and therefore to be infertile. As Sphk1 and Sphk2 are involved in metabolizing fats known as sphingolipids, the authors suggested that disturbances in sphingolipid metabolism might be a cause of early pregnancy loss in humans.
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New fat, same old problem with an added twist?
01-16-2007 · EurekAlert!
Last month, New York City outlawed the use of partially hydrogenated oils, known as trans fats, in restaurants, a ban now under consideration in other cities, including Boston and Chicago. But novel research conducted in Malaysia and at Brandeis University shows that a new method of modifying fat in commercial products to replace unhealthy trans fats raises blood glucose and depresses insulin in humans, common precursors to diabetes. Furthermore, like trans fat, it still adversely depressed the beneficial HDL-cholesterol.
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