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Common cause of heart disease, diabetes may be treatable with malaria drug

11-07-2006 · EurekAlert!

Studies of a rare genetic condition that increases cancer risk have unveiled a potential treatment for metabolic syndrome, a common disorder that afflicts as many as one in every four American adults and puts them at sharply increased risk of type 2 diabetes and clogged arteries.

Keywords: cause, heart, disease, diabetes, treatable, malaria, drug, diabete

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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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Hopkins scientists uncover cause of antipsychotic drug weight gain
02-12-2007 · EurekAlert!
Johns Hopkins brain scientists have hit on how and why some powerful drugs used for treating mental illnesses cause patients to gain so much weight that they often develop life-threatening complications such as diabetes and heart disease.
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Enzyme structure reveals new drug targets for cancer and other diseases
02-14-2008 · EurekAlert!
Researchers now have a clearer understanding of how a key protein controls gene activity and how mutations in the protein may cause disease. The work could provide new avenues to design drugs aimed at cancer, diabetes, HIV, and heart disease.
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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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Type 1 diabetes and heart disease -- Heavier may mean healthier
06-23-2007 · EurekAlert!
Researchers at the University of Pittsburgh Schools of the Health Sciences studying links between an early sign of heart disease called coronary artery calcification and body fat have found that, paradoxically, more fat may have some advantages, at least for people -- particularly women -- who have type 1 diabetes. Cardiovascular complications, including heart disease, are a leading cause of death for people with diabetes, who tend to suffer cardiovascular disease decades earlier than non-diabetics.
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Does being overweight in old age cause memory problems?
09-19-2007 · EurekAlert!
While obesity has been shown to contribute to high blood pressure, heart disease and diabetes, being overweight in old age does not lead to memory problems, according to a study published Sept. 19, 2007, in the online edition of Neurology, the medical journal of the American Academy of Neurology.
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Single genetic defect causes early heart disease
03-01-2007 · EurekAlert!
A team of researchers from the United States and Iran has identified a genetic mutation that causes early onset coronary artery disease in members of a large Iranian family. The genetic mutation leads to heart disease by causing high blood pressure, high blood levels of "bad cholesterol" and diabetes, all risk factors for heart disease. Coronary artery disease is the leading cause of death worldwide.
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UCSD researchers discover inflammation, not obesity, cause of insulin resistance
11-06-2007 · EurekAlert!
Researchers at the University of California, San Diego School of Medicine have discovered that inflammation provoked by immune cells called macrophages leads to insulin resistance and type 2 diabetes. Their discovery may pave the way to novel drug development to fight the epidemic of type 2 diabetes associated with obesity, the most prevalent metabolic disease worldwide.
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Mitochondrial 'bottleneck' cracked
01-27-2008 · EurekAlert!
Scientists have shown for the first time how a particular family of diseases are passed down from mother to child and how this can lead to the severity of the disease differing widely. The research, funded by the Wellcome Trust, offers hope of being able to predict a child's risk of developing a mitochondrial disease which can cause muscle weakness, diabetes, strokes, heart failure and epilepsy.
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Triptolide: A potential drug for polycystic kidney disease
03-05-2007 · EurekAlert!
A treatment for polycystic kidney disease (PKD), a leading cause of fatal kidney failure worldwide, has been identified by a research team led by Yale biochemist Craig Crews, according to a report in the Proceedings of the National Academy of Sciences.
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