Primary Arterial Hypertension News - Menu Ingredient in garlic protects against severe chronic pulmonary hypertension in rats
2-Apr-2005 - Small daily doses of allicin, the active metabolic in garlic, proved effective in preventing a severe form of pulmonary hypertension in rats, according to a study reported Saturday, April 2 by University of Alabama at Birmingham researchers at the Experimental Biology 2005 meeting in San Diego. The human form of the disease primary pulmonary hypertension often leads to cardiovascular complications such as right heart hypertrophy and failure and is frequently lethal.
Dr. David D. Ku says the findings confirm an earlier study by the team that garlic protects against a less lethal form of acute pulmonary hypertension in rats. The new study by Ku, graduate student Hsien Chin Wu and research assistant Xiaowei Sun, not only looks at a chronic form of the disease but also goes a big step further by pinpointing the effective ingredient in garlic and demonstrating that it achieves its protective effects through vasorelaxation. The presentation at Experimental Biology 2005 was part of the scientific sessions of the American Society for Pharmacology and Experimental Therapeutics. In the UAB study, rats were given a single dose of monocrotaline, a well-established mechanism for inducing vasoconstriction of the pulmonary arteries. Within three weeks, half the rats had developed chronic pulmonary hypertension, with markedly increased pulmonary arterial pressure, just as expected. But the other half experienced no such increase. These rats had received the hypertension-causing drug but their diets also had been supplemented daily for three weeks with small doses of allicin. And it was the allicin, not the garlic itself that protected the supplemented rats from developing the disease, emphasizes Dr. Ku. Animals that consumed garlic from which the active metabolite had been removed or inactivated with heat experienced no benefit. In a separate but related study also presented at Experimental Biology 2005, in the scientific sessions of the American Society for Pharmacology and Experimental Therapeutics, Dr. Ku's team found that garlic treatment also could protect coronary vascular function and lessen the severity of right heart hypertrophy, two of the serious byproducts of chronic pulmonary hypertension. Garlic has long been thought to have medicinal properties, and reports have suggested that garlic supplementation in humans could help lower blood pressure, decrease ischemic injury, reduce serum cholesterol, inhibit platelet function and enhance thrombolysis. Garlic also has been suggested to improve arterial oxygenation associated with pulmonary dysfunction in patients with hepatopulmonary syndrome. However, obtaining concrete scientific data to substantiate many of these claims has remained elusive, notes Dr. Ku, in part because it has been difficult to accurate detect and quantify the active garlic metabolite. Recently the UAB team developed a new highly effective method for doing just that, for quantifying the actual amount of metabolite included in treatments. In what the researchers describe as a "very simple" analytical method, reversed-phased high performance liquid chromatograph method is coupled to mass spectrometry with multiple ions reaction monitoring. Using this method, the team has been able to demonstrate that varying concentrations of garlic active metabolite from either pure allicin, freshly crushed garlic, or commercial freeze-dried garlic preparations, directly correlate to the extent of their vasorelaxation/vasodepressor responses in isolated pulmonary arteries and in living animals. What does this mean for human diets? Dr. Ku says studies are needed to prove similar beneficial effects from the allicin in garlic will occur in humans ·his new method should make such studies a little easier ·but in view of the low toxicity associated with eating garlic, including garlic in one's daily food intake seems a reasonable approach, especially for people with respiratory and pulmonary ailments. The amount of garlic that delivered the protective effects to the rats in his study was the equivalent, for humans, of two cloves of garlic a day. Contact: Sarah Goodwin ebpress@bellsouth.net 770-270-0989 Federation of American Societies for Experimental Biology
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Dr. Ku's study was supported by a grant from the national Center for Complementary and Alternative Medicine, National Institutes of Health.
Weight Loss - Why some Diet Supplements help Suppress Appetite
Appetite Controlled by serotonin
July 19th, 2006 - Scientists have new understandings why some weight loss drugs work by enhancing the serotonin levels in the brain. The diet drugs that have these mood boosting effects on serotonin include sibutramine (marketed as Meridia), and fenfluramine. Fenfluramine has been recalled because of the combination with dexfenfluramine, marketed as fen-phen because of the possibility of fatal heart valve abnormalities.
How does serotonin suppress appetite? The group of researchers, led by Michael Cowley of Oregon Health and Science University conducted research on mice to further investigate how serotonin works with the hypothalamus. They traced the receptors for serotonin and they saw that particular neurons were expressed in this circuitry which directly changed the mice food intake and body weight. They further found a protein called AgRP that stimulated appetite and another protein called áMSH that curbs appetite. These AgRP protein was reduced when the serotonin and drugs that affected serotonin was present while at the same time the áMSH protein was increased reducing the appetite.
The researchers tested mice to see what effects of the various drugs that enhance or interfere with serotonin would have on their eating behavior. The drugs helped to disrupt the function of receptors by a substance called melancortin. Melanocoritin has been known to act for receptors of the proteins AgRP and áMSH which control a persons appetite.
Another receptor called melanocortin receptor-4 was identified by the researchers as a critical target of the serotonin pathway, which seems to be the central location for appetite regulation.
The study was first reported in the July 20th issue in Neuron. Other researchers that have contributed to this study was Joel Elmquist of University of Texas Southwestern Medical Center at Dallas and formerly of Beth Israel Deaconess Medical Center and Harvard Medical School, and Lora K. Heisler of the University of Cambridge and formerly of Beth Israel Deaconess Medical Center and Harvard Medical School.
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