Help Huge Numbers Of Perpetual Dieters Stop Failing Diets. This Large Group Is Desperate For An Honest And Proven Solution To Losing Weight And Keeping It Off Permanently, Without Gimmicks, Without Starving And Without Spending A Fortune. 75% Commission
"Atherosclerosis begins in youth, and this process, from its earliest phases, is related to the presence and intensity of the known cardiovascular risk factors. Clinical events such as myocardial infarction, stroke, peripheral arterial disease, and ruptured aortic aneurysm are the culmination of the lifelong vascular process of atherosclerosis."They add that the earlier cardiovascular prevention starts the better.
email to a friend 
printer friendly 
opinions 
In a recent study by University of Kentucky researchers, watermelon was shown to reduce atherosclerosis in animals.
The animal model used for the study involved mice with diet-induced high cholesterol. A control group was given water to drink, while the experimental group was given watermelon juice. By week eight of the study, the animals given watermelon juice had lower body weight than the control group, due to decrease of fat mass. They experienced no decrease in lean mass. Plasma cholesterol concentrations were significantly lower in the experimental group, with modestly reduced intermediate and low-density lipoprotein cholesterol concentrations as compared to the control group.
A measurement of atherosclerotic lesion areas revealed that the watermelon juice group also experienced statistically significant reductions in atherosclerotic lesions, as compared to the control group.
"Melons have many health benefits," said lead investigator Dr. Sibu Saha. "This pilot study has found three interesting health benefits in mouse model of atherosclerosis. Our ultimate goal is to identify bioactive compounds that would improve human health."
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.MLA
Please note: If no author information is provided, the source is cited instead.
Maybe the weight loss was because of the decrease in calorie from the animal being full of watermelon juice. Or Maye it was because the Watermelon calories contain no fat. Do the experiment and control the fat and protein and just substitute the watermelon calories for some other carb/starch and then post the results.
| post followup | alert a moderator |
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
email to a friend printer friendly opinions 
Crestor is not significantly better at stabilizing plaque and reducing cholesterol, compared to Lipitor, a Pfizer drug that Ranbaxy Laboratories will launch in much cheaper generic versions in two weeks' time. AstraZeneca's Crestor (rosuvastatin) will be harder to sell because it is much more expensive than generic atorvastatin (Lipitor), now that no significant clinical advantage has been shown in a trial funded by AstraZeneca. Crestor's patent expires in 2016.
The SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin) trial results were presented at the American Heart Association's Scientific Sessions 2011, as well as being published today in NEJM (New England Journal of Medicine.
The 24-month trial, which included 1,385 participants, led by Stephen J. Nicholls, M.D., Ph.D., showed that high doses of Crestor and Lipitor - rosuvastatin (40 mg) and atorvastatin (80 mg) - reversed coronary artery disease by reducing the amount of plaque in arteries that supply blood to the heart. The SATURN trial was carried out in 215 different centers - it is the "largest study using intracoronary ultrasound to measure changes in the amount of plaque in coronary arteries."
The trial compared the impact of Crestor versus Lipitor in reducing LDL cholesterol, known as "bad cholesterol", and their varying effects on HDL cholesterol, known as "good cholesterol".
Previous trials had shown that Crestor raised good cholesterol by between 7% and 15%, while Lipitor's effect on HDL was only very slight.
In this study, atheroma volume dropped by 0.99% in the Lipitor group and 1.22% in the Crestor group - the researchers described the difference as "not statistically significant". The atheroma volume is the amount of plaque in the assessed part of the coronary artery.
Dr. Stephen J. Nicholls said:
"Regression of plaque has been the holy grail of heart disease treatment, and in this trial more than two-thirds of the patients had regression. It's a very positive outcome for patients and shows the benefits of high doses of statins."
Below are some additional findings from the SATURN trial: In a different method for analyzing atheroma volume (using ultrasound too), Lipitor lowered plaque by 4.4 cubic mm, while Crestor did so by 6.4 cubic mm.Lipitor lowered total plaque in 64.7% of participants, compared to 71.3% in the Crestor groupAverage LDL cholesterol levels in the Lipitor group were 70 mg/dl, compared to 62.6 mg/dl in the Crestor group (lower number is better, LDL is bad cholesterol)Average HDL cholesterol levels in the Lipitor group were 48.6 mg/dl, versus 50.4% in the Crestor group (higher number is better, HDL is good cholesterol)Dr. Nicholls said:
"The differences between the two drugs were modest and the difference in HDL levels was less than we were anticipating based on previous studies."
In the SATURN trial, incidence of stroke, heart attack or having to undergo an angioplasty was less than half, compared to prior trials with lower doses.
Dr. Nicholls said:
"Doctors have been reluctant to use high doses of statins, but in this study the drugs were safe, well tolerated and had a profound impact on lipid levels, the amount of plaque in vessel walls and the number of cardiovascular events."
Darwin Labarthe, professor of preventive medicine at Northwestern University's medical school, said during the AHA Scientific Meeting:
"The study provides no basis to infer differential clinical benefit between
the two interventions."
In September this year, AstraZeneca had warned that the SATURN trial had missed its primary goal - demonstrating Crestor's significant superiority to Lipitor in lowering arterial plaque. The company added that full details of the trial would not be revealed until today.
Even so, Crestor does improve cholesterol levels, as well as reducing plaque accumulation in the arteries, AstraZeneca stressed in a communiqué.
Howard Hutchinson, Chief Medical Officer, AstraZeneca, said:
"These results are good news for patients with cardiovascular disease and provide further support of what we already know about Crestor. Crestor consistently and significantly lowers LDL-C, increases HDL-C and helps patients get to target LDL-C of less than 70 mg/dL. In addition, SATURN once again shows us that Crestor helps to reduce plaque build-up in the arteries."
Written by Christian Nordqvist
MLA
Please note: If no author information is provided, the source is cited instead.
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
email to a friend printer friendly opinions
Patients unable to control their cholesterol levels with medications may someday be able to lower their "bad" cholesterol with a shot, according to research presented at the American Heart Association's Scientific Sessions 2011.
In its first preliminary human tests, the medicine in the new shot lowered low density lipoprotein, or "bad" cholesterol, in healthy volunteers who received the highest dose an average 64 percent more than those who received an inactive placebo injection.
The injected material - targeting a recently-identified cholesterol regulator - is a monoclonal antibody that's a laboratory-made human protein. Monoclonal antibodies are already used to treat certain cancers and other medical conditions.
In the study, scientists created the monoclonal antibody AMG145 to disable the cholesterol regulator PCSK9, which interferes with the liver's ability to remove bad cholesterol from the blood. Therefore, turning it off improves cholesterol levels.
"PCSK9 is the first target in lipid metabolism to be inhibited using a monoclonal antibody, and it appears to be a promising way to lower bad cholesterol," said Clapton Dias, Ph.D., lead researcher and medical sciences director of clinical pharmacology and early development at Amgen, Inc., in Thousand Oaks, Ca.
The study involved 54 men and two women, 18 to 45 years old, who were healthy and not taking other medications. Participants received a single injection that contained one of five doses of AMG145 or a placebo. Sixteen received the injections intravenously and the others got simple injections that delivered the drug just underneath the skin.
After the injections, bad cholesterol was measured frequently for 85-113 days, along with other laboratory measures related to heart disease.
With increasing doses of AMG145, blood tests revealed: Less of the active form of PCSK9; Lower levels of bad cholesterol, total cholesterol and apo-B (the primary protein component of bad cholesterol); No effect on triglycerides, high density lipoprotein ("good" cholesterol) or a protein associated with good cholesterol - all lipid measures were not influenced by the PCSK9 regulator. "The more PCSK9 was lowered, the more bad cholesterol levels went down," Dias said. "With higher doses, bad cholesterol stayed lower for a longer period."
The injections were tolerated well, with volunteers receiving AMG145 experiencing no more side effects than those receiving the placebo.
The study included a small number of participants, and they were healthy. So the company is conducting a similar study that gives multiple doses of AMG145 to adults who take statin medication to control their cholesterol.
If AMG145 proves safe and effective in further clinical trials, it could help people unable to control their cholesterol with current medications that work in different ways.
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.MLA
Please note: If no author information is provided, the source is cited instead.
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
email to a friend printer friendly opinions
Researchers at Emory University School of Medicine have identified hepcidin, a hormone that regulates iron levels in the body, as a potential target for treating atherosclerosis.
Suppressing hepcidin is a way to reduce the iron levels inside the white blood cells found in arterial plaques. Reducing iron levels pushes those cells to clean up harmful cholesterol in a process called "reverse cholesterol transport," interfering with atherosclerosis, researchers have found.
The data was presented by Aloke Finn, MD, assistant professor of medicine (cardiology) and colleague Omar Saeed at the American Heart Association Scientific Sessions meeting in Orlando. Charles Hong, MD, PhD, from Vanderbilt University and collaborators from CVPath Institute contributed to the research.
When mice modeling atherosclerosis are given a compound that reduces hepcidin levels, they have smaller atherosclerotic plaques and less fat in their plaques, as well as reduced foam cell formation. Foam cells are white blood cells that accumulate cholesterol and are signs of atherosclerosis, which can lead eventually to heart attacks and strokes.
The compound LDN 193189 reduces hepcidin levels by blocking its production. LDN 193189 is also being investigated as a treatment for inflammatory bowel disease and for anemia related to critical illness.
Finn is also presenting research on how hemoglobin, the iron-containing protein that allows red blood cells to carry oxygen, affects macrophages.
Finn and his colleagues used isolated human cells and a rabbit model of atherosclerosis to show that macrophages respond to hemoglobin by increasing production of proteins that transport cholesterol and pump iron out.
In the context of atherosclerosis, iron is toxic because it amplifies the action of reactive oxygen species, leading to more inflammation and more foam cells. Previous research has shown that hemorrhage within atherosclerotic plaques, leading to the release of hemoglobin from red blood cells, is linked to enlargement of the plaque's necrotic core - a sign of "vulnerable plaque."
"We were led to the hepcidin research by our work on macrophages," Finn says. "We discovered a different type of macrophages that detoxify iron. They take it up and spit it out again with an iron transport protein."
"Hemorrhage is bad, but as bad at it is, these macrophages seem to protect against the toxic effects of iron. Giving macrophages hemoglobin encourages them to behave in this detox mode," he says.
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.MLA
Please note: If no author information is provided, the source is cited instead.
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
email to a friend printer friendly opinions
New research reveals that patients with epilepsy who were treated for extended periods with older generation antiepileptic drugs (AEDs) may be at increased risk for developing atherosclerosis, a common disorder known as hardening of the arteries. According to the findings now available in Epilepsia, the journal of the International League Against Epilepsy (ILAE), the vascular risk is significantly associated with the duration of AED monotherapy.
While the majority of epilepsy patients have good results with treatment, more than 30% of patients continue to have seizures even with AED therapy. In these cases of refractory epilepsy, long-term or lifelong AED therapy is needed. Prolonged treatment can lead to diabetes, thyroid issues, psychiatric problems and adverse drug reactions. Prior studies suggest that older-generation AEDs such as phenytoin, carbamazepine, phenobarbital, and valproic acid may alter metabolic pathways, contributing to increased vascular risks.
Lead author, Dr. Yao-Chung Chuang from Kaohsiung Chang Gung Memorial Hospital in Taiwan, and colleagues compared the long-term impact of different categories of AED monotherapy on atherosclerosis development. The team recruited 160 adult patients with epilepsy who had received AED monotherapy for more than 2 years, along with 60 healthy controls. Ultrasonography was used to measure participants' common carotid artery (CCA) intima media thickness (IMT) -- a measurement used to assess the extent of atherosclerosis.
"Our study found patients with epilepsy who were under long-term monotherpy with phenytoin, carbamazepine and valproic acid displayed significantly increased CCA IMT measurements," said Dr. Chuang. "These altered circulatory markers from prolonged AED therapy may accelerate the atherosclerotic process." Analysis showed that CCA IMT is positively correlated with the duration of AED therapy.
Researchers also investigated specific vascular risk factors associated with the type of AED therapy. Epilepsy patients taking carbamazepine or phenytoin for long periods exhibited increased levels of cholesterol and of the amino acid, total homocysteine (tHcy), and lower levels of folate, all of which increase risk of adverse cardiovascular and cerebrovascular events. Patients who were treated with valproic acid displayed elevated levels of uric acid, tHcy, and thiobarbituric acid reactive substances (TBARS), increasing atherosclerosis risk which the authors believe is based on oxidative mechanisms.
The authors argue that drug choice should be carefully selected for epilepsy patients requiring long-term AED treatment, particularly in elderly or individuals at high-risk of vascular events. Dr. Chuang concluded, "Our findings suggest that newer AEDs, such as lamotrigine, may minimize metabolic disturbances, and therefore reduce the risk of atherosclerosis brought on by long-term AED therapy."
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.MLA
Please note: If no author information is provided, the source is cited instead.
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
email to a friend printer friendly opinions
Collaborative research from Perelman School of Medicine at the University of Pennsylvania has shown that psoriasis patients have an increased risk of heart attack, stroke and cardiovascular death, especially if the psoriasis is moderate to severe. Now, Penn researchers have discovered the potential underlying mechanism by which the inflammatory skin disease impacts cardiovascular health. In two new studies presented at the 2011 American Heart Association Scientific Sessions, Penn researchers show that the systemic inflammatory impact of psoriasis may alter both the makeup of cholesterol particles and numbers, as well as impair the function of high density lipoprotein (HDL), the "good" cholesterol.
"Anecdotally, many researchers have observed that HDL levels may be lower in states of inflammation, such as rheumatoid arthritis, psoriasis and even obesity," said lead study author Nehal Mehta, MD, MSCE, director of Inflammatory Risk in Preventive Cardiology at Penn. "However, these new findings suggest that in addition to lower levels, chronic inflammation associated with conditions like psoriasis may change the composition and decrease the function of HDL as well."
In the current studies, researchers enrolled 78 patients with psoriasis and 84 control subjects. In the first study, the authors measured fasting lipid levels and examined the number and size of cholesterol particles using nuclear magnetic resonance (NMR) spectroscopy. This analysis revealed that patients with psoriasis had a higher number of smaller LDL particles, or "bad" cholesterol, which was independent of traditional risk factors and obesity. "It was striking that the NMR profiles from patients with psoriasis resembled those seen in patients with diabetes, and that these patients with psoriasis had otherwise normal traditional lipid panels" Dr. Mehta added.
In the second study, the researchers measured HDL efflux, which is the ability of a patient's HDL to remove cholesterol from cells involved in atherosclerosis. This process, known as 'reverse cholesterol transport', is why HDL may have protective properties. In a previous study, researchers at Penn have demonstrated that measuring HDL efflux capacity may be a more effective barometer of protection from heart disease than measuring HDL levels alone.
In this same group of patients who had normal cholesterol levels compared to controls, patients with psoriasis demonstrated dramatically reduced HDL efflux capacity compared to control patients. This negative association observed between psoriasis and HDL efflux persisted after adjusting for traditional lipid levels and other traditional risk factors, including body mass index (BMI).
"Patients with psoriasis had an approximate 25 percent reduction in the HDL efflux capacity than the controls, despite their relatively normal overall lipid profiles which leads to the question of whether function is more important than concentration in chronic inflammatory states" Dr. Mehta noted.
The new findings may provide a critical clue to the link between psoriasis and heart disease, but the researchers say larger studies are needed to validate their findings. Joel M. Gefland, MD, MSCE, assistant professor of Dermatology and Epidemiology, and a senior author on the studies, said "We've been able to show that psoriasis is an important risk factor for vascular disease, and now we may finally be able to identify and ultimately treat the pathways by which psoriasis increases these risks."
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.MLA
Please note: If no author information is provided, the source is cited instead.
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
email to a friend printer friendly opinions
A new study suggests that blocking cancer cells' access to cholesterol may offer a new strategy for treating glioblastoma, the most common and deadly form of brain cancer, and perhaps other malignancies. The potential treatment could be appropriate for tumors with a hyperactive PI3K signaling pathway, which accounts for up to 90 percent of glioblastomas cases.
Researchers at the Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James) and at UCLA's Jonsson Comprehensive Cancer Center who led the study discovered that the hyperactive signaling pathway is linked to cholesterol metabolism, and that inhibiting this pathway leads to the death of glioblastoma cells in an animal model.
The findings are published in the journal Cancer Discovery.
"Our research shows that the tumor cells depend on large amounts of cholesterol for growth and survival, and that pharmacologically depriving tumor cells of cholesterol may offer a novel therapeutic strategy to treat glioblastoma," says first author and researcher Dr. Deliang Guo, assistant professor of radiation oncology at the OSUCCC - James.
"This study uncovers a mechanism that links a common oncogene with altered cell metabolism, and it potentially offers a strategy for blocking that mechanism and causing specific tumor-cell death without significant toxicity," says principal investigator Dr. Paul S. Mischel, professor of pathology at UCLA's Jonsson Cancer Center and an adjunct professor of radiation oncology at the OSUCCC - James.
"Overall, our findings suggest that the development of drugs to target this pathway may lead to significantly more effective treatments for patients with this lethal form of brain cancer."
Glioblastomas strike about 18,500 Americans annually and kill nearly 13,000 of them. Glioblastoma multiforme is the most common and lethal form of the malignancy, with an average survival of 15 months after diagnosis. The tumors are difficult to surgically remove because malignant cells invade surrounding brain tissue.
In addition, genetic differences leave some glioblastoma cells in the tumor resistant to chemo- and radiation therapy, the researchers say.
"Some glioblastomas respond well to treatment initially when the therapy-sensitive cells are killed, but the tumor then returns relatively quickly as the therapy-resistant cells proliferate," says co-author Dr. Arnab Chakravarti, chair and professor of Radiation Oncology and co-director of the OSUCCC - James Brain Tumor Program.
"Because glioblastomas are among the most treatment-resistant of cancers, new therapeutic strategies are urgently needed," says Chakravarti.
The study used tumor-cell lines, cells from patients and an animal model. Key technical findings include the following: In nearly 50 percent of glioblastomas, a mutation called EGFRvIII hyperactivates the PI3K signaling pathway and a master transcriptional regulator called SREBP-1. Activating this pathway upregulates the low-density lipoprotein (LDL) receptor and promotes LDL uptake, enabling tumor cells to import large amounts of cholesterol that feed tumor-cell growth and survival. Pharmacological activation of the nuclear Liver X Receptor leads to the loss of LDL receptors and to upregulation of the ABCA1 protein pump, which transports cholesterol out of the malignant cells. Together, these actions starve tumor cells of cholesterol, causing their death. "Because this pathway is activated in other types of cancer, this work may have significant implications for a broad range of cancer types," Mischel says. Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:
MLA
Please note: If no author information is provided, the source is cited instead.
This piece of scientific work dovetails nicely with the work of T.Colin Campbell, Ph.D. in his work The China Study. If you want to know what you, individually, can actually DO to prevent cancer or control it if you have it read his book. Read also SuperImmunity by Joel Fuhrman, M.D. and AntiCancer-A New Way of Life, by David Servan-Schreiber, M.D., Ph.D. Dr. Servan-Schreiber dealt with and healed from his own brain cancer over 22 years ago now (a time frame unheard of in brain cancer) and is still a practicing physician in Pittsburgh, PA and Paris, France.
| post followup | alert a moderator |
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
email to a friend printer friendly opinions
Researchers at NYU Langone Medical Center announce findings published in the October 20 issue of Nature that show for the first time the inhibition of both microRNA-33a and microRNA-33b (miR-33a/b) with chemically modified anti-miR oligonucleotides markedly suppress triglyceride levels and cause a sustained increase in high density lipoprotein cholesterol (HDL-C) "good" cholesterol.
"The discovery of microRNAs in the last decade has opened new insights for up new avenues for the development of therapies targeted at these potent regulators of gene pathways," said lead author Kathryn Moore, PhD, associate professor in the Department of Medicine, The Leon H. Charney Division of Cardiology and The Marc and Ruti Bell Vascular Biology and Disease Program at NYU Langone Medical Center. "The current study is the first to show that inhibition of miR-33a, as well as miR-33b which is only found in larger mammals can suppress plasma triglyceride levels and increase circulating levels of HDL-C. This study highlights the benefits of modulating miR-33a/b and its downstream metabolic pathways for the treatment of conditions that increase cardiovascular disease risks, such as dyslipidemias and metabolic syndrome."
Metabolic syndrome is a combination of medical disorders that increase the risk of developing cardiovascular disease and diabetes. Cholesterol is a growing public concern worldwide characterized by an increase in triglycerides, decrease in plasma HDL-C, obesity and resistance to insulin that can lead to both cardiovascular disease and diabetes.
Recent studies have indicated miR-33a/b regulate genes involved in cholesterol and fatty acid metabolism pathways. miR-33a/b strongly represses the cholesterol transporter ABCA1, resulting in decreased generation of HDL-C and reverse cholesterol transport. In addition, miR-33a/b also inhibit key genes involved in fatty acid metabolism resulting in the accumulation of triglycerides. The ability to inhibit miR-33a/b to reverse these events provides a novel therapeutic approach to correct dyslipidemia and metabolic syndrome.
"This study represents a significant advance from our proof-of-concept studies in mice showing that anti-miR-33 can both raise HDL and improve existing atherosclerotic vascular disease," said Katey Rayner, PhD in the Department of Medicine at NYU Langone Medical Center and co-author of the study. "These exciting results now bring the use of miR-33 inhibitors one step closer to the clinic."
Article adapted by Medical News Today from original press release. Source: New York University Langone Medical CenterMLA
Please note: If no author information is provided, the source is cited instead.
Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.
If you write about specific medications or operations, please do not name health care professionals by name.
All opinions are moderated before being included (to stop spam)
Contact Our News Editors
For any corrections of factual information, or to contact the editors please use our feedback form.
Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
