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General interest items edited by Janice Flahiff

[Press release] That’s using your head: Brain regulates fat metabolism, potentially stopping disease

[Press release] That’s using your head: Brain regulates fat metabolism, potentially stopping disease
Jessica Yue poses in her lab.

Jessica Yue

 

From the University of Alberta press release By Cait Wills on January 26, 2015

Recent research into brain control of liver lipid production could cause break in obesity and diabetes treatment

Ways of keeping the heart healthy has widened, with the discovery that the brain can help fight off hardening of the arteries.

Atherosclerosis—hardening and narrowing of the arteries—can be caused by fat build up that causes plaque deposits, and is one of the main causes of cardiovascular disease. Jessica Yue, a newly recruited researcher in the Department of Physiology in the Faculty of Medicine & Dentistry, has shown a link between how the brain can regulate fat metabolism, potentially stopping the development of this disease risk factor in obesity and diabetes.

Her findings, published this month in Nature Communications, the online version of the high-impact Nature publication, outlines how the brain can use the presence of fatty acids, which are building blocks of fat molecules, to trigger the liver to reduce its own lipid production.

“We know that when there is dyslipidemia, or an abnormal amount of fat in the bloodstream, it’s dangerous for health—largely because this can lead to obesity, obesity-related disorders such as Type 2 diabetes, and atherosclerosis,” says Yue, and that “if you can find ways to lower fats in the bloodstream, it helps to lower these chances of diabetes and cardiovascular disease as a result of this atherosclerosis.”

Yue trained at the Toronto General Research Institute under Tony Lam, where she was a recipient of fellowships from the Canadian Institutes of Health Research (CIHR) and the Canadian Diabetes Association. With her associates in Toronto and with Peter Light, professor of pharmacology in the Faculty of Medicine & Dentistry, she looked at how the infusion of oleic acid, a naturally occurring monounsaturated fatty acid, in the brain “triggers” a signal from the hypothalamus to the liver to lower its fat secretion, which Yue says is a “triglyceride-rich, very-low-density lipoprotein. Light is the co-author of Yue’s paper in Nature Communications and is the director of the Alberta Diabetes Institute (ADI), where Yue is applying for membership.

“This fat complex is the kind of lipoprotein that is dangerous when its levels in the blood are elevated because it promotes atherosclerosis,” she says.

The catch, though, is that this “trigger” doesn’t work in obesity, a setting in which blood lipid levels are usually high. “In a model of diet-induced obesity, which then leads to insulin resistance and pre-diabetes, oleic acid no longer provides the fat-lowering trigger to the liver.” Yue’s findings, though, demonstrate how this faulty signal can be bypassed, unveiling potentially other ways to trigger this same function in obese patients.

This study could potentially impact how obesity and diabetes are treated, says Yue, which is the focus of her future research.

The next steps, she says, will be to look at how the brain can sense other compounds to regulate not only liver secretion of fats, but also liver glucose production, a significant contributing factor to diabetes. As a member of the Group on Molecular and Cell Biology of Lipids and with the strength of the ADI, she feels enthusiastic and inspired by her new research environment at the University of Alberta.

January 28, 2015 Posted by | Medical and Health Research News | , , , , , , , , , , , , | Leave a comment

[Great article critique] Eating Egg Yolks as Bad as Smoking?

 

From the 14 August 2012 article at Understanding Nutrition

This article refers to the article and paper below:
http://www.sciencedaily.com/releases/2012/08/120813155640.htm
http://www.sciencedirect.com/science/article/pii/S0021915012005047

egg yolksOn August 13, 2012, ScienceDaily.com published an article entitled, “Eating Egg Yolks as Bad as Smoking?” ScienceDaily.com concludes “eating egg yolks accelerates atherosclerosis in a manner similar to smoking cigarettes.”

Unfortunately, ScienceDaily.com and many other news networks fail to accurately describe the details and outcomes of the study. Here, I carefully examine the study and suggest an alternative conclusion from the data.

First, it is important to look at the participants of the study. The data was collected from individuals soon after they had a stroke or transient ischeamic attack (known as a “mini stroke”). This study is not examining healthy individuals or comparing the number of strokes in people who ate lots of eggs vs. those who ate few eggs. All participants in the study already had a stroke regardless of their egg consumption….

 

 

 

August 22, 2012 Posted by | Medical and Health Research News, Nutrition | , , , | Leave a comment

Bacteria eyed for possible role in atherosclerosis

Bacteria eyed for possible role in atherosclerosis
Enterobacter hormaechei — normally associated with pneumonia and sepsis — found in excised atherosclerotic plaque tissue

From a January 5, 2011 Eurkea news alert

Dr. Emil Kozarov and a team of researchers at the Columbia University College of Dental Medicine have identified specific bacteria that may have a key role in vascular pathogenesis, specifically atherosclerosis, or what is commonly referred to as “hardening of the arteries” – the number one cause of death in the United States.

Fully understanding the role of infections in cardiovascular diseases has been challenging because researchers have previously been unable to isolate live bacteria from atherosclerotic tissue. Using tissue specimens from the Department of Surgery and the Herbert Irving Comprehensive Cancer Center at Columbia University, Dr. Kozarov and his team, however, were able to isolate plaques from a 78-year-old male who had previously suffered a heart attack. Their findings are explained in the latest Journal of Atherosclerosis and Thrombosis.

In the paper, researchers describe processing the tissue using cell cultures and genomic analysis to look for the presence of culturable bacteria. In addition, they looked at five pairs of diseased and healthy arterial tissue. The use of cell cultures aided in the isolation of the bacillus Enterobacter hormaechei from the patient’s tissue. Implicated in bloodstream infections and other life-threatening conditions, the isolated bacteria were resistant to multiple antibiotics. Surprisingly, using quantitative methods, this microbe was further identified in very high numbers in diseased but not in healthy arterial tissues.

The data suggest that a chronic infection may underlie the process of atherosclerosis, an infection that can be initiated by the systemic dissemination of bacteria though different “gates” in the vascular wall – as in the case of a septic patient, through intestinal infection. The data support Dr. Kozarov’s previous studies, where his team identified periodontal bacteria in carotid artery, thus pointing to tissue-destructing periodontal infections as one possible gate to the circulation.

Bacteria can gain access to the circulation through different avenues, and then penetrate the vascular walls where they can create secondary infections that have been shown to lead to atherosclerotic plaque formation, the researchers continued. “In order to test the idea that bacteria are involved in vascular pathogenesis, we must be able not only to detect bacterial DNA, but first of all to isolate the bacterial strains from the vascular wall from the patient,” Dr. Kozarov said.

One specific avenue of infection the researchers studied involved bacteria getting access to the circulatory system via internalization in white blood cells (phagocytes) designed to ingest harmful foreign particles. The model that Dr. Kozarov’s team was able to demonstrate showed an intermediate step where Enterobacter hormaechei is internalized by the phagocytic cells, but a step wherein bacteria are able to avoid immediate death in phagocytes. Once in circulation, Dr. Kozarov said, bacteria using this “Trojan horse” approach can persist in the organism for extended periods of time while traveling to and colonizing distant sites. This can lead to multitude of problems for the patients and for the clinicians: failure of antibiotic treatment, vascular tissue colonization and initiation of an inflammatory process, or atherosclerosis, which ultimately can lead to heart attack or stroke.

“Our findings warrant further studies of bacterial infections as a contributing factor to cardiovascular disease, and of the concept that ‘bacterial persistence’ in phagocytic cells likely contributes to systemic dissemination,” said Dr. Kozarov, an associate professor of oral biology at the College of Dental Medicine. Dr. Jingyue Ju, co-author and director of the Columbia Center for Genome Technology & Bio-molecular Engineering, also contributed to this research, which was supported in part by a grant from the National Heart, Lung, and Blood Institute of the National Institutes of Health and by the Columbia University Section of Oral and Diagnostic Sciences.

The article appeared in Volume 18 of the Journal of Atherosclerosis and Thrombosis.

January 7, 2011 Posted by | Medical and Health Research News | , , , , | Leave a comment

   

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