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We're a little crazy, about science!

Your brain is hardening your arteries, but not on purpose!

arteries

Your brain might just be killing you slowly. Atherosclerosis — or hardening and narrowing of the arteries — can be caused by fat buildup that causes plaque deposits, and is one of the main causes of cardiovascular disease. What does that have to do with the brain? Well new research has shown a link between how the brain regulates fat metabolism, which has the potential of stopping the development of this disease risk factor in obesity and diabetes.

The findings outline 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 Jessica Yue, a newly recruited researcher in the Department of Physiology in the Faculty of Medicine & Dentistry,. 

“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.”

The team of researchers 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 researchers say is a “triglyceride-rich, very-low-density lipoprotein.

“This fat complex is the kind of lipoprotein that is dangerous when its levels in the blood are elevated because it promotes atherosclerosis,” Yue 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.The 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, which is the focus of the future research from the group.

The next steps 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.

“It’s a big field and it’s emerging,” says Yue about neuroscience research in the areas of metabolic disease.

“Whereas the peripheral organs have gained a lot of attention in terms of how they release glucose and lipids, it’s exciting to see that within the last decade and a half that the brain now is emerging as an organ that has a lot of control over our health.”

The truth is, our world is changing faster than our brain can evolve. These mechanisms made sense not all that long ago in an evolutionary time scale. However, long gone are our hunter gatherer roots that we came from and unfortunately our brain hasn’t gotten the memo. While in many aspects our brain is the little black box we don’t understand, we are making outstanding progress in the field of neuroscience and with it, the hope that the brain will finally catch up to modern civilization.

Sources:
Yue JT, Abraham MA, LaPierre MP, Mighiu PI, Light PE, Filippi BM, & Lam TK (2015). A fatty acid-dependent hypothalamic-DVC neurocircuitry that regulates hepatic secretion of triglyceride-rich lipoproteins. Nature communications, 6 PMID: 25580573

Ginsberg, H. (2002). New Perspectives on Atherogenesis: Role of Abnormal Triglyceride-Rich Lipoprotein Metabolism Circulation, 106 (16), 2137-2142 DOI: 10.1161/01.CIR.0000035280.64322.31

Duez, H., Lamarche, B., Valero, R., Pavlic, M., Proctor, S., Xiao, C., Szeto, L., Patterson, B., & Lewis, G. (2008). Both Intestinal and Hepatic Lipoprotein Production Are Stimulated by an Acute Elevation of Plasma Free Fatty Acids in Humans Circulation, 117 (18), 2369-2376 DOI: 10.1161/CIRCULATIONAHA.107.739888

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