Scientists recently discovered surprising evidence that more brown fat (as a result of cold treatment) could increase a person’s risk of getting a stroke or a heart attack. The finding could explain why more people die of cardiovascular diseases during the winter months.
Brown fat consists of fat cells with a high metabolic rate, and the high metabolism in these cells can help burn fat and generate heat. These are unlike white fat cells, which have a much lower metabolic rate, and function mainly to store fat, contributing to obesity. Interestingly, white fat cells can acquire the properties of brown fat cells in response to cold temperatures, specifically by turning on a switch that can boost the fat cell’s metabolism. The switch is a protein known as UCP-1 (or uncoupled protein 1), a typical protein found in the cell’s mitochondria (power-house) where metabolism is controlled. The UCP-1 switch is activated by the nervous system’s response to cold, specifically through specific nerve connections that innervate fat tissue. The activation of UCP-1 turns on a cascade of signaling events that can rewire the fat cell’s overall metabolism, turning white fat cells brown by boosting their metabolic rate and driving the breakdown of fat.
Researchers recognize that converting white fat cells to brown fat cells with cold treatment can boost the person’s ability to burn off their excess fat, providing an ideal solution for people suffering from obesity. However, scientists recently discovered that UCP-1 activation in cold-induced brown fat cells can also increase the breakdown of fats in a process known as lipolysis, which produces the bad LDL cholesterol as a product. Released into the bloodstream, LDL would accumulate along blood vessels and arteries, forming deposits (called plaques) that can harden and form clots in a condition known as atherosclerosis, which can increase the risk of strokes and heart attacks.
This finding is recently reported in Cell Metabolism (July 2nd, 2013 issue) by Dr. Yihai Cao of Linköping University in Sweden and his colleagues in China. In this study, Cao tested how mice respond to cold treatment, specifically by placing the animals in 4 degrees Celsius for 2 hours each day. The mice selected for this study included healthy mice, as well as mutant mice with cholesterol uptake deficiency (APOE and LDL knockouts) that are susceptible to atherosclerosis. Assessing the animals after several weeks, Cao discovered that cold treatment can induce the production of more brown fat cells in mice. However, only animals that are susceptible to atherosclerosis actually had more bad LDL cholesterol in their blood stream, an effect that can be reversed with cholesterol lowering medications such as acipimox and simvastatin, and prevented by knocking out the UCP-1 gene. While it still unclear as to why the healthy animals still retained normal LDL levels in their bloodstream, even after cold treatment, Cao suggests that healthy animals have intact cholesterol uptake pathways that probably eliminated excessive cholesterol produced after cold treatment.
The study has enormous clinical implications, suggesting that cold winter temperatures could be harmful to people with atherosclerosis, specifically by driving even higher LDL accumulation in their bloodstream, which can put them at an even greater risk of dying from a heart attack or a stroke. “It might be wise to recommend that people who suffer from cardiovascular disease to avoid exposure to the cold and to put on warm clothes when they are outside during the winter,” says Cao.
Yet for healthy people without atherosclerosis, cold treatment can still help shape leaner and healthier bodies by activating brown fat cells and burning off excess fat.
Reference: Dong et al (2013). Cold Exposure Promotes Atherosclerotic Plaque Growth and Instability via UCP1-Dependent Lipolysis. Cell Metabolism. 18, 1: 118-129. 10.1016/j.cmet.2013.06.00
Front page image: Atlas of Microscopic Anatomy
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