More people die from heart-disease during the winter months because brown fat is activated by the cold, a new study has suggested.
The present study, which has been conducted by researchers at Karolinska Institutet, and Linkoping University in Sweden, and three universities in China, demonstrates a new principle by which the cold increases the risk of atherosclerosis.
The researchers conducted their study on a strain of mice genetically modified with a propensity for atherosclerosis. Mice, like humans, have both white and brown body fat. Normal rolls of fat consist mainly of white fat, which is a repository of surplus calories; brown adipose tissue, on the other hand, can convert fat into heat.
This heat-generation process is activated by cold temperatures and has been considered beneficial to the health since it can reduce the amount of unnecessary white adipose tissue in the body.
Yihao Cao at the Department of Microbiology, Tumour and Cell Biology at Karolinska Institutet, and the Department of Medicine and Health at Linkoping University, said that I the beginning they thought that the cold activation of brown fat would only make the mice thinner and healthier.
However, the team found that that mice ended up with more fat stored in the blood vessels.
It turned out that exposure to low temperatures accelerated the formation of atherosclerotic plaque in the mice, which can cause myocardial infarction and brain haemorrhaging.
Moreover, the cold made the plaque less stable, and if such plaque ruptures, stored fat can leak into the blood, blocking vessels in the heart and brain. The cold-activated breakdown of fatty acids in the mice's brown fat led to the accumulation of low-density lipoproteins (LDL) in the blood and an increase in fat storage in the plaque.
Cao said that if this is also true for humans, it might be wise to recommend that people who suffer from cardiovascular disease should avoid exposure to the cold and to put on warm clothes when they are outside during the winter.
The researchers hope to be able to extend their work on mice to studies on humans.
The new study has been published in the journal Cell Metabolism.
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