The Endless Summer: Thermoneutrality Prevents Monocytosis and Reduces Atherosclerosis.

Abstract

People with metabolic syndrome and obesity are at an increased risk of mortality from cardiovascular disease. Over the past decade, there has been intensive research into new ways to stimulate weight loss to lower this risk. One of the key tissues is the metabolically active brown adipose tissue (BAT). Given that this is a thermogenic tissue, it can be stimulated by cold and is suggested by some as a new frontier in weight loss and improvements in other aspects of human health. But what does this mean for the health of our arteries? In the current issue of Circulation Research , Williams et al,1 reveal that ambient cool temperature may not correlate to benefit in our blood vessels. By comparing atherosclerotic lesion development over a series of temperatures and in 2 atherosclerotic prone models, they reveal stark differences in plaque size, such that larger lesions are found in animals under cold conditions. Their studies reveal a novel temperature-sensitive modulation of monocyte release from the bone marrow that ultimately impacts atherogenesis. Importantly, Williams et al1 have also uncoupled the metabolic protective role of the heat-generating UCP1 (uncoupling protein 1) from atherosclerosis. Article, see p 662 Cooler temperatures have long been associated with an increased mortality because of cardiovascular disease; however, the causality has been indirect, rationalized by changes in traditional risk factors (eg, lipids and blood pressure).2 In line with this, Dong et al3 originally found that cold housing (4°C) compared with thermoneutrality (the temperature at which energy expenditure is not needed to maintain body temperature) stimulated BAT and the browning of white adipose tissue. Cold temperature through UCP1 caused lipolysis and resulted in elevated levels of atherogenic lipoproteins. However, the role of ambient temperature and cholesterol seems controversial, with the current study reporting no changes.1 …