Abstract
Due to its high energy consuming characteristics, brown adipose tissue (BAT) has been suggested as a key player in energy metabolism. Cold exposure is a physiological activator of BAT. Intermittent cold exposure (ICE), unlike persistent exposure, is clinically feasible. The main objective of this study was to investigate whether ICE reduces adiposity in C57BL/6 mice. Surprisingly, we found that ICE actually increased adiposity despite enhancing Ucp1 expression in BAT and inducing beige adipocytes in subcutaneous white adipose tissue. ICE did not alter basal systemic insulin sensitivity, but it increased liver triglyceride content and secretion rate as well as blood triglyceride levels. Gene profiling further demonstrated that ICE, despite suppressing lipogenic gene expression in white adipose tissue and liver during cold exposure, enhanced lipogenesis between the exposure periods. Together, our results indicate that despite enhancing BAT recruitment, ICE in mice increases fat accumulation by stimulating de novo lipogenesis.
Highlights
Obesity is a metabolic disease characterized by overexpansion of white adipose tissue (WAT)
We found that after cold exposure (ACE) for 5 hours induced progressive loss of body weight, fat mass, and even lean mass (Fig. 1A–C)
These results indicate that ACE enhances catabolism and weight loss in mice
Summary
Obesity is a metabolic disease characterized by overexpansion of white adipose tissue (WAT). WAT and BAT are the two main types of fat in mammals. BAT is considered as an energy dispenser that consumes significant amounts of chemical energy toward thermogenesis [1,2,3]. Recent studies have demonstrated the presence of metabolically active BAT in adults [4,5,6,7,8]. Cold temperature stimulates BAT activation and increases energy expenditure [5,7,8]. BAT activation is correlated with decreased adiposity in humans [5,6,7,9]. BAT activation has been proposed as a potential new therapeutic approach for obesity
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