Why the study?
Does intermittent cold exposure reduce adiposity in C57BL/6 mice?
Does intermittent cold exposure reduce adiposity in C57BL/6 mice?
Intermittent cold exposure in mice paradoxically increases fat accumulation by stimulating de novo lipogenesis between exposure periods, despite enhancing brown adipose tissue recruitment.
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ICE increases adiposity in mice despite BAT recruitment; leaves open whether compensatory lipogenesis limits cold-exposure strategies in humans.
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.
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Yoo et al. (2014) studied this question.
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