Intermittent cold exposure enhances fat accumulation in mice.
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.
Department of Pediatrics, University of California San Diego, La Jolla, California, United States of America.
Hyung Sun
HS
Yoo
Department of Pediatrics, University of California San Diego, La Jolla, California, United States of America.
Liping
L
Qiao
Department of Pediatrics, University of California San Diego, La Jolla, California, United States of America.
Chris
C
Bosco
Department of Pediatrics, University of California San Diego, La Jolla, California, United States of America.
Lok-Hei
LH
Leong
Department of Pediatrics, University of California San Diego, La Jolla, California, United States of America.
Nikki
N
Lytle
Department of Pathology, University of California San Diego, La Jolla, California, United States of America.
Gen-Sheng
GS
Feng
Veterans Affairs San Diego Healthcare system, and Department of Medicine, University of California San Diego, La Jolla, California, United States of America.
Nai-Wen
NW
Chi
Department of Pediatrics, University of California San Diego, La Jolla, California, United States of America.
Jianhua
J
Shao
D017667:Adipocytes / Q000378:metabolism*; D002001:Adipose Tissue, Brown / Q000166:cytology / Q000378:metabolism*; D050154:Adiposity / Q000235:genetics; D000704:Analysis of Variance; D000818:Animals; D003080:Cold Temperature; D004435:Eating; D004734:Energy Metabolism; D020869:Gene Expression Profiling; D015151:Immunoblotting; D007333:Insulin Resistance; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D050155:Lipogenesis / Q000235:genetics; D008099:Liver / Q000378:metabolism; D008810:Mice, Inbred C57BL; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050151:Subcutaneous Fat / Q000166:cytology / Q000378:metabolism; D013997:Time Factors; D014280:Triglycerides / Q000097:blood / Q000378:metabolism; D000071256:Uncoupling Protein 1
D007473:Ion Channels; D024101:Mitochondrial Proteins; D014280:Triglycerides; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1