Pronounced expression of the lipolytic inhibitor G0/G1 Switch Gene 2 (G0S2) in adipose tissue from brown bears (Ursus arctos) prior to hibernation
Jessen, Niels; Nielsen, Thomas S.; Vendelbo, Mikkel H.; Viggers, Rikke; Støen, Ole-Gunnar; Evans, Alina L.; Frøbert, Ole
Journal article, Peer reviewed
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http://hdl.handle.net/11250/2388889Utgivelsesdato
2016Metadata
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Originalversjon
Jessen, N., Nielsen, T. S., Vendelbo, M. H., Viggers, R., Støen, O.-G., Evans, A., & Frøbert, O. (2016). Pronounced expression of the lipolytic inhibitor G0/G1 Switch Gene 2 (G0S2) in adipose tissue from brown bears (Ursus arctos) prior to hibernation. Physiological Reports, 4(8). doi:10.14814/phy2.12781 10.14814/phy2.12781Sammendrag
Prior to hibernation, the brown bear (Ursus arctos) exhibits unparalleled
weight gain. Unlike humans, weight gain in bears is associated with lower
levels of circulating free fatty acids (FFA) and increased insulin sensitivity.
Understanding how free-ranging brown bears suppress lipolysis when gaining
weight may therefore provide novel insight toward the development of human
therapies. Blood and subcutaneous adipose tissue were collected from immobilized
free-ranging brown bears (fitted with GPS-collars) during hibernation
in winter and from the same bears during the active period in summer in
Dalarna, Sweden. The expression of lipid droplet-associated proteins in adipose
tissue was examined under the hypothesis that bears suppress lipolysis
during summer while gaining weight by increased expression of negative regulators
of lipolysis. Adipose triglyceride lipase (ATGL) expression did not differ
between seasons, but in contrast, the expression of ATGL coactivator Comparative
gene identification-58 (CGI-58) was lower in summer. In addition, the
expression of the negative regulators of lipolysis, G0S2 and cell-death inducing
DNA fragmentation factor-a-like effector (CIDE)C markedly increased during
summer. Free-ranging brown bears display potent upregulation of inhibitors
of lipolysis in adipose tissue during summer. This is a potential mechanism
for increased insulin sensitivity during weight gain and G0S2 may serve as a
target to modulate insulin sensitivity.