Cell ReportsArticleGlucocorticoid-Induced ObesityDevelops Independently of UCP1

Ineke H.N. Luijten, Katie Brooks, Nathalie Boulet, Irina G. Shabalina, Ankita Jaiprakash, Bo Carlsson, Alexander W. Fischer, Barbara Cannon, and Jan Nedergaard
https://doi.org/10.1016/j.celrep.2019.04.041

SUMMARY

An excess of glucocorticoids leads to the develop-ment of obesity in both mice and humans, but themechanism for this is unknown. Here, we determinethe extent to which decreased BAT thermogenic ca-pacity (as a result of glucocorticoid treatment) con-tributes to the development of obesity. Contrary toprevious suggestions, we show that only in micehoused at thermoneutrality (30C) does corticoste-rone treatment reduce total BAT UCP1 protein. Thisreduction is reflected in reduced brown adipocytecellular and mitochondrial UCP1-dependent respira-tion. However, glucocorticoid-induced obesity de-velops to the same extent in animals housed at21C and 30C, whereas total BAT UCP1 proteinlevels differ 100-fold between the two groups.In corticosterone-treated wild-type and UCP1knockout mice housed at 30C, obesity also de-velops to the same extent. Thus, our results demon-strate that the development of glucocorticoid-induced obesity is not caused by a decreasedUCP1-dependent thermogenic capacity.