Skip to main content
. Author manuscript; available in PMC: 2022 May 24.
Published in final edited form as: J Endocrinol. 2021 May 24;249(3):223–237. doi: 10.1530/JOE-21-0009

Figure 8.

Figure 8

The hypothesized mechanism of the exercise-induced increase in insulin resistance (IR) in ERbDBDKO mice. Exercise increases mitochondrial activity, which associates with increased reactive oxygen species (ROS) and inflammation. UCP1 is an insulin-sensitizing protein that is often upregulated by exercise in adipose tissue for reasons that are not clear and via mechanisms that are not fully known. We propose that UCP1 upregulation is protective against adipocyte stress (e.g. exercise) and buffers exercise-induced stress. Further, when exercise is not coupled with an appropriate increase in UCP1, as seen in these mutant mice lacking the ERb DBD, exercise-induced adipose tissue cell stress leads to increased adipocyte and systemic IR. A full color version of this figure is available at https://doi.org/10.1530/JOE-21–0009.