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PGC1beta coactivator and the Metabolic Syndrome:Functional characterisation in vivo using genetically modified mouse models.

Final Activity Report Summary - PGC1B METSYND (PGC1beta coactivator and the Metabolic Syndrome:Functional characterisation in vivo using genetically modified mouse models)

Recently, the research team have demonstrated that a specific group of proteins termed PGCs are important for the function of mitochondria, the component of the cell that makes energy. Here we wanted to study, specifically if the loss of one of these proteins, so called PGC1beta have any effect in the development of obesity and diabetes. For this purpose, we used a genetically modified mouse model and a second to none batch of techniques to study it.

Our results indicate that PGC1beta plays a role in controlling the activity of mitochondria (in many different organs) but seems that the deletion of this gene does not cause major metabolic failure as obesity and diabetes in normal conditions, because of a partial compensation mechanism due to their partner PGC1alpha in important metabolic tissues such as brown and white adipose tissue. Nevertheless, the loss of PGC1beta provokes several defects in other relevant tissues as skeletal muscle, heart and liver that were not recovered for PGC1alpha, specially when challenged with metabolic stressors (such as a high fat diet).

Our results indicate that, although having some overlapping functions, PGC1beta seems to cover basal energetic needs whereas their partner PGC1alpha provides the extra energetic support required under conditions of increased energy demand.