Functional disturbances of adipocyte mitochondria can affect systemic glucose tolerance via adipocyte-intrinsic mechanisms like impaired glucose uptake and altered differentiation processes (e.g. browning of WAT) as well as via metabolic- or endocrine-derived signals to remote tissues. Using new conditional knockout mouse models and high-fat diet feeding in combination with interventional studies employing pharmacological relevant substances, this project aims to unravel the role of MT-UPR signaling for the maintenance of adipocyte functions in WAT and BAT and its contribution to sustain whole body glucose homeostasis.