@misc{KoenigGruneOtt2019,
  author    = {K{\"o}nig, Jeannette and Grune, Tilman and Ott, Christiane},
  title     = {Assessing autophagy in murine skeletal muscle: current findings to modulate and quantify the autophagic flux},
  series = {Current opinion in clinical nutrition and metabolic care},
  volume    = {22},
  journal   = {Current opinion in clinical nutrition and metabolic care},
  number    = {5},
  publisher = {Lippincott Williams \& Wilkins},
  address   = {Philadelphia},
  issn      = {1363-1950},
  doi       = {10.1097/MCO.0000000000000579},
  pages     = {355 -- 362},
  year      = {2019},
  abstract  = {Purpose of review In addition to the currently available lysosomotropic drugs and autophagy whole-body knockout mouse models, we provide alternative methods that enable the modulation and detection of autophagic flux in vivo, discussing advantages and disadvantages of each method. Recent findings With the autophagosome-lysosome fusion inhibitor colchicine in skeletal muscle and temporal downregulation of autophagy using a novel Autophagy related 5-short hairpin RNA (Atg5-shRNA) mouse model we mention two models that directly modulate autophagy flux in vivo. Furthermore, methods to quantify autophagy flux, such as mitophagy transgenic reporters, in situ immunofluorescent staining and multispectral imaging flow cytometry, in mature skeletal muscle and cells are addressed. To achieve clinical benefit, less toxic, temporary and cell-type-specific modulation of autophagy should be pursued further. A temporary knockdown as described for the Atg5-shRNA mice could provide a first insight into possible implications of autophagy inhibition. However, it is also important to take a closer look into the methods to evaluate autophagy after harvesting the tissue. In particular caution is required when experimental conditions can influence the final measurement and this should be pretested carefully.},
  language  = {en}
}
@misc{CastroGruneSpeckmann2016,
  author    = {Castro, Jos{\´e} Pedro and Grune, Tilman and Speckmann, Bodo},
  title     = {The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction},
  series = {Biological chemistry},
  volume    = {397},
  journal   = {Biological chemistry},
  publisher = {De Gruyter},
  address   = {Berlin},
  issn      = {1431-6730},
  doi       = {10.1515/hsz-2015-0305},
  pages     = {709 -- 724},
  year      = {2016},
  abstract  = {White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/ release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho) physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e. g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.},
  language  = {en}
}