@article{StadionSchuermann2020,
  author    = {Stadion, Mandy and Sch{\"u}rmann, Annette},
  title     = {Intermittierendes Fasten},
  series = {Der Diabetologe},
  volume    = {16},
  journal   = {Der Diabetologe},
  number    = {7},
  publisher = {Springer Medizin},
  address   = {Berlin},
  issn      = {1860-9716},
  doi       = {10.1007/s11428-020-00666-z},
  pages     = {641 -- 646},
  year      = {2020},
  abstract  = {Obesity increases the risk of metabolic disorders and can lead to type 2 diabetes. Therefore, the treatment and prevention of obesity represent important medical challenges. Increased physical activity and a reduction in daily caloric intake of 25-30\% are often recommended. Another possibility is intermittent fasting, by limiting dietary caloric content over certain times, i.e. one or more days a week or for more than 14 h a day. Animal and human studies provide evidence that intermittent fasting in obesity leads to a reduction in body fat mass as well as to improvements of metabolic parameters and insulin sensitivity. These positive effects are mediated not only by the decrease in body mass, but also by the activation of metabolic pathways and cellular processes that are specific for fasting conditions. In this article, we describe the current knowledge about the mechanisms induced by intermittent fasting and present results from randomized controlled human trials.},
  language  = {de}
}
@misc{KlausOst2020,
  author    = {Klaus, Susanne and Ost, Mario},
  title     = {Mitochondrial uncoupling and longevity},
  series = {Experimental gerontology},
  volume    = {130},
  journal   = {Experimental gerontology},
  publisher = {Elsevier Science},
  address   = {Amsterdam},
  issn      = {0531-5565},
  doi       = {10.1016/j.exger.2019.110796},
  year      = {2020},
  abstract  = {Aging has been viewed both as a random process due to accumulation of molecular and cellular damage over time and as a programmed process linked to cellular pathway important for growth and maturation. These views converge on mitochondria as both the major producer of damaging reactive oxidant species (ROS) and as signaling organelles. A finite proton leak across the inner mitochondrial membrane leading to a slight uncoupling of oxidative phosphorylation and respiration is an intrinsic property of all mitochondria and according to the "uncoupling to survive" hypothesis it has evolved to protect against ROS production to minimize oxidative damage. This hypothesis is supported by evidence linking an increased endogenous, uncoupling protein (UCP1) mediated, as well as experimentally induced mitochondrial uncoupling to an increased lifespan in rodents. This is possibly due to the synergistic activation of molecular pathways linked to life extending effects of caloric restriction as well as a mitohormetic response. Mitohormesis is an adaptive stress response through mitonuclear signaling which increases stress resistance resulting in health promoting effects. Part of this response is the induction of fibroblast growth factor 21 (FGF21) and growth and differentiation factor 15 (GDF15), two stress-induced mitokines which elicit beneficial systemic metabolic effects via endocrine action.},
  language  = {en}
}