@phdthesis{Laeger2021,
  author    = {Laeger, Thomas},
  title     = {Protein-dependent regulation of feeding, metabolism, and development of type 2 diabetes},
  school      = {Universit{\"a}t Potsdam},
  pages     = {224},
  year      = {2021},
  abstract  = {Food intake is driven by the need for energy but also by the demand for essential nutrients such as protein. Whereas it was well known how diets high in protein mediate satiety, it remained unclear how diets low in protein induce appetite. Therefore, this thesis aims to contribute to the research area of the detection of restricted dietary protein and adaptive responses. This thesis provides clear evidence that the liver-derived hormone fibroblast growth factor 21 (FGF21) is an endocrine signal of a dietary protein restriction, with the cellular amino acid sensor general control nonderepressible 2 (GCN2) kinase acting as an upstream regulator of FGF21 during protein restriction. In the brain, FGF21 is mediating the protein-restricted metabolic responses, e.g. increased energy expenditure, food intake, insulin sensitivity, and improved glucose homeostasis. Furthermore, endogenous FGF21 induced by dietary protein or methionine restriction is preventing the onset of type 2 diabetes in the New Zealand Obese mouse. Overall, FGF21 plays an important role in the detection of protein restriction and macronutrient imbalance in rodents and humans, and mediates both the behavioral and metabolic responses to dietary protein restriction. This makes FGF21 a critical physiological signal of dietary protein restriction, highlighting the important but often overlooked impact of dietary protein on metabolism and eating behavior, independent of dietary energy content.},
  language  = {en}
}
@article{WiedmerJungCastroetal.2020,
  author    = {Wiedmer, Petra and Jung, Tobias and Castro, Jose Pedro and Pomatto, Laura C. D. and Sun, Patrick Y. and Davies, Kelvin J. A. and Grune, Tilman},
  title     = {Sarcopenia},
  series = {Ageing research reviews : ARR},
  volume    = {65},
  journal   = {Ageing research reviews : ARR},
  publisher = {Elsevier},
  address   = {Clare},
  issn      = {1568-1637},
  doi       = {10.1016/j.arr.2020.101200},
  pages     = {17},
  year      = {2020},
  abstract  = {Sarcopenia represents a muscle-wasting syndrome characterized by progressive and generalized degenerative loss of skeletal muscle mass, quality, and strength occurring during normal aging. Sarcopenia patients are mainly suffering from the loss in muscle strength and are faced with mobility disorders reducing their quality of life and are, therefore, at higher risk for morbidity (falls, bone fracture, metabolic diseases) and mortality. <br /> Several molecular mechanisms have been described as causes for sarcopenia that refer to very different levels of muscle physiology. These mechanisms cover e. g. function of hormones (e. g. IGF-1 and Insulin), muscle fiber composition and neuromuscular drive, myo-satellite cell potential to differentiate and proliferate, inflammatory pathways as well as intracellular mechanisms in the processes of proteostasis and mitochondrial function. <br /> In this review, we describe sarcopenia as a muscle-wasting syndrome distinct from other atrophic diseases and summarize the current view on molecular causes of sarcopenia development as well as open questions provoking further research efforts for establishing efficient lifestyle and therapeutic interventions.},
  language  = {en}
}