@article{TuckerBoehningGaeseFaganetal.2018,
  author    = {Tucker, Marlee A. and Boehning-Gaese, Katrin and Fagan, William F. and Fryxell, John M. and Van Moorter, Bram and Alberts, Susan C. and Ali, Abdullahi H. and Allen, Andrew M. and Attias, Nina and Avgar, Tal and Bartlam-Brooks, Hattie and Bayarbaatar, Buuveibaatar and Belant, Jerrold L. and Bertassoni, Alessandra and Beyer, Dean and Bidner, Laura and van Beest, Floris M. and Blake, Stephen and Blaum, Niels and Bracis, Chloe and Brown, Danielle and de Bruyn, P. J. Nico and Cagnacci, Francesca and Calabrese, Justin M. and Camilo-Alves, Constanca and Chamaille-Jammes, Simon and Chiaradia, Andre and Davidson, Sarah C. and Dennis, Todd and DeStefano, Stephen and Diefenbach, Duane and Douglas-Hamilton, Iain and Fennessy, Julian and Fichtel, Claudia and Fiedler, Wolfgang and Fischer, Christina and Fischhoff, Ilya and Fleming, Christen H. and Ford, Adam T. and Fritz, Susanne A. and Gehr, Benedikt and Goheen, Jacob R. and Gurarie, Eliezer and Hebblewhite, Mark and Heurich, Marco and Hewison, A. J. Mark and Hof, Christian and Hurme, Edward and Isbell, Lynne A. and Janssen, Rene and Jeltsch, Florian and Kaczensky, Petra and Kane, Adam and Kappeler, Peter M. and Kauffman, Matthew and Kays, Roland and Kimuyu, Duncan and Koch, Flavia and Kranstauber, Bart and LaPoint, Scott and Leimgruber, Peter and Linnell, John D. C. and Lopez-Lopez, Pascual and Markham, A. Catherine and Mattisson, Jenny and Medici, Emilia Patricia and Mellone, Ugo and Merrill, Evelyn and Mourao, Guilherme de Miranda and Morato, Ronaldo G. and Morellet, Nicolas and Morrison, Thomas A. and Diaz-Munoz, Samuel L. and Mysterud, Atle and Nandintsetseg, Dejid and Nathan, Ran and Niamir, Aidin and Odden, John and Oliveira-Santos, Luiz Gustavo R. and Olson, Kirk A. and Patterson, Bruce D. and de Paula, Rogerio Cunha and Pedrotti, Luca and Reineking, Bjorn and Rimmler, Martin and Rogers, Tracey L. and Rolandsen, Christer Moe and Rosenberry, Christopher S. and Rubenstein, Daniel I. and Safi, Kamran and Said, Sonia and Sapir, Nir and Sawyer, Hall and Schmidt, Niels Martin and Selva, Nuria and Sergiel, Agnieszka and Shiilegdamba, Enkhtuvshin and Silva, Joao Paulo and Singh, Navinder and Solberg, Erling J. and Spiegel, Orr and Strand, Olav and Sundaresan, Siva and Ullmann, Wiebke and Voigt, Ulrich and Wall, Jake and Wattles, David and Wikelski, Martin and Wilmers, Christopher C. and Wilson, John W. and Wittemyer, George and Zieba, Filip and Zwijacz-Kozica, Tomasz and Mueller, Thomas},
  title     = {Moving in the Anthropocene},
  series = {Science},
  volume    = {359},
  journal   = {Science},
  number    = {6374},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  issn      = {0036-8075},
  doi       = {10.1126/science.aam9712},
  pages     = {466 -- 469},
  year      = {2018},
  abstract  = {Animal movement is fundamental for ecosystem functioning and species survival, yet the effects of the anthropogenic footprint on animal movements have not been estimated across species. Using a unique GPS-tracking database of 803 individuals across 57 species, we found that movements of mammals in areas with a comparatively high human footprint were on average one-half to one-third the extent of their movements in areas with a low human footprint. We attribute this reduction to behavioral changes of individual animals and to the exclusion of species with long-range movements from areas with higher human impact. Global loss of vagility alters a key ecological trait of animals that affects not only population persistence but also ecosystem processes such as predator-prey interactions, nutrient cycling, and disease transmission.},
  language  = {en}
}
@article{McNultyGoupilAlbaradoetal.2020,
  author    = {McNulty, Margaret A. and Goupil, Brad A. and Albarado, Diana C. and Casta{\~n}o-Martinez, Teresa and Ambrosi, Thomas H. and Puh, Spela and Schulz, Tim Julius and Sch{\"u}rmann, Annette and Morrison, Christopher D. and Laeger, Thomas},
  title     = {FGF21, not GCN2, influences bone morphology due to dietary protein restrictions},
  series = {Bone Reports},
  volume    = {12},
  journal   = {Bone Reports},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {2352-1872},
  doi       = {10.1016/j.bonr.2019.100241},
  pages     = {1 -- 10},
  year      = {2020},
  abstract  = {Background: Dietary protein restriction is emerging as an alternative approach to treat obesity and glucose intolerance because it markedly increases plasma fibroblast growth factor 21 (FGF21) concentrations. Similarly, dietary restriction of methionine is known to mimic metabolic effects of energy and protein restriction with FGF21 as a required mechanism. However, dietary protein has been shown to be required for normal bone growth, though there is conflicting evidence as to the influence of dietary protein restriction on bone remodeling. The purpose of the current study was to evaluate the effect of dietary protein and methionine restriction on bone in lean and obese mice, and clarify whether FGF21 and general control nonderepressible 2 (GCN2) kinase, that are part of a novel endocrine pathway implicated in the detection of protein restriction, influence the effect of dietary protein restriction on bone. Methods: Adult wild-type (WT) or Fgf21 KO mice were fed a normal protein (18 kcal\%; CON) or low protein (4 kcal\%; LP) diet for 2 or 27 weeks. In addition, adult WT or Gcn2 KO mice were fed a CON or LP diet for 27 weeks. Young New Zealand obese (NZO) mice were placed on high-fat diets that provided protein at control (16 kcal\%; CON), low levels (4 kcal\%) in a high-carbohydrate (LP/HC) or high-fat (LP/HF) regimen, or on high-fat diets (protein, 16 kcal\%) that provided methionine at control (0.86\%; CON-MR) or low levels (0.17\%; MR) for up to 9 weeks. Long bones from the hind limbs of these mice were collected and evaluated with micro-computed tomography (mu CT) for changes in trabecular and cortical architecture and mass. Results: In WT mice the 27-week LP diet significantly reduced cortical bone, and this effect was enhanced by deletion of Fgf21 but not Gcn2. This decrease in bone did not appear after 2 weeks on the LP diet. In addition, Fgf21 KO mice had significantly less bone than their WT counterparts. In obese NZO mice dietary protein and methionine restriction altered bone architecture. The changes were mediated by FGF21 due to methionine restriction in the presence of cystine, which did not increase plasma FGF21 levels and did not affect bone architecture. Conclusions: This study provides direct evidence of a reduction in bone following long-term dietary protein restriction in a mouse model, effects that appear to be mediated by FGF21.},
  language  = {en}
}
@misc{McNultyGoupilAlbaradoetal.2020,
  author    = {McNulty, Margaret A. and Goupil, Brad A. and Albarado, Diana C. and Casta{\~n}o-Martinez, Teresa and Ambrosi, Thomas H. and Puh, Spela and Schulz, Tim Julius and Sch{\"u}rmann, Annette and Morrison, Christopher D. and Laeger, Thomas},
  title     = {FGF21, not GCN2, influences bone morphology due to dietary protein restrictions},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-51629},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-516297},
  pages     = {12},
  year      = {2020},
  abstract  = {Background: Dietary protein restriction is emerging as an alternative approach to treat obesity and glucose intolerance because it markedly increases plasma fibroblast growth factor 21 (FGF21) concentrations. Similarly, dietary restriction of methionine is known to mimic metabolic effects of energy and protein restriction with FGF21 as a required mechanism. However, dietary protein has been shown to be required for normal bone growth, though there is conflicting evidence as to the influence of dietary protein restriction on bone remodeling. The purpose of the current study was to evaluate the effect of dietary protein and methionine restriction on bone in lean and obese mice, and clarify whether FGF21 and general control nonderepressible 2 (GCN2) kinase, that are part of a novel endocrine pathway implicated in the detection of protein restriction, influence the effect of dietary protein restriction on bone. Methods: Adult wild-type (WT) or Fgf21 KO mice were fed a normal protein (18 kcal\%; CON) or low protein (4 kcal\%; LP) diet for 2 or 27 weeks. In addition, adult WT or Gcn2 KO mice were fed a CON or LP diet for 27 weeks. Young New Zealand obese (NZO) mice were placed on high-fat diets that provided protein at control (16 kcal\%; CON), low levels (4 kcal\%) in a high-carbohydrate (LP/HC) or high-fat (LP/HF) regimen, or on high-fat diets (protein, 16 kcal\%) that provided methionine at control (0.86\%; CON-MR) or low levels (0.17\%; MR) for up to 9 weeks. Long bones from the hind limbs of these mice were collected and evaluated with micro-computed tomography (mu CT) for changes in trabecular and cortical architecture and mass. Results: In WT mice the 27-week LP diet significantly reduced cortical bone, and this effect was enhanced by deletion of Fgf21 but not Gcn2. This decrease in bone did not appear after 2 weeks on the LP diet. In addition, Fgf21 KO mice had significantly less bone than their WT counterparts. In obese NZO mice dietary protein and methionine restriction altered bone architecture. The changes were mediated by FGF21 due to methionine restriction in the presence of cystine, which did not increase plasma FGF21 levels and did not affect bone architecture. Conclusions: This study provides direct evidence of a reduction in bone following long-term dietary protein restriction in a mouse model, effects that appear to be mediated by FGF21.},
  language  = {en}
}