@article{TomeNaegeleAdamoetal.2014,
  author    = {Tome, Filipa and N{\"a}gele, Thomas and Adamo, Mattia and Garg, Abhroop and Marco-Ilorca, Carles and Nukarinen, Ella and Pedrotti, Lorenzo and Peviani, Alessia and Simeunovic, Andrea and Tatkiewicz, Anna and Tomar, Monika and Gamm, Magdalena},
  title     = {The low energy signaling network},
  series = {Frontiers in Plant Science},
  volume    = {5},
  journal   = {Frontiers in Plant Science},
  number    = {353},
  issn      = {1664-462X},
  doi       = {10.3389/fpls.2014.00353},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-115813},
  year      = {2014},
  abstract  = {Stress impacts negatively on plant growth and crop productivity, causing extensive losses to agricultural production worldwide. Throughout their life, plants are often confronted with multiple types of stress that affect overall cellular energy status and activate energy-saving responses. The resulting low energy syndrome (LES) includes transcriptional, translational, and metabolic reprogramming and is essential for stress adaptation. The conserved kinases sucrose-non-fermenting-1-related protein kinase-1 (SnRK1) and target of rapamycin (TOR) play central roles in the regulation of LES in response to stress conditions, affecting cellular processes and leading to growth arrest and metabolic reprogramming. We review the current understanding of how TOR and SnRK1 are involved in regulating the response of plants to low energy conditions. The central role in the regulation of cellular processes, the reprogramming of metabolism, and the phenotypic consequences of these two kinases will be discussed in light of current knowledge and potential future developments.},
  language  = {en}
}
@article{DandekarFieselmannFischeretal.2014,
  author    = {Dandekar, Thomas and Fieselmann, Astrid and Fischer, Eva and Popp, Jasmin and Hensel, Michael and Noster, Janina},
  title     = {Salmonella—how a metabolic generalist adopts an intracellular lifestyle during infection},
  series = {Frontiers in Cellular and Infection Microbiology},
  volume    = {4},
  journal   = {Frontiers in Cellular and Infection Microbiology},
  number    = {191},
  issn      = {2235-2988},
  doi       = {10.3389/fcimb.2014.00191},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-120686},
  year      = {2014},
  abstract  = {The human-pathogenic bacterium Salmonella enterica adjusts and adapts to different environments while attempting colonization. In the course of infection nutrient availabilities change drastically. New techniques, "-omics" data and subsequent integration by systems biology improve our understanding of these changes. We review changes in metabolism focusing on amino acid and carbohydrate metabolism. Furthermore, the adaptation process is associated with the activation of genes of the Salmonella pathogenicity islands (SPIs). Anti-infective strategies have to take these insights into account and include metabolic and other strategies. Salmonella infections will remain a challenge for infection biology.},
  language  = {en}
}
@article{MirasSeyfriedPhinikaridouetal.2014,
  author    = {Miras, Alexander D. and Seyfried, Florian and Phinikaridou, Alkystis and Andia, Marcelo E. and Christakis, Ioannis and Spector, Alan C. and Botnar, Rene M. and le Roux, Carel W.},
  title     = {Rats Fed Diets with Different Energy Contribution from Fat Do Not Differ in Adiposity},
  series = {OBESITY FACTS},
  volume    = {7},
  journal   = {OBESITY FACTS},
  number    = {5},
  doi       = {10.1159/000368622},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-115249},
  pages     = {302-310},
  year      = {2014},
  abstract  = {Objective: To determine whether rats reaching the same body mass, having been fed either a low-fat (LFD) or a high-fat diet (HFD), differ in white adipose tissue (WAT) deposition. Methods: In experiment 1, 22 Sprague-Dawley rats of the same age were divided into 11 rats with body mass below the batch median and fed a HFD, and 11 above the median and fed a LFD. In experiment 2, 20 Sprague-Dawley rats of the same age and starting body mass were randomised to either a HFD or LFD. When all groups reached similar final body mass, WAT was quantified using magnetic resonance imaging (MRI), dissection, and plasma leptin. Results: In experiment 1, both groups reached similar final body mass at the same age; in experiment 2 the HFD group reached similar final body mass earlier than the LFD group. There were no significant differences in WAT as assessed by MRI or leptin between the HFD and LFD groups in both experiments. Dissection revealed a trend for higher retroperitoneal and epididymal adiposity in the HFD groups in both experiments. Conclusions: We conclude that at similar body mass, adiposity is independent of the macronutrient composition of the feeding regimen used to achieve it. (C) 2014 S Karger GmbH, Freiburg},
  language  = {en}
}
@article{BensaadFavaroLewisetal.2014,
  author    = {Bensaad, Karim and Favaro, Elena and Lewis, Caroline A. and Peck, Barrie and Lord, Simon and Collins, Jennifer M. and Pinnick, Katherine E. and Wigfield, Simon and Buffa, Francesca M. and Li, Ji-Liang and Zhang, Qifeng and Wakelam, Michael J. O. and Karpe, Fredrik and Schulze, Almut and Harris, Adrian L.},
  title     = {Fatty Acid Uptake and Lipid Storage Induced by HIF-1 alpha Contribute to Cell Growth and Survival after Hypoxia-Reoxygenation},
  series = {Cell Reports},
  volume    = {9},
  journal   = {Cell Reports},
  number    = {1},
  issn      = {2211-1247},
  doi       = {10.1016/j.celrep.2014.08.056},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-115162},
  pages     = {349-365},
  year      = {2014},
  abstract  = {An in vivo model of antiangiogenic therapy allowed us to identify genes upregulated by bevacizumab treatment, including Fatty Acid Binding Protein 3 (FABP3) and FABP7, both of which are involved in fatty acid uptake. In vitro, both were induced by hypoxia in a hypoxia-inducible factor-1 alpha (HIF-1 alpha)-dependent manner. There was a significant lipid droplet (LD) accumulation in hypoxia that was time and O-2 concentration dependent. Knockdown of endogenous expression of FABP3, FABP7, or Adipophilin (an essential LD structural component) significantly impaired LD formation under hypoxia. We showed that LD accumulation is due to FABP3/7-dependent fatty acid uptake while de novo fatty acid synthesis is repressed in hypoxia. We also showed that ATP production occurs via beta-oxidation or glycogen degradation in a cell-type-dependent manner in hypoxia-reoxygenation. Finally, inhibition of lipid storage reduced protection against reactive oxygen species toxicity, decreased the survival of cells subjected to hypoxia-reoxygenation in vitro, and strongly impaired tumorigenesis in vivo.},
  language  = {en}
}
@article{RiegerBaehrMaureretal.2014,
  author    = {Rieger, Johannes and B{\"a}hr, Oliver and Maurer, Gabriele D. and Hattingen, Elke and Franz, Kea and Brucker, Daniel and Walenta, Stefan and K{\"a}mmerer, Ulrike and Coy, Johannes F. and Weller, Michael and Steinbach, Joachim P.},
  title     = {ERGO: A pilot study of ketogenic diet in recurrent glioblastoma},
  series = {International Journal of Oncology},
  volume    = {44},
  journal   = {International Journal of Oncology},
  number    = {6},
  doi       = {10.3892/ijo.2014.2382},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-121170},
  pages     = {1843-52},
  year      = {2014},
  abstract  = {Limiting dietary carbohydrates inhibits glioma growth in preclinical models. Therefore, the ERGO trial (NCT00575146) examined feasibility of a ketogenic diet in 20 patients with recurrent glioblastoma. Patients were put on a low-carbohydrate, ketogenic diet containing plant oils. Feasibility was the primary endpoint, secondary endpoints included the percentage of patients reaching urinary ketosis, progression-free survival (PFS) and overall survival. The effects of a ketogenic diet alone or in combination with bevacizumab was also explored in an orthotopic U87MG glioblastoma model in nude mice. Three patients (15\%) discontinued the diet for poor tolerability. No serious adverse events attributed to the diet were observed. Urine ketosis was achieved at least once in 12 of 13 (92\%) evaluable patients. One patient achieved a minor response and two patients had stable disease after 6 weeks. Median PFS of all patients was 5 (range, 3-13) weeks, median survival from enrollment was 32 weeks. The trial allowed to continue the diet beyond progression. Six of 7 (86\%) patients treated with bevacizumab and diet experienced an objective response, and median PFS on bevacizumab was 20.1 (range, 12-124) weeks, for a PFS at 6 months of 43\%. In the mouse glioma model, ketogenic diet alone had no effect on median survival, but increased that of bevacizumab-treated mice from 52 to 58 days (p<0.05). In conclusion, a ketogenic diet is feasible and safe but probably has no significant clinical activity when used as single agent in recurrent glioma. Further clinical trials are necessary to clarify whether calorie restriction or the combination with other therapeutic modalities, such as radiotherapy or anti-angiogenic treatments, could enhance the efficacy of the ketogenic diet.},
  language  = {en}
}