@phdthesis{Meyer2015,
  author    = {Meyer, S{\"o}ren},
  title     = {Toxicity and toxicokinetics of arsenolipids and their metabolites},
  school      = {Universit{\"a}t Potsdam},
  pages     = {152, VIII},
  year      = {2015},
  language  = {en}
}
@phdthesis{Prandi2015,
  author    = {Prandi, Simone},
  title     = {Characterization of the expression and function of bitter taste receptor genes in gastrointestinal tissues},
  school      = {Universit{\"a}t Potsdam},
  pages     = {165},
  year      = {2015},
  language  = {en}
}
@phdthesis{Scherwinski2015,
  author    = {Scherwinski, Ann-Christin},
  title     = {Die Phyllosph{\"a}re},
  school      = {Universit{\"a}t Potsdam},
  pages     = {83},
  year      = {2015},
  language  = {de}
}
@phdthesis{Jacobs2015,
  author    = {Jacobs, Simone},
  title     = {Biological mechanisms of the association between proportions of fatty acids in erythrocyte membranes and type 2 diabetes risk in the EPIC-Potsdam-Study},
  pages     = {157},
  year      = {2015},
  language  = {en}
}
@phdthesis{Frenzel2015,
  author    = {Frenzel, Sabine},
  title     = {Die Rolle der Umamirezeptoruntereinheit Tas1r1 jenseits ihrer gustatorischen Bedeutung},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-79502},
  school      = {Universit{\"a}t Potsdam},
  pages     = {XV, 172},
  year      = {2015},
  abstract  = {Aminos{\"a}uren sind lebensnotwendige Molek{\"u}le f{\"u}r alle Organismen. Ihre Erkennung im K{\"o}rper erm{\"o}glicht eine bedarfsgerechte Regulation ihrer Aufnahme und ihrer Verwertung. Welcher Chemosensor f{\"u}r diese Erkennung jedoch hauptverantwortlich ist, ist bisher unklar. In der vorliegenden Arbeit wurde die Rolle der Umamigeschmacksrezeptoruntereinheit Tas1r1 jenseits ihrer gustatorischen Bedeutung f{\"u}r die Aminos{\"a}uredetektion in der Mundh{\"o}hle untersucht. In der histologischen Tas1r1-Expressionsanalyse nichtgustatorischer Gewebe der Mauslinie Tas1r1-Cre/ROSA26-tdRFP wurde {\"u}ber die Detektion des Reporterproteins tdRFP die Expression des Tas1r1 in allen untersuchten Geweben (Speiser{\"o}hre, Magen, Darm, Bauchspeicheldr{\"u}se, Leber, Niere, Muskel- und Fettgewebe, Milz, Thymus, Lymphknoten, Lunge sowie Hoden) nachgewiesen. Mit Ausnahme von D{\"u}nndarm und Hoden gelang hierbei der Nachweis erstmals spezifisch auf zellul{\"a}rer Ebene. Caecum und Lymphknoten wurden zudem neu als Expressionsorte des Tas1r1 identifiziert. Trotz der beobachteten weiten Verbreitung des Tas1r1 im Organismus - unter anderem auch in Geweben, die f{\"u}r den Proteinstoffwechsel besonders relevant sind - waren im Zuge der durchgef{\"u}hrten Untersuchung potentieller extraoraler Funktionen des Rezeptors durch ph{\"a}notypische Charakterisierung der Mauslinie Tas1r1-BLiR nur schwache Auswirkungen auf Aminos{\"a}urestoffwechsel bzw. Stickstoffhaushalt im Falle eines Tas1r1-Knockouts detektierbar. W{\"a}hrend sich Ern{\"a}hrungsverhalten, Gesamtphysiologie, Gewebemorphologie sowie Futterverdaulichkeit unver{\"a}ndert zeigten, war die renale Stickstoffausscheidung bei Tas1r1-Knockout-M{\"a}usen auf eiweißarmer sowie auf eiweißreicher Di{\"a}t signifikant verringert. Eine {\"U}berdeckung der Auswirkungen des Tas1r1-Knockouts aufgrund kompensatorischer Effekte durch den Aminos{\"a}uresensor CaSR oder den Peptidsensor Gpr93 war nicht nachweisbar. Es bleibt offen, ob andere Mechanismen oder andere Chemosensoren an einer Kompensation beteiligt sind oder aber Tas1r1 in extraoralem Gewebe andere Funktionen als die der Aminos{\"a}uredetektion {\"u}bernimmt. Unterschiede im extraoralen Expressionsmuster der beiden Umamirezeptor-untereinheiten Tas1r1 und Tasr3 lassen Spekulationen {\"u}ber andere Partner, Liganden und Funktionen zu.},
  language  = {de}
}
@phdthesis{Bojahr2015,
  author    = {Bojahr, Juliane},
  title     = {Aktivierung des humanen S{\"u}ßgeschmacksrezeptors im zellbasierten Testsystem},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-93331},
  school      = {Universit{\"a}t Potsdam},
  pages     = {XIII, 174},
  year      = {2015},
  abstract  = {Zellbasierte heterologe Expressionssysteme bieten ein einfaches und schnelles Verfahren, um neue S{\"u}ßstoffe oder S{\"u}ßverst{\"a}rker zu finden. Unter Verwendung eines solchen Testsystems, konnte ich in Zusammenarbeit mit der Symrise AG, Holzminden und dem Institut f{\"u}r Pflanzenbiochemie in Halle/Saale die vietnamesische Pflanze Mycetia balansae als Quelle eines neuen S{\"u}ßstoffs identifizieren. Deren Hauptkomponenten, genannt Balansine, aktivieren spezifisch den humanen S{\"u}ßrezeptor. Chim{\"a}re Rezeptoren zeigten, dass die amino-terminalen Dom{\"a}nen der S{\"u}ßrezeptoruntereinheiten, welche ein Großteil der Liganden des S{\"u}ßrezeptors binden, f{\"u}r dessen Aktivierung durch Balansin A nicht notwendig sind. Voraussetzung f{\"u}r die Anwendung zellbasierter Testsysteme zum Auffinden neuer S{\"u}ßstoffe ist jedoch, dass s{\"u}ße Substanzen gesichert identifiziert werden, w{\"a}hrend nicht s{\"u}ße Substanzen zuverl{\"a}ssig keine Rezeptoraktivierung aufweisen. W{\"a}hrend in HEK293 TAS1R2 TAS1R3To Galpha15i3-Zellen S{\"u}ßrezeptoraktivierung gegen{\"u}ber nicht s{\"u}ß schmeckenden Substanzen beobachtet wurde, konnte mit den HEK293PEAKrapid Galpha15-Zellen ein zuverl{\"a}ssiges Testsystem identifiziert, welches den S{\"u}ßgeschmack der untersuchten Substanzen widerspiegelte. Es fanden sich keine Hinweise, dass akzessorische Proteine oder verwandte Rezeptoren des S{\"u}ßrezeptors das unterschiedliche Verhalten der Zellen verursachen. Es konnte gezeigt werden, dass die Verwendung unterschiedlicher G-Proteine die Signalamplituden des S{\"u}ßrezeptors beeinflusst, die Unterschiede zwischen den Zellsystemen jedoch nicht vollst{\"a}ndig erkl{\"a}rt. Keine der untersuchten Galpha-Proteinchim{\"a}ren spiegelte die intrinsische S{\"u}ße der Substanzen wider. Wenn auch nicht urs{\"a}chlich f{\"u}r die Diskrepanz zwischen S{\"u}ßrezeptoraktivierung in vitro und S{\"u}ßgeschmack in vivo, so weisen die Ergebnisse dieser Arbeit auf eine Interaktion der S{\"u}ßrezeptoruntereinheiten mit dem humanen Calcium-sensing Rezeptor hin. Vanillin und Ethylvanillin konnten als neue Agonisten des Calcium-sensing Rezeptors identifiziert werden. Wie die vorliegende Arbeit zeigt, k{\"o}nnen sich kleine Unterschiede im Zellhintergrund deutlich auf die Funktionsweise heterolog exprimierter Rezeptoren auswirken. Dies zeigt wie wichtig die Wahl der Zellen f{\"u}r solche Screeningsysteme ist.},
  language  = {de}
}
@phdthesis{Brachs2015,
  author    = {Brachs, Maria},
  title     = {Genome wide expression analysis and metabolic mechanisms predicting body weight maintenance},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-100767},
  school      = {Universit{\"a}t Potsdam},
  pages     = {106},
  year      = {2015},
  abstract  = {Obesity is a major health problem for many developing and industrial countries. Increasing rates reach almost 50 \% of the population in some countries and related metabolic diseases including cardiovascular events and T2DM are challenging the health systems. Adiposity, an increase in body fat mass, is a major hallmark of obesity. Adipose tissue is long known not only to store lipids but also to influence whole-body metabolism including food intake, energy expenditure and insulin sensitivity. Adipocytes can store lipids and thereby protect other tissue from lipotoxic damage. However, if the energy intake is higher than the energy expenditure over a sustained time period, adipose tissue will expand. This can lead to an impaired adipose tissue function resulting in higher levels of plasma lipids, which can affect other tissue like skeletal muscle, finally leading to metabolic complications. Several studies showed beneficial metabolic effects of weight reduction in obese subjects immediately after weight loss. However, weight regain is frequently observed along with potential negative effects on cardiovascular risk factors and a high intra-individual response. We performed a body weight maintenance study investigating the mechanisms of weight maintenance after intended WR. Therefore we used a low caloric diet followed by a 12-month life-style intervention. Comprehensive phenotyping including fat and muscle biopsies was conducted to investigate hormonal as well as metabolic influences on body weight regulation. In this study, we showed that weight reduction has numerous potentially beneficial effects on metabolic parameters. After 3-month WR subjects showed significant weight and fat mass reduction, lower TG levels as well as higher insulin sensitivity. Using RNA-Seq to analyse whole fat and muscle transcriptome a strong impact of weight reduction on adipose tissue gene expression was observed. Gene expression alterations over weight reduction included several cellular metabolic genes involved in lipid and glucose metabolism as well as insulin signalling and regulatory pathways. These changes were also associated with anthropometric parameters assigning body composition. Our data indicated that weight reduction leads to a decreased expression of several lipid catabolic as well as anabolic genes. Long-term body weight maintenance might be influenced by several parameters including hormones, metabolic intermediates as well as the transcriptional landscape of metabolic active tissues. Our data showed that genes involved in biosynthesis of unsaturated fatty acids might influence the BMI 18-month after a weight reduction phase. This was further supported by analysing metabolic parameters including RQ and FFA levels. We could show that subjects maintaining their lost body weight had a higher RQ and lower FFA levels, indicating increased metabolic flexibility in subjects. Using this transcriptomic approach we hypothesize that low expression levels of lipid synthetic genes in adipose tissue together with a higher mitochondrial activity in skeletal muscle tissue might be beneficial in terms of body weight maintenance.},
  language  = {en}
}
@unpublished{SeelaenderLavianoBusquetsetal.2015,
  author    = {Seelaender, Marilia and Laviano, A. and Busquets, S. and P{\"u}schel, Gerhard Paul and Margaria, T. and Batista Jr., Miguel Luiz},
  title     = {Inflammation in Cachexia},
  series = {Mediators of inflammation},
  journal   = {Mediators of inflammation},
  publisher = {Hindawi Publishing Corp.},
  address   = {New York},
  issn      = {0962-9351},
  doi       = {10.1155/2015/536954},
  pages     = {2},
  year      = {2015},
  language  = {en}
}
@article{GereckeScholtkaLoewensteinetal.2015,
  author    = {Gerecke, Christian and Scholtka, Bettina and Loewenstein, Yvonne and Fait, Isabel and Gottschalk, Uwe and Rogoll, Dorothee and Melcher, Ralph and Kleuser, Burkhard},
  title     = {Hypermethylation of ITGA4, TFPI2 and VIMENTIN promoters is increased in inflamed colon tissue: putative risk markers for colitis-associated cancer},
  series = {Journal of cancer research and clinical oncology : official organ of the Deutsche Krebsgesellschaft},
  volume    = {141},
  journal   = {Journal of cancer research and clinical oncology : official organ of the Deutsche Krebsgesellschaft},
  number    = {12},
  publisher = {Springer},
  address   = {New York},
  issn      = {0171-5216},
  doi       = {10.1007/s00432-015-1972-8},
  pages     = {2097 -- 2107},
  year      = {2015},
  abstract  = {Epigenetic silencing of tumor suppressor genes is involved in early transforming events and has a high impact on colorectal carcinogenesis. Likewise, colon cancers that derive from chronically inflamed bowel diseases frequently exhibit epigenetic changes. But there is little data about epigenetic aberrations causing colorectal cancer in chronically inflamed tissue. The aim of the present study was to evaluate the aberrant gain of methylation in the gene promoters of VIM, TFPI2 and ITGA4 as putative early markers in the development from inflamed tissue via precancerous lesions toward colorectal cancer. Initial screening of different cancer cell lines by using methylation-specific PCR revealed a putative colon cancer-specific methylation pattern. Additionally, a demethylation assay was performed to investigate the methylation-dependent gene silencing of ITGA4. The candidate markers were analyzed in colonic tissue specimens from patients with colorectal cancer (n = 15), adenomas (n = 76), serrated lesions (n = 13), chronic inflammation (n = 10) and normal mucosal samples (n = 9). A high methylation frequency of VIM (55.6 \%) was observed in normal colon tissue, whereas ITGA4 and TFPI2 were completely unmethylated in controls. A significant gain of methylation frequency with progression of disease as well as an age-dependent effect was detectable for TFPI2. ITGA4 methylation frequency was high in precancerous and cancerous tissues as well as in inflammatory bowel diseases (IBD). The already established methylation marker VIM does not permit a specific and sensitive discrimination of healthy and neoplastic tissue. The methylation markers ITGA4 and TFPI2 seem to be suitable risk markers for inflammation-associated colon cancer.},
  language  = {en}
}
@article{SchraplauScheweNeuschaeferRubeetal.2015,
  author    = {Schraplau, Anne and Schewe, Bettina and Neusch{\"a}fer-Rube, Frank and Ringel, Sebastian and Neuber, Corinna and Kleuser, Burkhard and P{\"u}schel, Gerhard Paul},
  title     = {Enhanced thyroid hormone breakdown in hepatocytes by mutual induction of the constitutive androstane receptor (CAR, NR1I3) and arylhydrocarbon receptor by benzo[a]pyrene and phenobarbital},
  series = {Toxicology},
  volume    = {328},
  journal   = {Toxicology},
  publisher = {Elsevier},
  address   = {Clare},
  issn      = {0300-483X},
  doi       = {10.1016/j.tox.2014.12.004},
  pages     = {21 -- 28},
  year      = {2015},
  abstract  = {Xenobiotics may interfere with the hypothalamic-pituitary-thyroid endocrine axis by inducing enzymes that inactivate thyroid hormones and thereby reduce the metabolic rate. This induction results from an activation of xeno-sensing nuclear receptors. The current study shows that benzo[a]pyrene, a frequent contaminant of processed food and activator of the arylhydrocarbon receptor (AhR) activated the promoter and induced the transcription of the nuclear receptor constitutive androstane receptor (CAR, NR1I3) in rat hepatocytes. Likewise, phenobarbital induced the AhR transcription. This mutual induction of the nuclear receptors enhanced the phenobarbital-dependent induction of the prototypic CAR target gene Cyp2b1 as well as the AhR-dependent induction of UDP-glucuronosyltransferases. In both cases, the induction by the combination of both xenobiotics was more than the sum of the induction by either substance alone. By inducing the AhR, phenobarbital enhanced the benzo[a]pyrene-dependent reduction of thyroid hormone half-life and the benzo[a]pyrene-dependent increase in the rate of thyroid hormone glucuronide formation in hepatocyte cultures. CAR ligands might thus augment the endocrine disrupting potential of AhR activators by an induction of the AhR. (C) 2014 Elsevier Ireland Ltd. All rights reserved.},
  language  = {en}
}