Ramadori, Giuliano

[["dc.bibliographiccitation.firstpage","565"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.lastpage","572"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Haralanova-Ilieva, B."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Armbrust, T."],["dc.date.accessioned","2018-11-07T11:12:14Z"],["dc.date.available","2018-11-07T11:12:14Z"],["dc.date.issued","2005"],["dc.description.abstract","Background/Aims: The transmembrane glycoprotein osteoactivin is expressed in osteoblasts, dendritic cells and tumor cells. It is suggested to influence osteoblast maturation, cell adhesion and migration. We studied osteoactivin expression within the liver. Methods: Expression of osteoactivin was analysed by RT-PCR, Northern blotting, in situ hybridisation (ISH) and immunohistochemistry (IHC) comparing normal and acutely injured rat liver [induced by carbon tetrachloride (CCl4) administration], liver cell populations, and normal or diseased human liver. Results: By ISH osteoactivin expression was detected in sinusoid-lining cells found by IHC to be positive for the common mononuclear phagocyte marker antibody anti-CD68. While total liver contained only traces, isolated Kupffer cells expressed abundant amounts of osteoactivin mRNA further increasing during culture. In acutely injured rat liver osteoactivin expression was strongly increased reaching maximum of expression 48 h after CCl4. By ISH osteoactivin expression was localised in pericentral inflammatory cells and sinusoid-lining cells again anti-CD68 positive. Dexamethasone and lipopolysaccharide decreased osteoactivin expression in cultured mononuclear phagocytes of normal as well as of acutely injured liver. In human liver osteoactivin was increased in fulminant hepatitis and paracetamol intoxication. Conclusions: Osteoactivin is expressed at high levels in normal and inflammatory liver macrophages suggesting a significant role in acute liver injury. (C) 2005 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jhep.2004.12.021"],["dc.identifier.isi","000228302700025"],["dc.identifier.pmid","15763343"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53615"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0168-8278"],["dc.title","Expression of osteoactivin in rat and human liver and isolated rat liver cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Liver Transplantation"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Homayounfar, Kia"],["dc.contributor.author","Goralczyk, Armin"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Lorf, Thomas"],["dc.contributor.author","Obed, Aiman"],["dc.date.accessioned","2018-11-07T08:28:21Z"],["dc.date.available","2018-11-07T08:28:21Z"],["dc.date.issued","2009"],["dc.format.extent","S148"],["dc.identifier.isi","000267792300256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16399"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Inc"],["dc.publisher.place","Hoboken"],["dc.relation.conference","15th Annual Congress of the International-Liver-Transplantation-Society"],["dc.relation.eventlocation","New York, NY"],["dc.relation.issn","1527-6465"],["dc.title","LONG TERM SURVIVAL, AFTER LIVER TRANSPLANTATION IN PATIENTS WITH NEUROENDOCRINE LIVER METASTASES: GERMAN SINGLE CENTER EXPERIENCE"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Zocco, Maria Assunta"],["dc.contributor.author","Carloni, E."],["dc.contributor.author","Nista, E. C."],["dc.contributor.author","Candelli, M."],["dc.contributor.author","Cazzato, I. A."],["dc.contributor.author","Di Campli, C."],["dc.contributor.author","Nestola, M."],["dc.contributor.author","Gasbarrini, G."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Gasbarrini, A."],["dc.date.accessioned","2018-11-07T10:49:58Z"],["dc.date.available","2018-11-07T10:49:58Z"],["dc.date.issued","2004"],["dc.identifier.doi","10.1016/S0168-8278(04)90536-3"],["dc.identifier.isi","000220950800537"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48553"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","39th Annual Meeting of the European-Association-for-the-Study-of-the-Liver"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","0168-8278"],["dc.title","Characterization of gene expression profile in Kupffer cells stimulated with IFN alpha and gamma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2325"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Cancer"],["dc.bibliographiccitation.lastpage","2333"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Joensuu, Heikki"],["dc.contributor.author","Eriksson, Mikael"],["dc.contributor.author","Hall, Kirsten Sundby"],["dc.contributor.author","Hartmann, Joerg Thomas"],["dc.contributor.author","Pink, Daniel"],["dc.contributor.author","Schuette, Jochen"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Hohenberger, Peter"],["dc.contributor.author","Duyster, Justus"],["dc.contributor.author","Al-Batran, Salah-Eddin"],["dc.contributor.author","Schlemmer, Marcus"],["dc.contributor.author","Bauer, Sebastian"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Sarlomo-Rikala, Maarit"],["dc.contributor.author","Nilsson, Bengt"],["dc.contributor.author","Sihto, Harri"],["dc.contributor.author","Ballman, Karla V."],["dc.contributor.author","Leinonen, Mika"],["dc.contributor.author","DeMatteo, Ronald P."],["dc.contributor.author","Reichardt, Peter"],["dc.date.accessioned","2018-11-07T09:37:08Z"],["dc.date.available","2018-11-07T09:37:08Z"],["dc.date.issued","2014"],["dc.description.abstract","BACKGROUND: Little is known about the factors that predict for gastrointestinal stromal tumor (GIST) recurrence in patients treated with adjuvant imatinib. METHODS: Risk factors for GIST recurrence were identified, and 2 risk stratification scores were developed using the database of the Scandinavian Sarcoma Group (SSG) XVIII trial, where 358 patients with high-risk GIST with no overt metastases were randomly assigned to adjuvant imatinib 400 mg/day either for 12 or 36 months after surgery. The findings were validated in the imatinib arm of the American College of Surgeons Oncology Group Z9001 trial, where 359 patients with GIST were randomized to receive imatinib and 354 were to receive placebo for 12 months. RESULTS: Five factors (high tumor mitotic count, nongastric location, large size, rupture, and adjuvant imatinib for 12 months) were independently associated with unfavorable recurrence-free survival (RFS) in a multivariable analysis in the SSGXVIII cohort. A risk score based on these 5 factors had a concordance index with GIST recurrence of 78.9%. When a simpler score consisting of the 2 strongest predictive factors (mitotic count and tumor site) was devised, the groups with the lowest, intermediate high, and the highest risk had 5-year RFS of 76.7%, 47.5%, and 8.4%, respectively. Both scores were strongly associated with RFS in the validation cohort (P<.001 for each comparison). CONCLUSIONS: The scores generated were effective in stratifying the risk of GIST recurrence in patient populations treated with adjuvant imatinib. Patients with nongastric GIST with a high mitotic count are at a particularly high risk for recurrence. (C) 2014 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made."],["dc.identifier.doi","10.1002/cncr.28669"],["dc.identifier.isi","000340241500015"],["dc.identifier.pmid","24737415"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12825"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32770"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0142"],["dc.relation.issn","0008-543X"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Risk Factors for Gastrointestinal Stromal Tumor Recurrence in Patients Treated With Adjuvant Imatinib"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Strahlentherapie und Onkologie"],["dc.bibliographiccitation.volume","183"],["dc.contributor.author","Christiansen, H."],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Hess, C. F."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T11:02:14Z"],["dc.date.available","2018-11-07T11:02:14Z"],["dc.date.issued","2007"],["dc.format.extent","49"],["dc.identifier.isi","000247071800131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51329"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.publisher.place","Munich"],["dc.relation.conference","13th Congress of the Deutschen-Gesellschaft-fur-Radioonkologie"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","0179-7158"],["dc.title","Radiation-induced reduced expression of Hsp27 in in vitro liver macrophages leads to apoptosis and release of TNF-alpha"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2374"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","World Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","2382"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Attar, Bashar M."],["dc.contributor.author","Moore, Christopher M."],["dc.contributor.author","George, Magdalena"],["dc.contributor.author","Ion-Nedelcu, Nicolae"],["dc.contributor.author","Turbay, Rafael"],["dc.contributor.author","Zachariah, Annamma"],["dc.contributor.author","Ramadori, Guiliano"],["dc.contributor.author","Fareed, Jawed"],["dc.contributor.author","van Thiel, David H."],["dc.date.accessioned","2018-11-07T09:42:39Z"],["dc.date.available","2018-11-07T09:42:39Z"],["dc.date.issued","2014"],["dc.description.abstract","AIM: To quantitate the simultaneous serum and ascitic fluid levels of procalcitonin and inflammatory markers in cirrhotics with and without ascites. METHODS: A total of 88 consecutive severe cirrhotic patients seen in a large city hospital liver clinic were studied and divided into two groups, those with and without ascites. Group 1 consisted of 41 cirrhotic patients with massive ascites, as demonstrated by necessity for therapeutic large-volume paracentesis. Group 2 consisted of 47 cirrhotic patients without any clinically documented ascites to include either a recent abdominal computed tomography scan or ultrasound study. Serum and ascitic fluid levels of an array of inflammatory markers, including procalcitonin, were measured and compared to each other and a normal plasma panel (NPP). RESULTS: The values for inflammatory markers assayed in the serum of Groups 1 and 2, and ascitic fluid of the Group 1. The plasma levels of the inflammatory cytokines interleukin (IL)-2, IL-4, IL-6, IL-8, interferon gamma (IFN gamma) and epidermal growth factor (EGF) were all significantly greater in the serum of Group 1 as compared to that of the serum obtained from the Group 2 subjects (all P < 0.05). There were significantly greater serum levels of IL-6, IL-8, IL-10, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, vascular endothelial growth factor and EGF when comparing Group 2 to the NPP. There was no significant difference for IL-1A, IL-1B, IL-2, IL-4 and IFN gamma levels between these two groups. Serum procalcitonin levels were increased in cirrhotics with ascites compared to cirrhotics without ascites, but serum levels were similar to ascites levels within the ascites group. Furthermore, many of these cytokines, but not procalcitonin, demonstrate an ascites-to-serum gradient. Serum procalcitonin does not demonstrate any significant difference segregated by liver etiology in the ascites group; but ascitic fluid procalcitonin is elevated significantly in cardiac cirrhosis/miscellaneous subgroup compared to the hepatitis C virus and alcoholic cirrhosis subgroups. CONCLUSION: Procalcitonin in the ascitic fluid, but not in the serum, differentiates between cirrhotic subgroup reflecting the dynamic interplay of ascites, bacterial translocation and the peri-peritoneal cytokine. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved."],["dc.identifier.doi","10.3748/wjg.v20.i9.2374"],["dc.identifier.isi","000332692300025"],["dc.identifier.pmid","24605035"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34005"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Baishideng Publ Grp Co Ltd"],["dc.relation.issn","2219-2840"],["dc.relation.issn","1007-9327"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Procalcitonin, and cytokines document a dynamic inflammatory state in non-infected cirrhotic patients with ascites"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","301"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","311"],["dc.bibliographiccitation.volume","313"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","El-Armouche, H."],["dc.contributor.author","Aprigliano, Isabella"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:36:23Z"],["dc.date.available","2018-11-07T10:36:23Z"],["dc.date.issued","2003"],["dc.description.abstract","Hepatic stellate cells (HSCs), the pericytes of hepatic sinusoids, and liver myofibroblasts (rMFs), cells located in the portal field and around the pericentral area, are the principal fibrogenic cell types of the liver. In cases of liver damage HSCs undergo 'activation,' i.e., they acquire a myofibroblast-like appearance and synthesize huge amounts of extracellular matrix proteins (ECMs). Their proliferation ability, however, is a matter of debate. In fact, during culture the number of rat HSCs decreases, while DNA synthesis activity and DNA content per cell increase (4+/-0.6 times). Together with the decrease in cell number (60+/-19% at day 6 of primary culture compared to day 3), cell volume increases and many HSCs become multinuclear. On the other hand, in cultures of rMFs, cell number increases along with DNA synthesis, and these cells do not become multinuclear. 'Activated' HSCs produce higher levels of cyclin D-1 and E-1 transcripts than rMFs, which correlates with their increased levels of phosphorylated retinoblastoma (Rb) protein. In activated HSCs DNA synthesis seems to be associated with polyploidy and increase in cell volume, while DNA synthesis is followed by mitosis in rMFs."],["dc.identifier.doi","10.1007/s00441-003-0768-3"],["dc.identifier.isi","000185457000006"],["dc.identifier.pmid","12898209"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45309"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0302-766X"],["dc.title","Endoreplication and polyploidy in primary culture of rat hepatic stellate cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","279"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","291"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Triebel, Jakob"],["dc.contributor.author","Posselt, Jessica"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Ramadori, Pierluigi"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:13:12Z"],["dc.date.available","2018-11-07T09:13:12Z"],["dc.date.issued","2012"],["dc.description.abstract","MCRs are known to be expressed predominantly in the brain where they mediate metabolic and anti-inflammatory functions. Leptin plays an important role in appetite and energy regulation via signaling through melanocortin receptors (MCRs) in the brain. As serum levels of MCR ligands are elevated in a clinical situation [acute-phase response (APR)] to tissue damage, where the liver is responsible for the metabolic changes, we studied hepatic gene expression of MCRs in a model of muscle tissue damage induced by turpentine oil (TO) injection in rats. A significant increase in gene expression of all five MCRs (MC4R was the highest) in liver at the RNA and protein level was detected after TO injection. A similar pattern of increase was also found in the brain. Immunohistology showed MC4R in the cytoplasm, but also in the nucleus of parenchymal and non-parenchymal liver cells, whereas MC3R-positivity was mainly cytoplasmic. A time-dependent migration of MC4R protein from the cytoplasm into the nucleus was observed during APR, in parallel with an increase in alpha-MSH and leptin serum levels. An increase of MC4R was detected at the protein level in wild-type mice, while such an increase was not observed in IL-6ko mice during APR. Moreover, treatment of isolated liver cells with melanocortin agonists (alpha-MSH and THIQ) inhibited the endotoxin-induced upregulation of the acute-phase cytokine (IL-6, IL1 beta and TNF-alpha) gene expression in Kupffer cells and of chemokine gene expression in hepatocytes. MCRs are expressed not only in the brain, but also in liver cells and their gene expression in liver and brain tissue is upregulated during APR. Due to the presence of specific ligands in the serum, they may mediate metabolic changes and exert a protective effect on liver cells."],["dc.identifier.doi","10.1007/s00418-011-0899-7"],["dc.identifier.isi","000300326100002"],["dc.identifier.pmid","22183812"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7321"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27120"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Melanocortin receptors in rat liver cells: change of gene expression and intracellular localization during acute-phase response"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","285"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","18"],["dc.contributor.affiliation","Alwahsh, Salamah; \t\t \r\n\t\t Clinic for Gastroenterology and Endocrinology, University Medical Center, Georg-August-University Goettingen, Goettingen D-37075, Germany, salwahsh@exseed.ed.ac.uk\t\t \r\n\t\t MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK, salwahsh@exseed.ed.ac.uk"],["dc.contributor.affiliation","Dwyer, Benjamin; \t\t \r\n\t\t MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK, bdwyer@exseed.ed.ac.uk"],["dc.contributor.affiliation","Forbes, Shareen; \t\t \r\n\t\t Endocrinology Unit, University/BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, UK, Shareen.Forbes@ed.ac.uk"],["dc.contributor.affiliation","Van Thiel, David; \t\t \r\n\t\t Advanced Liver and Gastrointestinal Disease Center, Chicago, IL 60611, USA, dvanthiel@dr.com"],["dc.contributor.affiliation","Starkey Lewis, Philip; \t\t \r\n\t\t MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK, pstarkey@exseed.ed.ac.uk"],["dc.contributor.affiliation","Ramadori, Giuliano; \t\t \r\n\t\t Clinic for Gastroenterology and Endocrinology, University Medical Center, Georg-August-University Goettingen, Goettingen D-37075, Germany, gramado@med.uni-goettingen.de"],["dc.contributor.author","Alwahsh, Salamah Mohammad"],["dc.contributor.author","Dwyer, Benjamin J."],["dc.contributor.author","Forbes, Shareen"],["dc.contributor.author","van Thiel, David H."],["dc.contributor.author","Lewis, Philip J. Starkey"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:27:50Z"],["dc.date.available","2018-11-07T10:27:50Z"],["dc.date.issued","2017"],["dc.date.updated","2022-09-06T10:50:57Z"],["dc.description.abstract","The role of the liver and the endocrine pancreas in development of hyperinsulinemia in different types of obesity remains unclear. Sedentary rats (160 g) were fed a low-fat-diet (LFD, chow 13% kcal fat), high-fat-diet (HFD, 35% fat), or HFD+ 30% ethanol+ 30% fructose (HF-EFr, 22% fat). Overnight-fasted rats were culled after one, four or eight weeks. Pancreatic and hepatic mRNAs were isolated for subsequent RT-PCR analysis. After eight weeks, body weights increased three-fold in the LFD group, 2.8-fold in the HFD group, and 2.4-fold in the HF-EFr (p < 0.01). HF-EFr-fed rats had the greatest liver weights and consumed less food during Weeks 4-8 (p < 0.05). Hepatic-triglyceride content increased progressively in all groups. At Week 8, HOMA-IR values, fasting serum glucose, C-peptide, and triglycerides levels were significantly increased in LFD-fed rats compared to that at earlier time points. The greatest plasma levels of glucose, triglycerides and leptin were observed in the HF-EFr at Week 8. Gene expression of pancreatic-insulin was significantly greater in the HFD and HF-EFr groups versus the LFD. Nevertheless, insulin: C-peptide ratios and HOMA-IR values were substantially higher in HF-EFr. Hepatic gene-expression of insulin-receptor-substrate-1/2 was downregulated in the HF-EFr. The expression of phospho-ERK-1/2 and inflammatory-mediators were greatest in the HF-EFr-fed rats. Chronic intake of both LFD and HFD induced obesity, MetS, and intrahepatic-fat accumulation. The hyperinsulinemia is the strongest in rats with the lowest body weights, but having the highest liver weights. This accompanies the strongest increase of pancreatic insulin production and the maximal decrease of hepatic insulin signaling, which is possibly secondary to hepatic fat deposition, inflammation and other factors."],["dc.description.sponsorship","German Research Foundation (DFG); Gottingen University"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3390/ijms18020285"],["dc.identifier.isi","000395457700054"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14271"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43306"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Mdpi Ag"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Insulin Production and Resistance in Different Models of Diet-Induced Obesity and Metabolic Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S479"],["dc.bibliographiccitation.journal","Radiotherapy and Oncology"],["dc.bibliographiccitation.lastpage","S480"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Christiansen, H."],["dc.contributor.author","Thello, K."],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Hess, C. F."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T09:13:58Z"],["dc.date.available","2018-11-07T09:13:58Z"],["dc.date.issued","2006"],["dc.identifier.isi","000242719101490"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27292"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.publisher.place","Clare"],["dc.relation.conference","Conference of the Spanish-Portuguese-and -Latin-American-Association"],["dc.relation.eventlocation","Leipzig, GERMANY"],["dc.relation.issn","0167-8140"],["dc.title","Irradiation leads to sensitization of hepatocytes to TNF-alpha- mediated apoptosis by upregulation of IKB expression"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]