Raddatz, Dirk

[["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.firstpage","389"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Journal of Gastroenterology & Hepatology"],["dc.bibliographiccitation.lastpage","395"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Wietzke-Braun, Perdita"],["dc.contributor.author","Schindler, C."],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Braun, F."],["dc.contributor.author","Armbrust, T."],["dc.contributor.author","Nolte, W."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:49:51Z"],["dc.date.available","2018-11-07T10:49:51Z"],["dc.date.issued","2004"],["dc.description.abstract","Objective Patients with non-resectable liver metastases of colorectal cancer have poor prognosis and are mainly treated by palliative chemotherapy. Laser interstitial thereto-therapy is an innovative minimal invasive procedure for local tumour destruction within solid organs. The aim of the study was to investigate quality of life and outcome of ultrasound-guided laser interstitial thermotherapy (US-LITT) in patients with liver metastases of colorectal cancer. Methods In this prospective non-randomized study, 45 patients with liver metastases of colorectal cancer were palliatively treated by US-LITT. Patient survival was analysed by the Kaplan-Meier method and the quality of life by questionnaire C30 of the European Organisation for Research and Treatment of Cancer before, and 1 week, 1 month, and 6 months after initiation of US-LITT. Results Median survival after initiation of US-LITT was 8.5 +/- 0.7 months with a range of 1.5-18 months. Body weight was constant 1 month after US-LITT. In the multivariate analyses, quality-of-life symptoms and functioning scales did not deteriorate in patients alive at 6 months after initiation of US-LITT. Univariate analyses outlined a significant increase of the pain subscale before and at 1 week after US-LITT. Conclusions This study first describes the quality of life in patients with liver metastases of colorectal cancer treated by US-LITT. Potential benefits of the minimal invasive procedure could be prolonged survival time by preserved quality of life, but this first impression needs to be verified in a comparative study."],["dc.identifier.doi","10.1097/00042737-200404000-00004"],["dc.identifier.isi","000220655900004"],["dc.identifier.pmid","15028971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48527"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0954-691X"],["dc.title","Quality of life and outcome of ultrasound-guided laser interstitial thereto-therapy for non-resectable liver metastases of colorectal cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","162"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Radiation Research"],["dc.bibliographiccitation.lastpage","169"],["dc.bibliographiccitation.volume","169"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Rave-Fraenk, Mararet"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:18:56Z"],["dc.date.available","2018-11-07T11:18:56Z"],["dc.date.issued","2008"],["dc.description.abstract","The aim of the study was to analyze the effect of a single irradiation on chemokine gene expression in the rat liver and in isolated rat hepatocytes. RNA extracted from livers and from hepatocytes within the first 48 h after irradiation was analyzed by real-time PCR and the Northern blot assay. The chemokine concentrations in the serum of irradiated rats were measured quantitatively by ELISA. A significant radiation-induced increase of CINC1, IP10, MCP1, MIP3 alpha, MIP3 beta, MIG and ITAC gene expression could be detected at the RNA level in the liver. CINC1, MCP1 and IP10 serum levels were significantly increased. In rat hepatocytes in vitro, only MIP3a showed a radiation-induced increase in expression, while CINC1, IP10, MIP3 beta, MIG, MIP1 alpha, ITAC and SDF1 RNA levels were significantly down-regulated. However, incubation of irradiated hepatocytes in vitro with either TNF-alpha, IL1 beta, or IL6 plus TNF-alpha led to up-regulation of MCP1, IP10 and MCP1 or CINC1 and MIP3 beta, respectively. Irradiation of the liver induces up-regulation of the genes of the main proinflammatory chemokines, probably through the action of locally synthesized proinflammatory cytokines. The reason for the lack of liver inflammation in this model has still to be clarified. (C) 2008 by Radiation Research Society."],["dc.identifier.doi","10.1667/RR1006.1"],["dc.identifier.isi","000252633000004"],["dc.identifier.pmid","18220462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55150"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Radiation Research Soc"],["dc.relation.issn","0033-7587"],["dc.title","Effect of radiation on gene expression of rat liver chemokines: In vivo and in vitro studies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","166"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.lastpage","177"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:14:00Z"],["dc.date.available","2018-11-07T09:14:00Z"],["dc.date.issued","2012"],["dc.description.abstract","Chronic inflammatory bowel diseases can be successfully treated with antibodies against the acute phase mediator TNF-alpha. The process of activation and of extravasation of inflammatory cells from the blood into the 'stressed' tissue site is controlled by cytokines and chemokines, which attract leukocytes and by adhesion molecules, which mediate their attachment and transmigration toward the affected cell(s). The changes in the gene expression of adhesion molecules taking place in those cells before attachment have been less investigated. Changes of PECAM-1, ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1) gene expression were studied in phytohaemagglutinin (PHA)- and lipolysaccharide (LPS)-treated human peripheral blood leukocytes (PBLs), granulocytes and the human monocyte cell line U-937. Cells were treated either with PHA or with LPS in the presence or absence of infliximab and incubated with TNF-alpha, IFN-gamma and/or transforming growth factor beta (TGF-beta) and treated as above. Activation of PBLs by PHA or LPS treatment triggered a sharp upregulation of ICAM-1, VCAM-1 gene expression and a time-dependent downregulation of PECAM-1 gene expression reaching a minimum 4 h from start of the experiment. The anti-TNF-alpha antibody infliximab, by neutralizing TNF-alpha and IFN-gamma production, completely reversed PECAM-1 mRNA downregulation and ICAM-1 and VCAM-1 upregulation. Immunostaining of PBLs cytospins with antibodies against PECAM-1 and ICAM-1 confirmed RT-PCR and western blot results. PBLs IFN-gamma or TNF-alpha treatment downregulated PECAM-1 in parallel with the upregulation of ICAM-1 and VCAM-1 gene expression, whereas TGF-beta upregulated PECAM-1- and downregulated ICAM-1 and VCAM-1 gene expression counteracting the effect of TNF-alpha or IFN-gamma. Similar results were obtained in human U937 cells and in granulocyte cultures by TNF-alpha or IFN-gamma treatment. Taken together, these results suggest that infliximab, blocking TNF-alpha and IFN-gamma production, exerts its anti-inflammatory effect through inhibiting downregulation of PECAM-1 gene expression and upregulation of ICAM-1 and VCAM-1 expression in leukocytes of the peripheral blood. These results also suggest that TGF-beta may thus be of therapeutic importance as an anti-inflammatory agent. Laboratory Investigation (2012) 92, 166-177; doi:10.1038/labinvest.2011.160; published online 31 October 2011"],["dc.identifier.doi","10.1038/labinvest.2011.160"],["dc.identifier.isi","000299799700001"],["dc.identifier.pmid","22042082"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27298"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0023-6837"],["dc.title","The anti-TNF-alpha antibody infliximab indirectly regulates PECAM-1 gene expression in two models of in vitro blood cell activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","51"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Zeitschrift für Gastroenterologie"],["dc.bibliographiccitation.lastpage","62"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:07:46Z"],["dc.date.available","2018-11-07T11:07:46Z"],["dc.date.issued","2007"],["dc.description.abstract","The liver plays a unique role in controlling carbohydrate metabolism by maintaining glucose concentrations in a normal range. This is achieved by a tightly regulated system of enzymes and kinases regulating either glucose breakdown or synthesis in hepatocytes. This process is under the control of glucoregulatory mediators among which insulin plays a key role. In type 2 diabetes, as well as in liver disease, alterations in hepatic glucose metabolism like an increased post-absorptive glucose production together with diminished glucose uptake following carbohydrate ingestion occur, implying insulin resistance as a central pathological principle. Knowledge of the processes involved in maintaining glucose homeostasis as well as insulin resistance is a prerequisite to develop new therapeutic approaches in diabetes as well as in liver disease. In the recent years, genetically-altered mouse models that have helped to identify enzymes, transcription factors and mediators that are essential for maintaining glucose homeostasis in the liver and provide a valuable tool to study carbohydrate metabolism in liver disease. In this current review, genetically manipulated animals either overexpressing or lacking key gluconeogenic enzymes, hepatic transcription factors, IGF-1, hepatic insulin receptors, adipokines and hepatitis C core antigen will be discussed in the context of human disease."],["dc.identifier.doi","10.1055/s-2006-927394"],["dc.identifier.isi","000244109100007"],["dc.identifier.pmid","17236121"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52650"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0044-2771"],["dc.title","Carbohydrate metabolism and the liver: Actual aspects from physiology and disease"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2273"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The American Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","96"],["dc.contributor.author","Schworer, H."],["dc.contributor.author","Bohn, M."],["dc.contributor.author","Waezsada, S. Y."],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:53:17Z"],["dc.date.available","2018-11-07T08:53:17Z"],["dc.date.issued","2001"],["dc.identifier.isi","000169839600062"],["dc.identifier.pmid","11467676"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22373"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0002-9270"],["dc.title","Successful treatment of megacolon associated with colitis with a nitric oxide synthase inhibitor"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e104220"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Alwahsh, Salamah Mohammad"],["dc.contributor.author","Xu, Min"],["dc.contributor.author","Schultze, Frank Christian"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:36:45Z"],["dc.date.available","2018-11-07T09:36:45Z"],["dc.date.issued","2014"],["dc.description.abstract","Although both alcohol and fructose are particularly steatogenic, their long-term effect in the development of a metabolic syndrome has not been studied in vivo. Consumption of fructose generally leads to obesity, whereas ethanol can induce liver damage in the absence of overweight. Here, Sprague-Dawley rats were fed ad libitum for 28 days on five diets: chow (control), liquid Lieber-DeCarli (LDC) diet, LDC +30%J of ethanol (L-Et) or fructose (L-Fr), and LDC combined with 30%J ethanol and 30%J fructose (L-EF). Body weight (BW) and liver weight (LW) were measured. Blood and liver samples were harvested and subjected to biochemical tests, histopathological examinations, and RT-PCR. Alcohol-containing diets substantially reduced the food intake and BW (<= 3rd week), whereas fructose-fed animals had higher LW than controls ( P < 0.05). Additionally, leukocytes, plasma AST and leptin levels were the highest in the fructose-administered rats. Compared to the chow and LDC diets, the L-EF diet significantly elevated blood glucose, insulin, and total-cholesterol levels (also vs. the L-Et group). The albumin and Quick-test levels were the lowest, whereas ALT activity was the highest in the L-EF group. Moreover, the L-EF diet aggravated plasma triglyceride and reduced HDL-cholesterol levels more than 2.7-fold compared to the sum of the effects of the L-Et and L-Fr diets. The decreased hepatic insulin clearance in the L-EF group vs. control and LDC groups was reflected by a significantly decreased C-peptide: insulin ratio. All diets except the control caused hepatosteatosis, as evidenced by Nile red and H&E staining. Hepatic transcription of insulin receptor substrate-1/2 was mainly suppressed by the L-Fr and L-EF diets. The L-EF diet did not enhance the mitochondrial beta-oxidation of fatty acids (Cpt1 alpha and Ppar-alpha expressions) compared to the L-Et or L-Fr diet. Together, our data provide evidence for the coaction of ethanol and fructose with a high-fat-diet on dyslipidemia and insulin resistance-accompanied liver damage."],["dc.description.sponsorship","Open Access Publikationsfonds 2014"],["dc.identifier.doi","10.1371/journal.pone.0104220"],["dc.identifier.isi","000339993900050"],["dc.identifier.pmid","25101998"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10788"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32686"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Combination of Alcohol and Fructose Exacerbates Metabolic Imbalance in Terms of Hepatic Damage, Dyslipidemia, and Insulin Resistance in Rats"],["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","461"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Experimental and Clinical Endocrinology & Diabetes"],["dc.bibliographiccitation.lastpage","467"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Nolte, W."],["dc.contributor.author","Rossbach, C."],["dc.contributor.author","Leonhardt, U."],["dc.contributor.author","Buchwald, A."],["dc.contributor.author","Scholz, Karl Heinrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:12:26Z"],["dc.date.available","2018-11-07T11:12:26Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Diabetes in liver cirrhosis is associated with a blunted insulin response, which might be explained by an impaired release of the incretin hormone glucagon-like peptide 1 (GLP-1) into the portal circulation. Aims: To investigate basal and stimulated portal venous and peripheral GLP-1 concentrations in non-diabetic (ND) and diabetic (D) patients with liver cirrhosis undergoing transjugular intrahepatic portosystemic stent shunt (TIPSS) implantation. Patients and Methods: After elective TIPSS portalvenous and peripheral probes were drawn from 10 ND and 10 D patients with stable liver disease during an oral metabolic test and plasma glucose, immunoreactive GLP-1, insulin and C-peptide were measured. Results: The study meal led to a significant rise in portal GLP-1 levels in ND and D. Basal and stimulated portal GLP-1 concentrations were not significantly different between ND and D. Peripheral GLP-1 did not differ significantly from portal venous levels. Insulin response in ND was more pronounced in the portal blood than in the periphery and was absent in D. Conclusion: TIPSS allows a direct evaluation of hormonal changes in the portal circulation during an oral metabolic tolerance test. A disturbed GLP-1 secretion does not play a role in blunting the insulin response observed in patients with hepatogenous diabetes."],["dc.identifier.doi","10.1055/s-2007-1004596"],["dc.identifier.isi","000259927300002"],["dc.identifier.pmid","18770489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53665"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Johann Ambrosius Barth Verlag Medizinverlage Heidelberg Gmbh"],["dc.relation.issn","0947-7349"],["dc.title","Measuring the effect of a study meal on portal concentrations of glucagon-like peptide 1 (GLP-1) in non diabetic and diabetic patients with liver cirrhosis: Transjugular intrahepatic portosystemic stent shunt (TIPSS) as a new method for metabolic measurements"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","268"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Experimental and Clinical Endocrinology & Diabetes"],["dc.bibliographiccitation.lastpage","274"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Rossbach, C."],["dc.contributor.author","Buchwald, A."],["dc.contributor.author","Scholz, Karl Heinrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Nolte, W."],["dc.date.accessioned","2018-11-07T11:03:20Z"],["dc.date.available","2018-11-07T11:03:20Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: Hyperglucagonemia has been described to be associated with insulin resistance in patients with liver cirrhosis. Portosystemic shunts may be involved in the etiology of hyperglucagonemia. To test this hypothesis we investigated fasting peripheral plasma glucagon levels before and after portal decompression by transjugular intrahepatic portosystemic shunting (TIPS). Methods: Glucagon, insulin, plasma glucose, HbA1c, and C-peptide were determined in peripheral venous samples from 21 non-diabetic (ND)- and 15 diabetic patients (1); 3 treated with insulin, 3 with sulfonylurea, 9 with diet alone) with liver cirrhosis, showing comparable clinical features (gender, age, BMI, creatinine, Child-Pugh-score, complications, and etiology of liver cirrhosis) before, 3 and 9 months after elective TIPS implantation. insulin resistance was calculated as R-HOMA according to the homeostasis model assessment (HOMA). Results: Glucagon levels before TIPS were elevated in patients with diabetes compared to patients without diabetes (1): 145.4 &PLUSMN; 52.1 pg/ml vs. ND: 97.3 &PLUSMN; 49.8 pg/ml; p = 0.057). 3 and 9 months after TIPS implantation glucagon levels increased significantly in ND (188.9 &PLUSMN; 80.3 pg/ml and 187.2 &PLUSMN; 87.6 pg/ml) but not in D (169.6 &PLUSMN; 62.4 pg/ml and 171.9 &PLUSMN; 58.4 pg/ml). While plasma glucose, HbA1c, and C-peptide were significantly higher in D than in ND, they did not change significantly 3 and 9 months after TIPS implantation. Insulin was increased in D before TIPS (1): 31.6 &PLUSMN; 15.9 mU/l vs. ND: 14.8 &PLUSMN; 7.1 mU/l; p = 0.0001). 3 and 9 months after TIPS insulin significantly increased in ND (26.6 &PLUSMN; 14.7 mU/l and 23.2 &PLUSMN; 10.9 mU/l vs. 14.8 &PLUSMN; 7.1 mU/l before TIPS) but not in D. In ND R-HOMA also increased from 3.5 &PLUSMN; 2 mU x mmol/l(2) to 5.7 &PLUSMN; 3.3 mU x mmol/l(2) after 3 and 5.4 &PLUSMN; 2.6 mU x mmol/l(2) after 9 months. BMI, liver and kidney function did not change with time. Conclusion: In nondiabetic cirrhotic patients TIPS implantation is followed by an increase of glucagon. However, this does not result in a worsening of glycemic control, probably because of a simultaneous increase of insulin."],["dc.identifier.doi","10.1055/s-2005-837546"],["dc.identifier.isi","000229605500006"],["dc.identifier.pmid","15926112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51593"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Johann Ambrosius Barth Verlag Medizinverlage Heidelberg Gmbh"],["dc.relation.issn","0947-7349"],["dc.title","Fasting hyperglucagonemia in patients with transjugular intrahepatic portosystemic shunts (TIPS)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alimentary Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","61"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Middel, Peter"],["dc.contributor.author","Bockemühl, Miriam"],["dc.contributor.author","Benöhr, Peter"],["dc.contributor.author","Wissmann, C."],["dc.contributor.author","Schworer, H."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:51:53Z"],["dc.date.available","2018-11-07T10:51:53Z"],["dc.date.issued","2004"],["dc.description.abstract","Background: Glucocorticoids (GC) play a major role in the attenuation of inflammation. Glucocorticoid receptor (GR) expression is an important determinant of steroid sensitivity. Aims: To investigate whether GR mRNA expression is altered in inflammatory bowel disease, and whether GR mRNA expression correlates with disease activity and may predict response to GC therapy. Methods: Mucosal biopsies were taken from 33 patients with ulcerative colitis, 21 with Crohn's disease and 11 controls. Peripheral blood mononuclear cells were isolated from 24 ulcerative colitis and 18 Crohn's disease patients and 11 controls. GR mRNA was measured by quantitative reverse transcriptase polymerase chain reaction (RT-PCR), and correlated to endoscopic findings, clinical activity and outcome of GC therapy. In a subset of subjects GR localisation was shown by immunohistochemistry. Results: In patients with inflammatory bowel disease GR expression was not different from controls. However, GR was decreased in biopsies from ulcerative colitis patients with impaired GC response. The inhibitory subtype GRbeta was expressed 100-1000 times lower than GRalpha. GR immunoreactivity was identified in immune and epithelial cells except for colonic crypts. Conclusion: In inflammatory bowel disease systemic and mucosal GR mRNA expression is not altered. However, in ulcerative colitis patients, low mucosal GR expression may predict the outcome of GC therapy. The low expression of GRbeta challenges its role in steroid refractoriness in inflammatory bowel disease."],["dc.identifier.doi","10.1046/j.1365-2036.2003.01802.x"],["dc.identifier.isi","000187549200004"],["dc.identifier.pmid","14687166"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48987"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0269-2813"],["dc.title","Glucocorticoid receptor expression in inflammatory bowel disease: evidence for a mucosal down-regulation in steroid-unresponsive ulcerative colitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]