Skip to main content
Erschienen in: Inflammation 1/2013

01.02.2013

Curcumin Protects Against Concanavalin A-Induced Hepatitis in Mice Through Inhibiting the Cytoplasmic Translocation and Expression of High Mobility Group Box 1

verfasst von: Chuan-tao Tu, Qun-yan Yao, Bei-li Xu, Shun-cai Zhang

Erschienen in: Inflammation | Ausgabe 1/2013

Einloggen, um Zugang zu erhalten

Abstract

The aims of this study were to examine the anti-inflammatory effect of curcumin on concanavalin A (ConA) induced hepatitis in mice, and to elucidate its underlying molecular mechanisms. Mice received curcumin by gavage before ConA intravenous administration. The results showed that curcumin pretreatment attenuated ConA-induced hepatitis. Enzyme linked immunosorbent assay (ELISA) results showed that serum levels of high mobility group box 1 (HMGB1) increased at 4 h and reached its peak value at 12 h after challenge with ConA; but this increase was significantly inhibited by curcumin. Furthermore, curcumin significantly decreased the HMGB1 translocation from nucleus to cytoplasm of hepatocytes in ConA-induced mice. The levels of HMGB1 mRNA and protein expression in the liver were also significantly lowered in curcumin-treated mice. In addition, curcumin inhibited intrahepatic expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 protein. In conclusion, the results indicated that curcumin protected against ConA-induced hepatitis in mice; and the beneficial effects may be partly through inhibition of HMGB1 translocation in hepatocytes, release into the plasma and expression in livers.
Literatur
1.
Zurück zum Zitat Bozza, M., J.L. Bliss, R. Maylor, J. Erickson, L. Donnelly, P. Bouchard, A.J. Dorner, and W.L. Trepicchio. 1999. Interleukin-11 reduces T-cell-dependent experimental liver injury in mice. Hepatology 30: 1441–1447.PubMedCrossRef Bozza, M., J.L. Bliss, R. Maylor, J. Erickson, L. Donnelly, P. Bouchard, A.J. Dorner, and W.L. Trepicchio. 1999. Interleukin-11 reduces T-cell-dependent experimental liver injury in mice. Hepatology 30: 1441–1447.PubMedCrossRef
2.
Zurück zum Zitat Nunnari, G., and M.J. Schnell. 2011. MicroRNA-122: A therapeutic target for hepatitis C virus (HCV) infection. Frontiers in Bioscience (Schol Ed) 3: 1032–1037.CrossRef Nunnari, G., and M.J. Schnell. 2011. MicroRNA-122: A therapeutic target for hepatitis C virus (HCV) infection. Frontiers in Bioscience (Schol Ed) 3: 1032–1037.CrossRef
3.
Zurück zum Zitat Lupberger, J., M.B. Zeisel, F. Xiao, C. Thumann, I. Fofana, L. Zona, C. Davis, C.J. Mee, M. Turek, S. Gorke, C. Royer, B. Fischer, M.N. Zahid, D. Lavillette, J. Fresquet, F.L. Cosset, S.M. Rothenberg, T. Pietschmann, A.H. Patel, P. Pessaux, M. Doffoël, W. Raffelsberger, O. Poch, J.A. McKeating, L. Brino, and T.F. Baumert. 2011. EGFR and EphA2 are host factors for hepatitis C virus entry and possible targets for antiviral therapy. Nature Medicine 17: 589–595.PubMedCrossRef Lupberger, J., M.B. Zeisel, F. Xiao, C. Thumann, I. Fofana, L. Zona, C. Davis, C.J. Mee, M. Turek, S. Gorke, C. Royer, B. Fischer, M.N. Zahid, D. Lavillette, J. Fresquet, F.L. Cosset, S.M. Rothenberg, T. Pietschmann, A.H. Patel, P. Pessaux, M. Doffoël, W. Raffelsberger, O. Poch, J.A. McKeating, L. Brino, and T.F. Baumert. 2011. EGFR and EphA2 are host factors for hepatitis C virus entry and possible targets for antiviral therapy. Nature Medicine 17: 589–595.PubMedCrossRef
4.
Zurück zum Zitat Verma, S., and P.J. Thuluvath. 2007. Complementary and alternative medicine in hepatology: Review of the evidence of efficacy. Clinical Gastroenterology Hepatology 5: 408–416.CrossRef Verma, S., and P.J. Thuluvath. 2007. Complementary and alternative medicine in hepatology: Review of the evidence of efficacy. Clinical Gastroenterology Hepatology 5: 408–416.CrossRef
5.
Zurück zum Zitat Hong, F., B. Jaruga, W.H. Kim, S. Radaeva, O.N. El-Assal, Z. Tian, V.A. Nguyen, and B. Gao. 2002. Opposing roles of STAT1 and STAT3 in T cell-mediated hepatitis: Regulation by SOCS. The Journal of Clinical Investigation 110: 1503–1513.PubMed Hong, F., B. Jaruga, W.H. Kim, S. Radaeva, O.N. El-Assal, Z. Tian, V.A. Nguyen, and B. Gao. 2002. Opposing roles of STAT1 and STAT3 in T cell-mediated hepatitis: Regulation by SOCS. The Journal of Clinical Investigation 110: 1503–1513.PubMed
6.
Zurück zum Zitat Tu, C.T., B. Han, H.C. Liu, and S.C. Zhang. 2011. Curcumin protects mice against concanavalin A-induced hepatitis by inhibiting intrahepatic intercellular adhesion molecule-1 (ICAM-1) and CXCL10 expression. Molecular and Cellular Biochemistry 358: 53–60.PubMedCrossRef Tu, C.T., B. Han, H.C. Liu, and S.C. Zhang. 2011. Curcumin protects mice against concanavalin A-induced hepatitis by inhibiting intrahepatic intercellular adhesion molecule-1 (ICAM-1) and CXCL10 expression. Molecular and Cellular Biochemistry 358: 53–60.PubMedCrossRef
7.
Zurück zum Zitat Tiegs, G., J. Hentschel, and A. Wendel. 1992. A T cell-dependent experimental liver injury in mice inducible by concanavalin A. The Journal of Clinical Investigation 90: 196–203.PubMedCrossRef Tiegs, G., J. Hentschel, and A. Wendel. 1992. A T cell-dependent experimental liver injury in mice inducible by concanavalin A. The Journal of Clinical Investigation 90: 196–203.PubMedCrossRef
8.
Zurück zum Zitat Wang, H., O. Bloom, M. Zhang, J.M. Vishnubhakat, M. Ombrellino, J. Che, A. Frazier, H. Yang, S. Ivanova, L. Borovikova, K.R. Manogue, E. Faist, E. Abraham, J. Andersson, U. Andersson, P.E. Molina, N.N. Abumrad, A. Sama, and K.J. Tracey. 1999. HMG-1 as a late mediator of endotoxin lethality in mice. Science 285: 248–251.PubMedCrossRef Wang, H., O. Bloom, M. Zhang, J.M. Vishnubhakat, M. Ombrellino, J. Che, A. Frazier, H. Yang, S. Ivanova, L. Borovikova, K.R. Manogue, E. Faist, E. Abraham, J. Andersson, U. Andersson, P.E. Molina, N.N. Abumrad, A. Sama, and K.J. Tracey. 1999. HMG-1 as a late mediator of endotoxin lethality in mice. Science 285: 248–251.PubMedCrossRef
9.
Zurück zum Zitat Lotze, M.T., and K.J. Tracey. 2005. High-mobility group box 1 protein (HMGB1): Nuclear weapon in the immune arsenal. Nature Review Immunology 5: 331–542.CrossRef Lotze, M.T., and K.J. Tracey. 2005. High-mobility group box 1 protein (HMGB1): Nuclear weapon in the immune arsenal. Nature Review Immunology 5: 331–542.CrossRef
10.
Zurück zum Zitat Erlandsson Harris, H., and U. Andersson. 2004. Mini-review: The nuclear protein HMGB1 as a proinflammatory mediator. European Journal of Immunology 34: 1503–1512.PubMedCrossRef Erlandsson Harris, H., and U. Andersson. 2004. Mini-review: The nuclear protein HMGB1 as a proinflammatory mediator. European Journal of Immunology 34: 1503–1512.PubMedCrossRef
11.
Zurück zum Zitat Sims, G.P., D.C. Rowe, S.T. Rietdijk, R. Herbst, and A.J. Coyle. 2010. HMGB1 and RAGE in inflammation and cancer. Annual Review Immunology 28: 367–388.CrossRef Sims, G.P., D.C. Rowe, S.T. Rietdijk, R. Herbst, and A.J. Coyle. 2010. HMGB1 and RAGE in inflammation and cancer. Annual Review Immunology 28: 367–388.CrossRef
12.
Zurück zum Zitat Andersson, U., and K.J. Tracey. 2011. HMGB1 is a therapeutic target for sterile inflammation and infection. Annual Review Immunology 29: 139–162.CrossRef Andersson, U., and K.J. Tracey. 2011. HMGB1 is a therapeutic target for sterile inflammation and infection. Annual Review Immunology 29: 139–162.CrossRef
13.
Zurück zum Zitat Sass, G., S. Heinlein, A. Agli, R. Bang, J. Schümann, and G. Tiegs. 2002. Cytokine expression in three mouse models of experimental hepatitis. Cytokine 19: 115–120.PubMedCrossRef Sass, G., S. Heinlein, A. Agli, R. Bang, J. Schümann, and G. Tiegs. 2002. Cytokine expression in three mouse models of experimental hepatitis. Cytokine 19: 115–120.PubMedCrossRef
14.
Zurück zum Zitat Zhou, R.R., S.S. Zhao, M.X. Zou, P. Zhang, B.X. Zhang, X.H. Dai, N. Li, H.B. Liu, H. Wang, and X.G. Fan. 2011. HMGB1 cytoplasmic translocation in patients with acute liver failure. BMC Gastroenterology 11: 21.PubMedCrossRef Zhou, R.R., S.S. Zhao, M.X. Zou, P. Zhang, B.X. Zhang, X.H. Dai, N. Li, H.B. Liu, H. Wang, and X.G. Fan. 2011. HMGB1 cytoplasmic translocation in patients with acute liver failure. BMC Gastroenterology 11: 21.PubMedCrossRef
15.
Zurück zum Zitat Gong, Q., H. Zhang, J.H. Li, L.H. Duan, S. Zhong, X.L. Kong, F. Zheng, Z. Tan, P. Xiong, G. Chen, M. Fang, and F.L. Gong. 2010. High-mobility group box 1 exacerbates concanavalin A-induced hepatic injury in mice. Journal of Molecular Medicine 88: 1289–1298.PubMedCrossRef Gong, Q., H. Zhang, J.H. Li, L.H. Duan, S. Zhong, X.L. Kong, F. Zheng, Z. Tan, P. Xiong, G. Chen, M. Fang, and F.L. Gong. 2010. High-mobility group box 1 exacerbates concanavalin A-induced hepatic injury in mice. Journal of Molecular Medicine 88: 1289–1298.PubMedCrossRef
16.
Zurück zum Zitat Takano, K., M. Shinoda, M. Tanabe, T. Miyasho, S. Yamada, S. Ono, Y. Masugi, K. Suda, K. Fukunaga, T. Hayashida, T. Hibi, H. Obara, H. Takeuchi, S. Kawachi, K. Kawasako, M. Okamoto, H. Yokota, I. Maruyama, and Y. Kitagawa. 2010. Protective effect of high-mobility group box 1 blockade on acute liver failure in rats. Shock 34: 573–579.PubMedCrossRef Takano, K., M. Shinoda, M. Tanabe, T. Miyasho, S. Yamada, S. Ono, Y. Masugi, K. Suda, K. Fukunaga, T. Hayashida, T. Hibi, H. Obara, H. Takeuchi, S. Kawachi, K. Kawasako, M. Okamoto, H. Yokota, I. Maruyama, and Y. Kitagawa. 2010. Protective effect of high-mobility group box 1 blockade on acute liver failure in rats. Shock 34: 573–579.PubMedCrossRef
17.
Zurück zum Zitat Tsung, A., R. Sahai, H. Tanaka, A. Nakao, M.P. Fink, M.T. Lotze, H. Yang, J. Li, K.J. Tracey, D.A. Geller, and T.R. Billiar. 2005. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia–reperfusion. Journal of Experimental Medicine 201: 1135–1143.PubMedCrossRef Tsung, A., R. Sahai, H. Tanaka, A. Nakao, M.P. Fink, M.T. Lotze, H. Yang, J. Li, K.J. Tracey, D.A. Geller, and T.R. Billiar. 2005. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia–reperfusion. Journal of Experimental Medicine 201: 1135–1143.PubMedCrossRef
18.
Zurück zum Zitat Tsung, A., J.R. Klune, X. Zhang, G. Jeyabalan, Z. Cao, X. Peng, D.B. Stolz, D.A. Geller, M.R. Rosengart, and T.R. Billiar. 2007. HMGB1 release induced by liver ischemia involves Toll-like receptor 4 dependent reactive oxygen species production and calcium-mediated signaling. Journal of Experimental Medicine 204: 2913–2923.PubMedCrossRef Tsung, A., J.R. Klune, X. Zhang, G. Jeyabalan, Z. Cao, X. Peng, D.B. Stolz, D.A. Geller, M.R. Rosengart, and T.R. Billiar. 2007. HMGB1 release induced by liver ischemia involves Toll-like receptor 4 dependent reactive oxygen species production and calcium-mediated signaling. Journal of Experimental Medicine 204: 2913–2923.PubMedCrossRef
19.
Zurück zum Zitat Corson, T.W., and C.M. Crews. 2007. Molecular understanding and modern application of traditional medicines: Triumphs and trials. Cell 130: 769–774.PubMedCrossRef Corson, T.W., and C.M. Crews. 2007. Molecular understanding and modern application of traditional medicines: Triumphs and trials. Cell 130: 769–774.PubMedCrossRef
20.
Zurück zum Zitat Aggarwal, B.B., and K.B. Harikumar. 2009. Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. International Journal of Biochemical Cell Biology 41: 40–59.CrossRef Aggarwal, B.B., and K.B. Harikumar. 2009. Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. International Journal of Biochemical Cell Biology 41: 40–59.CrossRef
21.
Zurück zum Zitat Tu, C.T., B. Han, Q.Y. Yao, Y.A. Zhang, H.C. Liu, and S.C. Zhang. 2012. Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression. International Immunopharmacology 12: 151–157.PubMedCrossRef Tu, C.T., B. Han, Q.Y. Yao, Y.A. Zhang, H.C. Liu, and S.C. Zhang. 2012. Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression. International Immunopharmacology 12: 151–157.PubMedCrossRef
22.
Zurück zum Zitat Tang, D., R. Kang, H.J. Zeh 3rd, and M.T. Lotze. 2011. High-mobility group box 1, oxidative stress, and disease. Antioxidants & Redox Signaling 14: 1315–1335.CrossRef Tang, D., R. Kang, H.J. Zeh 3rd, and M.T. Lotze. 2011. High-mobility group box 1, oxidative stress, and disease. Antioxidants & Redox Signaling 14: 1315–1335.CrossRef
23.
Zurück zum Zitat Kim, D.C., W. Lee, and J.S. Bae. 2011. Vascular anti-inflammatory effects of curcumin on HMGB1-mediated responses in vitro. Inflammation Research 60: 1161–1168.PubMedCrossRef Kim, D.C., W. Lee, and J.S. Bae. 2011. Vascular anti-inflammatory effects of curcumin on HMGB1-mediated responses in vitro. Inflammation Research 60: 1161–1168.PubMedCrossRef
24.
Zurück zum Zitat Liu, A., O. Dirsch, H. Fang, W. Dong, H. Jin, H. Huang, J. Sun, and U. Dahmen. 2011. HMGB1 translocation and expression is caused by warm ischemia reperfusion injury, but not by partial hepatectomy in rats. Experimental and Molecular Pathology 91: 502–508.PubMedCrossRef Liu, A., O. Dirsch, H. Fang, W. Dong, H. Jin, H. Huang, J. Sun, and U. Dahmen. 2011. HMGB1 translocation and expression is caused by warm ischemia reperfusion injury, but not by partial hepatectomy in rats. Experimental and Molecular Pathology 91: 502–508.PubMedCrossRef
25.
Zurück zum Zitat Livak, K.J., and T.D. Schmittgen. 2001. Analysis of relative gene expression data using real-time quantitative PCR and the 2(−Delta Delta C(T)) Method. Methods 25: 402–408.PubMedCrossRef Livak, K.J., and T.D. Schmittgen. 2001. Analysis of relative gene expression data using real-time quantitative PCR and the 2(−Delta Delta C(T)) Method. Methods 25: 402–408.PubMedCrossRef
26.
Zurück zum Zitat Ghosh, N., R. Ghosh, V. Mandal, and S.C. Mandal. 2011. Recent advances in herbal medicine for treatment of liver diseases. Pharmaceutical Biology 49: 970–988.PubMedCrossRef Ghosh, N., R. Ghosh, V. Mandal, and S.C. Mandal. 2011. Recent advances in herbal medicine for treatment of liver diseases. Pharmaceutical Biology 49: 970–988.PubMedCrossRef
27.
Zurück zum Zitat Lubbad, A., M.A. Oriowo, and I. Khan. 2009. Curcumin attenuates inflammation through inhibition of TLR-4 receptor in experimental colitis. Molecular and Cellular Biochemistry 322: 127–135.PubMedCrossRef Lubbad, A., M.A. Oriowo, and I. Khan. 2009. Curcumin attenuates inflammation through inhibition of TLR-4 receptor in experimental colitis. Molecular and Cellular Biochemistry 322: 127–135.PubMedCrossRef
28.
Zurück zum Zitat Louis, H., O. Le Moine, M.O. Peny, E. Quertinmont, D. Fokan, M. Goldman, and J. Devière. 1997. Production and role of interleukin-10 in concanavalin A-induced hepatitis in mice. Hepatology 25: 1382–1389.PubMedCrossRef Louis, H., O. Le Moine, M.O. Peny, E. Quertinmont, D. Fokan, M. Goldman, and J. Devière. 1997. Production and role of interleukin-10 in concanavalin A-induced hepatitis in mice. Hepatology 25: 1382–1389.PubMedCrossRef
29.
Zurück zum Zitat Cardinal, J., P. Pan, R. Dhupar, M. Ross, A. Nakao, M. Lotze, T. Billiar, D. Geller, and A. Tsung. 2009. Cisplatin prevents high mobility group box 1 release and is protective in a murine model of hepatic ischemia/reperfusion injury. Hepatology 50: 565–574.PubMedCrossRef Cardinal, J., P. Pan, R. Dhupar, M. Ross, A. Nakao, M. Lotze, T. Billiar, D. Geller, and A. Tsung. 2009. Cisplatin prevents high mobility group box 1 release and is protective in a murine model of hepatic ischemia/reperfusion injury. Hepatology 50: 565–574.PubMedCrossRef
30.
Zurück zum Zitat Ogiku, M., H. Kono, M. Hara, M. Tsuchiya, and H. Fujii. 2011. Glycyrrhizin prevents liver injury by inhibition of high-mobility group box 1 production by Kupffer cells after ischemia-reperfusion in rats. Journal Pharmacology Experimental Therapeutics 339: 93–98.CrossRef Ogiku, M., H. Kono, M. Hara, M. Tsuchiya, and H. Fujii. 2011. Glycyrrhizin prevents liver injury by inhibition of high-mobility group box 1 production by Kupffer cells after ischemia-reperfusion in rats. Journal Pharmacology Experimental Therapeutics 339: 93–98.CrossRef
31.
Zurück zum Zitat Bonaldi, T., F. Talamo, P. Scaffidi, D. Ferrera, A. Porto, A. Bachi, A. Rubartelli, A. Agresti, and M.E. Bianchi. 2003. Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion. The EMBO Journal 22: 5551–5560.PubMedCrossRef Bonaldi, T., F. Talamo, P. Scaffidi, D. Ferrera, A. Porto, A. Bachi, A. Rubartelli, A. Agresti, and M.E. Bianchi. 2003. Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion. The EMBO Journal 22: 5551–5560.PubMedCrossRef
32.
Zurück zum Zitat Tang, D., R. Kang, K.M. Livesey, C.W. Cheh, A. Farkas, P. Loughran, G. Hoppe, M.E. Bianchi, K.J. Tracey, H.J. Zeh III, and M.T. Lotze. 2010. Endogenous HMGB1 regulates autophagy. The Journal of Cell Biology 190: 881–892.PubMedCrossRef Tang, D., R. Kang, K.M. Livesey, C.W. Cheh, A. Farkas, P. Loughran, G. Hoppe, M.E. Bianchi, K.J. Tracey, H.J. Zeh III, and M.T. Lotze. 2010. Endogenous HMGB1 regulates autophagy. The Journal of Cell Biology 190: 881–892.PubMedCrossRef
33.
Zurück zum Zitat Takeuchi, O., and S. Akira. 2010. Pattern recognition receptors and inflammation. Cell 140: 805–820.PubMedCrossRef Takeuchi, O., and S. Akira. 2010. Pattern recognition receptors and inflammation. Cell 140: 805–820.PubMedCrossRef
34.
Zurück zum Zitat Xu, J., X. Zhang, M. Monestier, N.L. Esmon, and C.T. Esmon. 2011. Extracellular histones are mediators of death through TLR2 and TLR4 in mouse fatal liver injury. Journal of Immunology 187: 2626–2631.CrossRef Xu, J., X. Zhang, M. Monestier, N.L. Esmon, and C.T. Esmon. 2011. Extracellular histones are mediators of death through TLR2 and TLR4 in mouse fatal liver injury. Journal of Immunology 187: 2626–2631.CrossRef
35.
Zurück zum Zitat Uesugi, T., M. Froh, G.E. Arteel, B.U. Bradford, and R.G. Thurman. 2001. Toll-like receptor 4 is involved in the mechanism of early alcohol-induced liver injury in mice. Hepatology 34: 101–108.PubMedCrossRef Uesugi, T., M. Froh, G.E. Arteel, B.U. Bradford, and R.G. Thurman. 2001. Toll-like receptor 4 is involved in the mechanism of early alcohol-induced liver injury in mice. Hepatology 34: 101–108.PubMedCrossRef
Metadaten
Titel
Curcumin Protects Against Concanavalin A-Induced Hepatitis in Mice Through Inhibiting the Cytoplasmic Translocation and Expression of High Mobility Group Box 1
verfasst von
Chuan-tao Tu
Qun-yan Yao
Bei-li Xu
Shun-cai Zhang
Publikationsdatum
01.02.2013
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 1/2013
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-012-9536-4

Weitere Artikel der Ausgabe 1/2013

Inflammation 1/2013 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

RAS-Blocker bei Hyperkaliämie möglichst nicht sofort absetzen

14.05.2024 Hyperkaliämie Nachrichten

Bei ausgeprägter Nierenfunktionsstörung steigen unter der Einnahme von Renin-Angiotensin-System(RAS)-Hemmstoffen nicht selten die Serumkaliumspiegel. Was in diesem Fall zu tun ist, erklärte Prof. Jürgen Floege beim diesjährigen Allgemeinmedizin-Update-Seminar.

Gestationsdiabetes: In der zweiten Schwangerschaft folgenreicher als in der ersten

13.05.2024 Gestationsdiabetes Nachrichten

Das Risiko, nach einem Gestationsdiabetes einen Typ-2-Diabetes zu entwickeln, hängt nicht nur von der Zahl, sondern auch von der Reihenfolge der betroffenen Schwangerschaften ab.

Labor, CT-Anthropometrie zeigen Risiko für Pankreaskrebs

13.05.2024 Pankreaskarzinom Nachrichten

Gerade bei aggressiven Malignomen wie dem duktalen Adenokarzinom des Pankreas könnte Früherkennung die Therapiechancen verbessern. Noch jedoch klafft hier eine Lücke. Ein Studienteam hat einen Weg gesucht, sie zu schließen.

Battle of Experts: Sport vs. Spritze bei Adipositas und Typ-2-Diabetes

11.05.2024 DDG-Jahrestagung 2024 Kongressbericht

Im Battle of Experts traten zwei Experten auf dem Diabeteskongress gegeneinander an: Die eine vertrat die Auffassung „Sport statt Spritze“ bei Adipositas und Typ-2-Diabetes, der andere forderte „Spritze statt Sport!“ Am Ende waren sie sich aber einig: Die Kombination aus beidem erzielt die besten Ergebnisse.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.