Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Typ-2-Diabetes und Adipositas Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende
Erweiterte Suche
Anmelden
nach oben
Inflammation Research
Erschienen in: Inflammation Research 5/2016

13.02.2016 | Original Research Paper

Contribution of PPARα/β/γ, AP-1, importin-α3, and RXRα to the protective effect of 5,14-HEDGE, a 20-HETE mimetic, against hypotension, tachycardia, and inflammation in a rat model of septic shock

verfasst von: Sefika Pinar Senol, Meryem Temiz, Demet Sinem Guden, Pelin Cecen, Ayse Nihal Sari, Seyhan Sahan-Firat, John R. Falck, Rambabu Dakarapu, Kafait U. Malik, Bahar Tunctan

Erschienen in: Inflammation Research | Ausgabe 5/2016

Einloggen, um Zugang zu erhalten

Abstract

Objectives

We have previously demonstrated that downregulation of the MyD88/TAK1-dependent signaling pathway associated with increased CYP4A1 expression and 20-HETE formation participates in the protective effect of N-(20-hydroxyeicosa-5[Z],14[Z]-dienoyl)glycine (5,14-HEDGE), a 20-HETE mimetic, against vascular hyporeactivity, hypotension, tachycardia, inflammation, and mortality in a rodent model of septic shock. The aim of this study was to determine whether increased renal and cardiovascular expression of PPARα/β/γ and RXRα associated with decreased expression and/or activity of AP-1 and importin-α3 participates in the protective effect of 5,14-HEDGE in response to systemic administration of lipopolysaccharide (LPS).

Methods

Conscious male Wistar rats received saline (4 ml/kg) or LPS (10 mg/kg) at time 0. Blood pressure and heart rate were measured using a tail-cuff device. Separate groups of LPS-treated rats were given 5,14-HEDGE (30 mg/kg) 1 h after injection of saline or LPS. The rats were killed 4 h after saline or LPS administration and the kidney, heart, thoracic aorta, and superior mesenteric artery were collected for measurement of protein expression.

Results

Blood pressure fell by 33 mmHg and heart rate rose by 72 beats/min at 4 h after LPS administration. In LPS-treated rats, tissue protein expressions of cytosolic/nuclear PPARα/β/γ and nuclear RXRα, in addition to nuclear translocation of PPARα/β/γ proteins, were decreased, while cytosolic/nuclear AP-1 subunit c-jun/phosphorylated c-jun and importin-α3 protein expression as well as their nuclear translocation were increased. The LPS-induced changes were prevented by 5,14-HEDGE.

Conclusions

The results suggest that an increase in the expression of PPARα/β/γ and RXRα as well as a decrease in AP-1 and importin-α3 expression/activity participates in the protective effect of 5,14-HEDGE against hypotension, tachycardia, and inflammation during endotoxemia and thus have a beneficial effect in septic shock treatment.
Literatur
1.
Elshenawy OH, Anwar-Mohamed A, El-Kadi AO. 20-Hydroxyeicosatetraenoic acid is a potential therapeutic target in cardiovascular diseases. Curr Drug Metab. 2013;14:706–19.CrossRefPubMed
2.
3.
Roman RJ. P-450 metabolites of arachidonic acid in the control of cardiovascular function. Physiol Rev. 2002;82:131–85.CrossRefPubMed
4.
Tunctan B, Korkmaz B, Sari AN, Kacan M, Unsal D, Serin MS, Buharalioglu CK, Sahan-Firat S, Schunck WH, Falck JR, Malik KU. A novel treatment strategy for sepsis and septic shock based on the interactions between prostanoids, nitric oxide, and 20-hydroxyeicosatetraenoic acid. Antiinflamm Antiallergy Agents Med Chem. 2012;11:121–50.CrossRefPubMed
5.
6.
Escalante B, Omata K, Sessa W, Lee SG, Falck JR, Schwartzman ML. 20-hydroxyeicosatetraenoic acid is an endothelium-dependent vasoconstrictor in rabbit arteries. Eur J Pharmacol. 1993;235:1–7.CrossRefPubMed
7.
Randriamboavonjy V, Busse R, Fleming I. 20-HETE-induced contraction of small coronary arteries depends on the activation of Rho-kinase. Hypertension. 2003;41:801–6.CrossRefPubMed
8.
Zou AP, Fleming JT, Falck JR, Jacobs ER, Gebremedhin D, Harder DR, Roman RJ. 20-HETE is an endogenous inhibitor of the large-conductance Ca(2+)-activated K+ channel in renal arterioles. Am J Physiol. 1996;270:R228–37.PubMed
9.
Carroll MA, Capparelli MF, Doumand AB, Cheng MK, Jiang H, McGiff JC. Renal vasoactive eicosanoids: interactions between cytochrome P450 and cyclooxygenase metabolites during salt depletion. Am J Hypertens. 2001;14:159A.CrossRef
10.
Pratt PF, Falck JR, Reddy KM, Kurian JB, Campbell WB. 20-HETE relaxes bovine coronary arteries through the release of prostacyclin. Hypertension. 1998;31:237–41.CrossRefPubMed
11.
Cheng J, Wu CC, Gotlinger KH, Zhang F, Falck JR, Narsimhaswamy D, Schwartzman ML. 20-hydroxy-5,8,11,14-eicosatetraenoic acid mediates endothelial dysfunction via IkappaB kinase-dependent endothelial nitric-oxide synthase uncoupling. J Pharmacol Exp Ther. 2010;332:57–65.CrossRefPubMedPubMedCentral
12.
Ishizuka T, Cheng J, Singh H, Vitto MD, Manthati VL, Falck JR, Laniado-Schwartzman M. 20-Hydroxyeicosatetraenoic acid stimulates nuclear factor-κB activation and the production of inflammatory cytokines in human endothelial cells. J Pharmacol Exp Ther. 2008;324:103–10.CrossRefPubMed
13.
Toth P, Csiszar A, Sosnowska D, Tucsek Z, Cseplo P, Springo Z, Tarantini S, Sonntag WE, Ungvari Z, Koller A. Treatment with the cytochrome P450 ω-hydroxylase inhibitor HET0016 attenuates cerebrovascular inflammation, oxidative stress and improves vasomotor function in spontaneously hypertensive rats. Br J Pharmacol. 2013;168:1878–88.CrossRefPubMedPubMedCentral
14.
Anwar-mohamed A, Zordoky BN, Aboutabl ME, El-Kadi AO. Alteration of cardiac cytochrome P450-mediated arachidonic acid metabolism in response to lipopolysaccharide-induced acute systemic inflammation. Pharmacol Res. 2010;61:410–8.CrossRefPubMed
15.
Theken KN, Deng Y, Kannon MA, Miller TM, Poloyac SM, Lee CR. Activation of the acute inflammatory response alters cytochrome P450 expression and eicosanoid metabolism. Drug Metab Dispos. 2011;39:22–9.CrossRefPubMedPubMedCentral
16.
17.
Gupta SC, Sundaram C, Reuter S, Aggarwal BB. Inhibiting NF-κB activation by small molecules as a therapeutic strategy. Biochim Biophys Acta. 2010;1799:775–87.CrossRefPubMedPubMedCentral
18.
19.
Liu SF, Malik AB. NF-kappa B activation as a pathological mechanism of septic shock and inflammation. Am J Physiol. 2006;290:L622–45.
20.
21.
Haddad JJ, Abdel-Karim NE. NF-κB cellular and molecular regulatory mechanisms and pathways: therapeutic pattern or pseudoregulation? Cell Immunol. 2011;271:5–14.CrossRefPubMed
22.
Ferreira AM, Minarrieta L, Lamas Bervejillo M, Rubbo H. Nitro-fatty acids as novel electrophilic ligands for peroxisome proliferator-activated receptors. Free Radic Biol Med. 2012;53:1654–63.CrossRefPubMed
23.
Grygiel-Gorniak B. Peroxisome proliferator-activated receptors and their ligands: nutritional and clinical implications-a review. Nutr J. 2014;13(17):23.
24.
Neher MD1, Weckbach S, Huber-Lang MS, Stahel PF. New insights into the role of peroxisome proliferator-activated receptors in regulating the inflammatory response after tissue injury. PPAR Res. 2012;2012:728461.
25.
Wright MB, Bortolini M, Tadayyon M, Bopst M. Minireview: challenges and opportunities in development of PPAR agonists. Mol Endocrinol. 2014;28:1756–68.CrossRefPubMed
26.
von Knethen A, Soller M, Brune B. Peroxisome proliferator-activated receptor gamma (PPAR gamma) and sepsis. Arch Immunol Ther Exp. 2007;55:19–25.CrossRef
27.
28.
Cautain B, Hill R, de Pedro N, Link W. Components and regulation of nuclear transport processes. FEBS J. 2015;282:445–62.CrossRefPubMed
29.
Tran EJ, King MC, Corbett AH. Macromolecular transport between the nucleus and the cytoplasm: advances in mechanism and emerging links to disease. Biochim Biophys Acta. 2014;1843:2784–95.CrossRefPubMedPubMedCentral
30.
Cuez T, Korkmaz B, Buharalioglu CK, Sahan-Firat S, Falck J, Malik KU, Tunctan B. A synthetic analogue of 20-HETE, 5,14-HEDGE, reverses endotoxin-induced hypotension via increased 20-HETE levels associated with decreased iNOS protein expression and vasodilator prostanoid production in rats. Basic Clin Pharmacol. 2010;106:378–88.CrossRef
31.
Sari AN, Korkmaz B, Serin MS, Kacan M, Unsal D, Buharalioglu CK, Sahan Firat S, Manthati VL, Falck JR, Malik KU, Tunctan B. Effects of 5,14-HEDGE, a 20-HETE mimetic, on lipopolysaccharide-induced changes in MyD88/TAK1/IKKβ/IκB-α/NF-κB pathway and circulating miR-150, miR-223, and miR-297 levels in a rat model of septic shock. Inflam Res. 2014;63:741–56.
32.
Tunctan B, Korkmaz B, Buharalioglu CK. Sahan Firat S, Anjaiah S, Falck J, Roman RJ, Malik KU. A 20-HETE agonist, N-[20-hydroxyeicosa-5(Z),14(Z)-dienoyl]glycine, opposes the fall in blood pressure and vascular reactivity in endotoxin-treated rats. Shock. 2008;30:329–35.CrossRefPubMedPubMedCentral
33.
Tunctan B, Korkmaz B, Sari AN, Kacan M, Unsal D, Serin MS, Buharalioglu CK, Sahan-Firat S, Cuez T, Schunck WH, Manthati VL, Falck JR, Malik KU. Contribution of iNOS/sGC/PKG pathway, COX-2, CYP4A1, and gp91phox to the protective effect of 5,14-HEDGE, a 20-HETE mimetic, against vasodilation, hypotension, tachycardia, and inflammation in a rat model of septic shock. Nitric Oxide. 2013;33:18–41.CrossRefPubMed
34.
Tunctan B, Korkmaz B, Sari AN, Kacan M, Unsal D, Serin MS, Buharalioglu CK, Sahan-Firat S, Cuez T, Schunck WH, Falck JR, Malik KU. 5,14-HEDGE, a 20-HETE mimetic, reverses hypotension and improves survival in a rodent model of septic shock: contribution of soluble epoxide hydrolase, CYP2C23, MEK1/ERK1/2/IKKβ/IκB-α/NF-κB pathway, and proinflammatory cytokine formation. Prostaglandins Other Lipid Mediat. 2013;102–103:31–41.CrossRefPubMed
35.
Tunctan B, Korkmaz B, Yildirim H, Tamer L, Atik U, Buharalioglu C. Increased production of nitric oxide contributes to renal oxidative stress in endotoxemic rat. Am J Infect Dis. 2005;1:111–5.CrossRef
36.
Gadjeva M, Tomczak MF, Zhang M, Wang YY, Dull K, Rogers AB, Erdman SE, Fox JG, Carroll M, Horwitz BH. A role for NF-kappa B subunits p50 and p65 in the inhibition of lipopolysaccharide-induced shock. J Immunol. 2004;173:5786–93.CrossRefPubMed
37.
38.
Birbach A, Gold P, Binder BR, Hofer E, de Martin R, Schmid JA. Signaling molecules of the NF-kappa B pathway shuttle constitutively between cytoplasm and nucleus. J Biol Chem. 2002;277:10842–51.CrossRefPubMed
39.
Huang TT, Kudo N, Yoshida M, Miyamoto S. A nuclear export signal in the N-terminal regulatory domain of IkappaBalpha controls cytoplasmic localization of inactive NF-kappaB/IkappaBalpha complexes. Proc Natl Acad Sci USA. 2000;97:1014–9.CrossRefPubMedPubMedCentral
40.
Johnson C, Van Antwerp D, Hope TJ. An N-terminal nuclear export signal is required for the nucleocytoplasmic shuttling of IkappaBalpha. EMBO J. 1999;18:6682–93.CrossRefPubMedPubMedCentral
41.
Shirakawa F, Mizel SB. In vitro activation and nuclear translocation of NF-kappa B catalyzed by cyclic AMP-dependent protein kinase and protein kinase C. Mol Cell Biol. 1989;9:2424–30.CrossRefPubMedPubMedCentral
42.
Fagerlund R, Melén K, Cao X, Julkunen I. NF-kappaB p52, RelB and c-Rel are transported into the nucleus via a subset of importin alpha molecules. Cell Signal. 2008;20:1442–51.CrossRefPubMed
43.
Fagerlund R, Kinnunen L, Köhler M, Julkunen I, Melen K. NF-{kappa}B is transported into the nucleus by importin {alpha}3 and importin {alpha}4. J Biol Chem. 2005;280:15942–51.CrossRefPubMed
44.
Zerfaoui M, Errami Y, Naura AS, Suzuki Y, Kim H, Ju J, Liu T, Hans CP, Kim JG, Abd Elmageed ZY, Koochekpour S, Catling A, Boulares AH. Poly(ADP-ribose) polymerase-1 is a determining factor in Crm1-mediated nuclear export and retention of p65 NF-kappa B upon TLR4 stimulation. J Immunol. 2010;185:1894–902.CrossRefPubMedPubMedCentral
45.
Iida A, Yoshidome H, Shida T, Takano S, Takeuchi D, Kimura F, Shimizu H, Ohtsuka M, Miyazaki M. Hepatocyte nuclear factor-kappa beta (NF-kappaB) activation is protective but is decreased in the cholestatic liver with endotoxemia. Surgery. 2010;148:477–89.CrossRefPubMed
46.
Jiang Q, Liu P, Wu X, Liu W, Shen X, Lan T, Xu S, Peng J, Xie X, Huang H. Berberine attenuates lipopolysaccharide-induced extracellular matrix accumulation and inflammation in rat mesangial cells: involvement of NF-κB signaling pathway. Mol Cell Endocrinol. 2011;331:34–40.CrossRefPubMed
47.
Kwon WY, Suh GJ, Kim KS, Kwak YH. Niacin attenuates lung inflammation and improves survival during sepsis by downregulating the nuclear factor-κB pathway. Crit Care Med. 2011;39:328–34.CrossRefPubMed
48.
Meyer-Schwesinger C, Dehde S, von Ruffer C, Gatzemeier S, Klug P, Wenzel UO, Stahl RA, Thaiss F, Meyer TN. Rho kinase inhibition attenuates LPS-induced renal failure in mice in part by attenuation of NF-kappaB p65 signaling. Am J Physiol. 2009;296:F1088–99.
49.
Zhang X, Song Y, Ci X, An N, Ju Y, Li H, Wang X, Han C, Cui J, Deng X. Ivermectin inhibits LPS-induced production of inflammatory cytokines and improves LPS-induced survival in mice. Inflamm Res. 2008;57:524–9.CrossRefPubMed
50.
Mandard S, Patsouris D. Nuclear control of the inflammatory response in mammals by peroxisome proliferator-activated receptors. PPAR Res. 2013;2013:613864.CrossRefPubMedPubMedCentral
51.
Ishizuka T, Ito O, Tan L, Ogawa S, Kohzuki M, Omata K, Takeuchi K, Ito S. Regulation of cytochrome P-450 4A activity by peroxisome proliferator-activated receptors in the rat kidney. Hypertens Res. 2003;26:929–36.CrossRefPubMed
52.
Ito O, Nakamura Y, Tan L, Ishizuka T, Sasaki Y, Minami N, Kanazawa M, Ito S, Sasano H, Kohzuki M. Expression of cytochrome P-450 4 enzymes in the kidney and liver: regulation by PPAR and species-difference between rat and human. Mol Cell Biochem. 2006;284:141–8.CrossRefPubMed
53.
Lee DL, Wilson JL, Duan R, Hudson T, El-Marakby A. Peroxisome proliferator-activated receptor-α activation decreases mean arterial pressure, plasma interleukin-6, and COX-2 while increasing renal CYP4A expression in an acute model of DOCA-salt hypertension. PPAR Res. 2011;2011:502631.CrossRefPubMedPubMedCentral
54.
Ng VY, Huang Y, Reddy LM, Falck JR, Lin ET, Kroetz DL. Cytochrome P450 eicosanoids are activators of peroxisome proliferator-activated receptor alpha. Drug Metab Dispos. 2007;35:1126–34.CrossRefPubMed
55.
Zhou Y, Luo P, Chang HH, Huang H, Yang T, Dong Z, Wang CY, Wang MH. Clofibrate attenuates blood pressure and sodium retention in DOCA-salt hypertension. Kidney Int. 2008;74:1040–8.CrossRefPubMedPubMedCentral
56.
Liang CJ, Tseng CP, Yang CM, Ma YH. 20-Hydroxyeicosatetraenoic acid inhibits ATP-induced COX-2 expression via peroxisome proliferator activator receptor-α in vascular smooth muscle cells. Br J Pharmacol. 2011;163:815–25.CrossRefPubMedPubMedCentral
57.
Barclay TB, Peters JM, Sewer MB, Ferrari L, Gonzalez FJ, Morgan ET. Modulation of cytochrome P-450 gene expression in endotoxemic mice is tissue specific and peroxisome proliferator-activated receptor-alpha dependent. J Pharmacol Exp Ther. 1999;290:1250–7.PubMed
58.
Iwamoto F, Umemoto T, Motojima K, Fujiki Y. Nuclear transport of peroxisome-proliferator activated receptor & alpha. J Biochem. 2011;149:311–9.CrossRefPubMed
59.
Umemoto T, Fujiki Y. Ligand-dependent nucleo-cytoplasmic shuttling of peroxisome proliferator-activated receptors. PPARα and PPARγ. Genes Cells. 2012;17:576–96.CrossRefPubMed
60.
von Knethen A, Tzieply N, Jennewein C, Brüne B. Casein-kinase-II-dependent phosphorylation of PPARgamma provokes CRM1-mediated shuttling of PPARgamma from the nucleus to the cytosol. J Cell Sci. 2010;123:192–201.CrossRef
61.
Forwood JK, Lam MH, Jans DA. Nuclear import of Creb and AP-1 transcription factors requires importin-beta 1 and Ran but is independent of importin-alpha. Biochemistry. 2001;40:5208–17.CrossRefPubMed
62.
Schreck I, Al-Rawi M, Mingot JM, Scholl C, Diefenbacher ME, O’Donnell P, Bohmann D, Weiss C. c-Jun localizes to the nucleus independent of its phosphorylation by and interaction with JNK and vice versa promotes nuclear accumulation of JNK. Biochem Biophys Res Commun. 2011;407:735–40.CrossRefPubMed
63.
Waldmann I, Wälde S, Kehlenbach RH. Nuclear import of c-Jun is mediated by multiple transport receptors. J Biol Chem. 2007;282:27685–892.CrossRefPubMed
64.
Burgermeister E, Seger R. MAPK kinases as nucleo-cytoplasmic shuttles for PPARgamma. Cell Cycle. 2007;6:1539–48.CrossRefPubMed
65.
Ramer R, Walther U, Borchert P, Laufer S, Linnebacher M, Hinz B. Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib. J Lipid Res. 2013;54:3116–29.CrossRefPubMedPubMedCentral
66.
Chen HH, Chen TW, Lin H. Pravastatin attenuates carboplatin-induced nephrotoxicity in rodents via peroxisome proliferator-activated receptor alpha-regulated heme oxygenase-1. Mol Pharmacol. 2010;78:36–45.CrossRefPubMed
67.
Shibuya A, Wada K, Nakajima A, Saeki M, Katayama K, Mayumi T, Kadowaki T, Niwa H, Kamisaki Y. Nitration of PPARgamma inhibits ligand-dependent translocation into the nucleus in a macrophage-like cell line, RAW 264. FEBS Lett. 2002;525:43–7.CrossRefPubMed
68.
Xue H, Chen B, Fan Y, Palikhe M, Li Y. The inhibitory effect of polypeptide cSN50 on alcoholic hepatic injuries through blocking the binding of NF-κB to importin α. Scand J Gastroenterol. 2011;46:931–40.CrossRefPubMed
Metadaten
Titel
Contribution of PPARα/β/γ, AP-1, importin-α3, and RXRα to the protective effect of 5,14-HEDGE, a 20-HETE mimetic, against hypotension, tachycardia, and inflammation in a rat model of septic shock
verfasst von
Sefika Pinar Senol
Meryem Temiz
Demet Sinem Guden
Pelin Cecen
Ayse Nihal Sari
Seyhan Sahan-Firat
John R. Falck
Rambabu Dakarapu
Kafait U. Malik
Bahar Tunctan
Publikationsdatum
13.02.2016
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 5/2016
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-016-0922-5

Weitere Artikel der Ausgabe 5/2016

Inflammation Research 5/2016 Zur Ausgabe

Original Research Paper

Rac1 regulates bacterial toxin-induced thrombin generation

Review

Calcium channels: the potential therapeutic targets for inflammatory bone destruction of rheumatoid arthritis

Original Research Paper

TGF-β signaling is activated in patients with chronic HBV infection and repressed by SMAD7 overexpression after successful antiviral treatment

Short Communication

Circulating soluble receptor for advanced glycation end products is decreased and inversely associated with acute phase response in chronic spontaneous urticaria

Original Research Paper

Characterisation of the clinical and activated T cell response to repeat delayed-type hypersensitivity skin challenges in human subjects, with KLH and PPD, as a potential model to test T cell-targeted therapies

Original Research Paper

Epigenetic factors MeCP2 and HDAC6 control α-tubulin acetylation in cardiac fibroblast proliferation and fibrosis

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

Herzinfarkt mit 85 – trotzdem noch intensive Lipidsenkung?

16.05.2024 Hypercholesterinämie Nachrichten

Profitieren nach einem akuten Myokardinfarkt auch Betroffene über 80 Jahre noch von einer intensiven Lipidsenkung zur Sekundärprävention? Um diese Frage zu beantworten, wurden jetzt Registerdaten aus Frankreich ausgewertet.

ADHS-Medikation erhöht das kardiovaskuläre Risiko

16.05.2024 Herzinsuffizienz Nachrichten

Erwachsene, die Medikamente gegen das Aufmerksamkeitsdefizit-Hyperaktivitätssyndrom einnehmen, laufen offenbar erhöhte Gefahr, an Herzschwäche zu erkranken oder einen Schlaganfall zu erleiden. Es scheint eine Dosis-Wirkungs-Beziehung zu bestehen.

Erstmanifestation eines Diabetes-Typ-1 bei Kindern: Ein Notfall!

16.05.2024 DDG-Jahrestagung 2024 Kongressbericht

Manifestiert sich ein Typ-1-Diabetes bei Kindern, ist das ein Notfall – ebenso wie eine diabetische Ketoazidose. Die Grundsäulen der Therapie bestehen aus Rehydratation, Insulin und Kaliumgabe. Insulin ist das Medikament der Wahl zur Behandlung der Ketoazidose.

CKD bei Diabetes: Neuheiten und Zukunftsaussichten

16.05.2024 DDG-Jahrestagung 2024 Kongressbericht

Jeder Mensch mit Diabetes muss auf eine chronische Nierenerkrankung gescreent werden – diese neue Empfehlung spricht die KDIGO aus. Die Therapie erfolgt individuell und je nach Szenario mit verschiedenen Substanzklassen. Künftig kommt wahrscheinlich, neben RAS-Hemmung, SGLT2-Inhibition und nsMRA, eine vierte Therapiesäule hinzu.

Update Innere Medizin

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

Newsletter bestellen
Bildnachweise