Adipozytokine bei chronisch entzündlichen Darmerkrankungen (CED)

Valentini, Luzia; Schaper, L.; Hengstermann, S.; Büning, Carsten; Koernicke, Thomas; Wirth, Erich; Schweizer, U.; Lochs, Herbert; Ockenga, J.

doi:10.1055/s-2007-988250

Cited by 2 publications

(2 citation statements)

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“…For instance, in obese patients undergoing bariatric surgery IBD has been reported to improve (20), but also to be aggravated or to be elicited de novo (2). Several adipokines like leptin, adiponectin, resistin, visfatin, grelin or apelin have been reported to be related with intestinal inflammation (4,18,38,45,47). However, the exact role of leptin in IBD is equivocal thus far, and its effects remain controversial and poorly described in many ways.…”

Section: Discussionmentioning

confidence: 99%

Leptin-resistant Zucker rats with trinitrobenzene sulfonic acid colitis present a reduced inflammatory response but enhanced epithelial damage

Rivero-Gutiérrez

Arredondo-Amador

Gámez‐Belmonte

et al. 2021

American Journal of Physiology-Gastrointestinal and Liver Physi

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The role of leptin in the development of intestinal inflammation remains controversial, since proinflammatory and anti-inflammatory effects have been described. This study describes the effect of the absence of leptin signaling in intestinal inflammation. Experimental colitis was induced by intrarectal administration of trinitrobenzene sulfonic acid (TNBS) to lean and obese Zucker rats (n=10). Effects on inflammation and mucosal barrier were studied. Bacterial translocation and LPS concentration were evaluated together with colonic permeability to 4 kDa FITC-dextran. Obese Zucker rats showed a lower intestinal myeloperoxidase and alkaline phosphatase activity, reduced alkaline phosphatase sensitivity to levamisole, and diminished colonic expression of Nos2, Tnf and Il6, indicating attenuated intestinal inflammation, associated with attenuated STAT3, AKT and ERK signaling in the colonic tissue. S100a8 and Cxcl1 mRNA levels were maintained, suggesting that in the absence of leptin signaling neutrophil activation rather than infiltration is hampered. In spite of the lower inflammatory response, leptin resistance enhanced intestinal permeability, reflecting an increased epithelial damage. This was shown by augmented LPS presence in the portal vein of colitic obese Zucker rats, associated with induction of tissue non-specific alkaline phosphatase, LPS-binding protein and CD14 hepatic expression (involved in LPS handling). This was linked to decreased ZO-1 immunoreactivity in tight junctions and lower occludin expression. Our results indicate that obese Zucker rats present an attenuated inflammatory response to TNBS, but increased intestinal epithelial damage allowing the passage of bacterial antigens.

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Section: Discussionmentioning

confidence: 99%

Leptin-resistant Zucker rats with trinitrobenzene sulfonic acid colitis present a reduced inflammatory response but enhanced epithelial damage

Rivero-Gutiérrez

Arredondo-Amador

Gámez‐Belmonte

et al. 2021

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Estudos associando doença inflamatória intestinal (DII), adiponectina e controle saudável apresentam resultados controversos. De acordo com Valentini e col. (2009) há redução da adiponectina sérica em DC e RCUI quando comparados ao controle 58 . Em outro esta redução foi observada apenas para o sexo feminino na DC quando comparado com o controle 69 .…”

Section: Avaliação Subjetiva Global (Asg)unclassified

Níveis séricos e teciduais de adipocinas, perfil nutricional e papel do tecido mesenterial na doença de Crohn

Rodrigues¹,

Ferreira²

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Adipozytokine bei chronisch entzündlichen Darmerkrankungen (CED)

Cited by 2 publications

References 0 publications

Leptin-resistant Zucker rats with trinitrobenzene sulfonic acid colitis present a reduced inflammatory response but enhanced epithelial damage

Leptin-resistant Zucker rats with trinitrobenzene sulfonic acid colitis present a reduced inflammatory response but enhanced epithelial damage

Níveis séricos e teciduais de adipocinas, perfil nutricional e papel do tecido mesenterial na doença de Crohn

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