Leptin, adiponectin, resistin, and ghrelin – Implications for inflammatory bowel disease
Identifieur interne : 002A71 ( Main/Exploration ); précédent : 002A70; suivant : 002A72Leptin, adiponectin, resistin, and ghrelin – Implications for inflammatory bowel disease
Auteurs : Konstantinos Karmiris ; Ioannis E. Koutroubakis [Grèce] ; Elias A. KouroumalisSource :
- Molecular Nutrition & Food Research [ 1613-4125 ] ; 2008-08.
English descriptors
- Teeft :
- Adipocytes, Adipokines, Adiponectin, Adiponectin levels, Adiponectin production, Adiponectin secretion, Adipose, Adipose tissue, Animal models, Biochem, Biophys, Bowel, Clin, Colitis, Colonic, Commun, Cytokine, Cytokine release, Endocrinol, Endogenous, Epithelial, Epithelial cells, Food intake, Gastroenterology, Ghrelin, Globular, Globular adiponectin, Globular domain, Gmbh, Human adipocytes, Human hepatic stelate cells, Human macrophages, Human monocytes, Human resistin, Ifnc, Immune, Immune cells, Immune response, Immune system, Immunol, Inflamed, Inflammation, Inflammatory, Inflammatory bowel disease, Inflammatory bowel diseases, Intestinal, Intestinal epithelial cells, Intestinal inflammation, Intestine, Karmiris, Kgaa, Leptin, Macrophage, Mesenteric, Metab, Metabolic syndrome, Monocyte, Mrna, Mrna expression, Mwat, Neutrophil, Neutrophil infiltration, Nutr, Other hand, Oxidative stress, Pbmc, Peptide, Peripheral blood, Plasma leptin, Pparc, Proinflammatory, Proinflammatory cytokines, Receptor, Resistin, Resistin expression, Resistin production, Secretion, Serum leptin levels, Synovial, Tnfa, Ulcerative colitis, Verlag, Verlag gmbh, Weinheim.
Abstract
Inflammatory bowel disease (IBD) is characterized by anorexia, malnutrition, altered body composition, and development of mesenteric white adipose tissue (WAT) hypertrophy. Increasing evidence suggests that adipokines synthesized either in WAT or in immune cells, are involved in these manifestations of IBD. Among adipokines leptin, adiponectin and resistin hold a fundamental role while the role of ghrelin in inflammation is not well established. Preliminary studies have shown overexpression of leptin, adiponectin, and resistin in mesenteric WAT of patients with Crohn's disease (CD) and significant alterations of circulating serum levels of these adipokines in IBD. It has also been demonstrated that intestinal inflammation causes an increase in endogenous ghrelin production. In animal models of intestinal inflammation, existing data suggest that leptin, adiponectin, and resistin are pivotal mediators of inflammation. Interesting therapeutic interventions based on these data have been suggested. A specific role for hypertrophic WAT has also been implicated in CD. Further efforts with experimental and clinical studies are needed to better understand the role of adipokines in IBD.
Url:
DOI: 10.1002/mnfr.200700050
Affiliations:
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Le document en format XML
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<term>Adiponectin levels</term>
<term>Adiponectin production</term>
<term>Adiponectin secretion</term>
<term>Adipose</term>
<term>Adipose tissue</term>
<term>Animal models</term>
<term>Biochem</term>
<term>Biophys</term>
<term>Bowel</term>
<term>Clin</term>
<term>Colitis</term>
<term>Colonic</term>
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<term>Cytokine</term>
<term>Cytokine release</term>
<term>Endocrinol</term>
<term>Endogenous</term>
<term>Epithelial</term>
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<term>Human hepatic stelate cells</term>
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<term>Human monocytes</term>
<term>Human resistin</term>
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<term>Immune</term>
<term>Immune cells</term>
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<term>Immune system</term>
<term>Immunol</term>
<term>Inflamed</term>
<term>Inflammation</term>
<term>Inflammatory</term>
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<term>Intestinal epithelial cells</term>
<term>Intestinal inflammation</term>
<term>Intestine</term>
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<term>Mesenteric</term>
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<term>Metabolic syndrome</term>
<term>Monocyte</term>
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<term>Mrna expression</term>
<term>Mwat</term>
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<term>Other hand</term>
<term>Oxidative stress</term>
<term>Pbmc</term>
<term>Peptide</term>
<term>Peripheral blood</term>
<term>Plasma leptin</term>
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<term>Proinflammatory cytokines</term>
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<term>Resistin</term>
<term>Resistin expression</term>
<term>Resistin production</term>
<term>Secretion</term>
<term>Serum leptin levels</term>
<term>Synovial</term>
<term>Tnfa</term>
<term>Ulcerative colitis</term>
<term>Verlag</term>
<term>Verlag gmbh</term>
<term>Weinheim</term>
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<front><div type="abstract" xml:lang="en">Inflammatory bowel disease (IBD) is characterized by anorexia, malnutrition, altered body composition, and development of mesenteric white adipose tissue (WAT) hypertrophy. Increasing evidence suggests that adipokines synthesized either in WAT or in immune cells, are involved in these manifestations of IBD. Among adipokines leptin, adiponectin and resistin hold a fundamental role while the role of ghrelin in inflammation is not well established. Preliminary studies have shown overexpression of leptin, adiponectin, and resistin in mesenteric WAT of patients with Crohn's disease (CD) and significant alterations of circulating serum levels of these adipokines in IBD. It has also been demonstrated that intestinal inflammation causes an increase in endogenous ghrelin production. In animal models of intestinal inflammation, existing data suggest that leptin, adiponectin, and resistin are pivotal mediators of inflammation. Interesting therapeutic interventions based on these data have been suggested. A specific role for hypertrophic WAT has also been implicated in CD. Further efforts with experimental and clinical studies are needed to better understand the role of adipokines in IBD.</div>
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