Mesenteric adipose tissue alterations resulting from experimental reactivated colitis

Gambero, Alessandra; Maróstica, Marta; Saad, Mário José Abdalla; Pedrazzoli, José

doi:10.1002/ibd.20222

Cited by 58 publications

(54 citation statements)

References 50 publications

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“…A local activation of production of peroxisome proliferators-activated receptor-c (PPARc) from adipocytes due to stimulation from translocated bacteria entering through a defective epithelial barrier in CD has also been implicated as the cause of hypertrophy of mWAT [96]. In line, repeated TNBS-induced intestinal inflammation in rats caused a site-specific increase in mesenteric fat content, a decrease in the diameter of the adjacent to the bowel wall but not of perinodal mesenteric adipocytes, an increase in lipolysis and TNFa production in both sites but interestingly a reduction in PPARc production and an elevation in leptin and adiponectin secretion only from perinodal adipocytes, indicating a site-specific interplay between these adipokines and the immune cells [97]. Also recently, 3T3-L1 preadipocytes were maintained in undifferentiated state, under continuous stimulation with LPS.…”

Section: Ghrelinmentioning

confidence: 86%

Leptin, adiponectin, resistin, and ghrelin – Implications for inflammatory bowel disease

Karmiris

Koutroubakis²,

Kouroumalis

2008

Molecular Nutrition Food Res

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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.

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Section: Ghrelinmentioning

confidence: 86%

Leptin, adiponectin, resistin, and ghrelin – Implications for inflammatory bowel disease

Karmiris

Koutroubakis²,

Kouroumalis

2008

Molecular Nutrition Food Res

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“…The results showed that colitis induced by DSS was significantly alleviated. These results were based on several crucial aspects of IBD: the MPO enzyme is a good marker of inflammatory status and tissue injury, and is expressed by neutrophils, which have a major function in causing colitis, as well as in the pathogenesis of the disease (Gambero et al, 2007;Hensel et al, 2014). In addition, TNF-a and IL-6 serve a critical function in the modulation of intestinal immunity and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Oral delivery of Bifidobacterium longum expressing α-melanocyte-stimulating hormone to combat ulcerative colitis

Wei

Yang

Ding

et al. 2016

Journal of Medical Microbiology

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a-Melanocyte-stimulating hormone (a-MSH) is a tridecapeptide derived from proopiomelanocortin that exhibits potent anti-inflammatory properties by regulating the production of inflammatory mediators. This peptide has been well established in several inflammatory models, including inflammatory bowel disease (IBD). However, its extremely short duration in vivo limits its clinical application. To address this limitation, Bifidobacterium was used here as a carrier to deliver a-MSH. We utilized a-MSH-engineered Bifidobacterium against IBD, which is closely linked to immune and intestinal microbiota dysfunction. First, we constructed a Bifidobacterium longum secreting a-MSH (B. longum-a-MSH). We then tested the recombinant a-MSH expression and determined its bioactivity in HT-29 cells. To assess its effectiveness, B. longum-a-MSH was used against an ulcerative colitis (UC) model in rats induced by dextran sulfate sodium. The data showed that a-MSH expression in B. longum-a-MSH was effective, and its biological activity was similar to the synthesized one. This UC model experiment indicated that B. longum-a-MSH successfully colonized the intestinal gut, expressed bioactive a-MSH and had a significant anti-inflammatory effect. The results demonstrate the feasibility of preventing IBD by using B. longum-a-MSH.

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“…It is probable that the signal transduction of Zn-provoked attenuation of mucosal inflammation is closely integrated with a reduction in disease activity. An increase in colonic MPO activity, a specific marker of PMN recruitment and activation, has been used as a measure of inflammatory status in experimental colitis (7). It has recently been reported that transepithelial resistance and lucifer yellow permeability in colonic tissues were maintained under marginal Zn deficiency (12).…”

Section: Discussionmentioning

confidence: 99%

Zinc deficiency induces dysregulation of cytokine productions in an experimental colitis of rats

et al. 2012

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Dextran sulfate sodium (DSS)-induced colitis is an experimental model of ulcerative colitis, although the precise mechanism has not yet been elucidated. We investigate whether Zn deficiency affects the pathogenesis of colitis induced by DSS with a focus on immune responses. Male WKAH/Hkm Slc rats were fed either a Zn-adequate (ZA, 30 mg Zn/kg diet) as a control or Zndeficient (ZD, 5 mg Zn/kg diet) diet for 21 days and then treated with 2% DSS via deionized drinking water for 7 days. The disease activity index (DAI) was recorded daily throughout DSS treatment. Serum Zn concentrations were significantly lowered in rats fed the ZD diet than those fed the ZA diet at day 7 and 14. Surprisingly, DSS treatment considerably reduced the serum Zn in both groups. The rats fed the ZD diet showed exacerbated colitis based on clinical outcomes, including weight loss, increased DAI, and shortened colon length. An in vitro study corroborated these results, showing that a large amount of TNFα was induced by rat mesenteric leukocytes in response to lipopolysaccharide in ZD medium, but not in ZA medium. These results indicate that a modulation of TNFα production due to Zn deficiency influences disease activity in DSS-induced colitis. In addition, more attention should be given to Zn for prevention of colitis.

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Mesenteric adipose tissue alterations resulting from experimental reactivated colitis

Cited by 58 publications

References 50 publications

Leptin, adiponectin, resistin, and ghrelin – Implications for inflammatory bowel disease

Leptin, adiponectin, resistin, and ghrelin – Implications for inflammatory bowel disease

Oral delivery of Bifidobacterium longum expressing α-melanocyte-stimulating hormone to combat ulcerative colitis

Zinc deficiency induces dysregulation of cytokine productions in an experimental colitis of rats

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