Serum adipokines in inflammatory bowel disease

Waluga, Marek; Hartleb, Marek; Boryczka, Grzegorz; Kukla, Michał; Żwirska-Korczala, K

doi:10.3748/wjg.v20.i22.6912

Cited by 75 publications

(88 citation statements)

References 31 publications

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“…In this cohort study, involving patients with active UC, we compared levels before treatment of the flare with anti‐inflammatory and/or immunosuppressive therapy, and the post‐treatment remission phase and a healthy control group. Unlike other studies, treatment decreased visfatin levels in the remission group . Although not diagnostic, elevation of CRP and ESR in IBD are well‐known markers for determining and monitoring disease activity.…”

Section: Discussionmentioning

confidence: 71%

“…Baseline serum concentrations of visfatin were significantly higher in subjects with UC than in healthy controls. None of the previously reported studies, between active and inactive groups, failed to detect a significant difference in visfatin levels . In this cohort study, involving patients with active UC, we compared levels before treatment of the flare with anti‐inflammatory and/or immunosuppressive therapy, and the post‐treatment remission phase and a healthy control group.…”

Section: Discussionmentioning

confidence: 94%

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Serum Visfatin Levels in Ulcerative Colitis

Doğan

Güven

Celıkbılek

et al. 2015

Clinical Laboratory Analysis

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 94%

Serum Visfatin Levels in Ulcerative Colitis

Doğan

Güven

Celıkbılek

et al. 2015

Clinical Laboratory Analysis

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“…2010; Waluga et al. 2014). Similarly, in our study neither the DSS-induced decrease in circulating total chemerin for all mice nor the overall higher circulating chemerin in older versus younger mice appeared to have any impact on the disease progression or severity.…”

Section: Discussionmentioning

confidence: 99%

Local chemerin levels are positively associated with DSS-induced colitis but constitutive loss of CMKLR1 does not protect against development of colitis

et al. 2015

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Inflammatory bowel disease (IBD) is a family of disorders including ulcerative colitis and Crohn’s disease that are characterized by chronic and relapsing intestinal inflammation. Increased production of proinflammatory mediators, possibly combined with low expression of anti-inflammatory mediators, is thought to promote the development and progression of IBD. In the current study, we demonstrate that expression, secretion, and processing of chemerin, a potent chemoattractant for cells expressing chemokine-like receptor 1 (CMKLR1), increased in the cecum and colon along a gradient positively associated with the severity of inflammation in dextran sodium sulfate (DSS)-induced colitis. We also show that levels of circulating bioactive chemerin increased following DSS treatment. At both 6–8 and 14–16 weeks of age, CMKLR1 knockout mice developed signs of clinical illness more slowly than wild type and had changes in circulating cytokine levels, increased spleen weight, and increased local chemerin secretion following DSS treatment. However, knockout mice ultimately developed similar levels of clinical illness and local inflammation as wild type. Finally, contrary to previous reports, intraperitoneal injection of bioactive chemerin had no effect on the severity of DSS-induced colitis. This suggests that local chemerin levels have a greater impact than circulating levels in the pathogenesis of colitis. Considered altogether, bioactive chemerin represents a novel biomarker for IBD severity, although strategies to modulate endogenous chemerin signaling other than chronic CMKLR1 loss are necessary in order to exploit chemerin as a therapeutic target for the treatment of IBD.

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“…Both Crohn’s disease and ulcerative colitis are associated with high levels of 2 adipokines (resistin and visfatin) and low levels of a third adipokine (leptin). 76 Another study showed that active Crohn’s disease was associated with significantly lower adiponectin levels compared with the control group. 77 Given the contradictory data in these 2 studies, the significance of these adipokine levels still is unclear.…”

Section: Small Intestinementioning

confidence: 99%

Gastrointestinal Complications of Obesity

2017

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Obesity usually is associated with morbidity related to diabetes mellitus and cardiovascular diseases. However, there are many gastrointestinal and hepatic diseases for which obesity is the direct cause (eg, nonalcoholic fatty liver disease) or is a significant risk factor, such as reflux esophagitis and gallstones. When obesity is a risk factor, it may interact with other mechanisms and result in earlier presentation or complicated diseases. There are increased odds ratios or relative risks of several gastrointestinal complications of obesity: gastroesophageal reflux disease, erosive esophagitis, Barrett’s esophagus, esophageal adenocarcinoma, erosive gastritis, gastric cancer, diarrhea, colonic diverticular disease, polyps, cancer, liver disease including nonalcoholic fatty liver disease, cirrhosis, hepatocellular carcinoma, gallstones, acute pancreatitis, and pancreatic cancer. Gastroenterologists are uniquely poised to participate in the multidisciplinary management of obesity as physicians caring for people with obesity-related diseases, in addition to their expertise in nutrition and endoscopic interventions.

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Serum adipokines in inflammatory bowel disease

Abstract: IBD modulates serum adipokine levels by increasing resistin and visfatin release and suppressing leptin production.

Cited by 75 publications

References 31 publications

Serum Visfatin Levels in Ulcerative Colitis

Serum Visfatin Levels in Ulcerative Colitis

Local chemerin levels are positively associated with DSS-induced colitis but constitutive loss of CMKLR1 does not protect against development of colitis

Gastrointestinal Complications of Obesity

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