Are adipocytokines inflammatory or metabolic mediators in patients with inflammatory bowel disease?

Kahraman, Resul; Çalhan, Turan; Şahin, Abdurrahman; Özdil, Kamil; Çalışkan, Zuhal; Bireller, Elif Sinem; Çakmakoğlu, Bedia

doi:10.2147/tcrm.s140618

Cited by 17 publications

(20 citation statements)

References 40 publications

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“…A similar observation was made by Tuzun et al, who found elevated levels of leptin in patients in the acute stage of UC [135]. In another study, Kahraman and colleagues [136] showed that leptin levels were much lower in patients with UC and CD than in healthy controls. In contrast, Karmiris et al [137] observed that serum levels of leptin were reduced in patients with IBD.…”

Section: Leptinsupporting

confidence: 75%

“…Similar to leptin, the data concerning APN serum levels in patients with IBD is controversial. For instance, Kahraman et al [136] find that, unlike in other studies, serum APN concentrations are decreased in both UC and CD patients. Similarly, Valentini et al [140] demonstrated that APN serum levels are decreased in active and inactive disease in both CD and UC individuals.…”

Section: Adiponectinmentioning

confidence: 70%

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Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

et al. 2019

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Inflammatory bowel diseases (IBDs) are a group of disorders which include ulcerative colitis and Crohn’s disease. Obesity is becoming increasingly more common among patients with inflammatory bowel disease and plays a role in the development and course of the disease. This is especially true in the case of Crohn’s disease. The recent results indicate a special role of visceral adipose tissue and particularly mesenteric adipose tissue, also known as “creeping fat”, in pathomechanism, leading to intestinal inflammation. The involvement of altered adipocyte function and the deregulated production of adipokines, such as leptin and adiponectin, has been suggested in pathogenesis of IBD. In this review, we discuss the epidemiology and pathophysiology of obesity in IBD, the influence of a Western diet on the course of Crohn’s disease and colitis in IBD patients and animal’s models, and the potential role of adipokines in these disorders. Since altered body composition, decrease of skeletal muscle mass, and development of pathologically changed mesenteric white adipose tissue are well-known features of IBD and especially of Crohn’s disease, we discuss the possible crosstalk between adipokines and myokines released from skeletal muscle during exercise with moderate or forced intensity. The emerging role of microbiota and the antioxidative and anti-inflammatory enzymes such as intestinal alkaline phosphatase is also discussed, in order to open new avenues for the therapy against intestinal perturbations associated with IBD.

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Section: Leptinsupporting

confidence: 75%

Section: Adiponectinmentioning

confidence: 70%

Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

et al. 2019

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“…In this framework, the overall objective of our study was to investigate the involvement of adipose tissue-derived hormones, immune- and neuromodulatory factors in the alterations of the s-IP in D-IBS patients categorised as having normal [D-IBS(−)] or increased s-IP [D-IBS(+)] by using the lactulose/mannitol (La/Ma) ratio and healthy subjects. In particular, the aims of the study were to (a) analyse the symptom profile in D-IBS patients using a validated questionnaire, such as the Gastrointestinal Symptom Rating Scale (GSRS), in relation to whether or not there are alterations in s-IP [15] and (b) assess the circulating levels of the adipo(cyto)kines interleukin 6 (IL-6), interleukin 8 (IL-8), and tumor necrosis factor alpha (TNF- α ) that play a role as mediators of inflammation and immune activation [16], along with circulating levels of lipopolysaccharide (LPS) and toll-like receptor 4 (TLR-4), as markers of endotoxemia; leptin and adiponectin as mediators of intestinal inflammation [17]; neurotensin, with its role in preserving gut barrier integrity [18]; and the metabotropic brain-derived neurotrophic factor (BDNF), a neuroendocrine factor expressed in adipose tissue [19]. Lastly, the familial aggregation suggests a genetic component as having a role in increasing the risk of developing the pathology, although the functional role of allelic variants in IBS is still an open field [20].…”

Section: Introductionmentioning

confidence: 99%

Adipose Tissue-Derived Biomarkers of Intestinal Barrier Functions for the Characterization of Diarrhoea-Predominant IBS

et al. 2018

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Background Alterations of the small-intestinal permeability (s-IP) might play an essential role in a subgroup of diarrhoea-predominant IBS (D-IBS) patients. Goals (a) To analyse in D-IBS patients the symptom profile in relation to the altered (+) or not (−) s-IP using the Gastrointestinal Symptom Rating Scale (GSRS). (b) To assess the circulating levels of the adipokines IL-6, IL-8, TNF-α, leptin, and adiponectin, along with LPS, TLR-4, neurotensin, and brain-derived neurotrophic factor (BDNF). The frequency distribution of SNPs at the loci for the investigated molecules and leptin receptor was evaluated. Study The study included 34 D-IBS patients and 17 healthy controls (HC). s-IP permeability was assayed by high-performance liquid chromatography determination in the urine of the lactulose to mannitol ratio. Concentrations of IL-6, IL-8, TNF-α, LPS, TLR-4, leptin, adiponectin, neurotensin, and BDNF were assayed by ELISA. Screening of genetic variants was done employing the restriction fragment length polymorphism-polymerase chain reaction method. Results D-IBS(−) patients had a significantly higher GSRS cluster pain and diarrhoea profile than D-IBS(+) ones. Significant correlations were found between the symptoms clusters and immune activation and inflammation markers. The levels of adipo(cyto)kines in D-IBS(+) patients were higher than those of controls, and IL-6 levels correlated with those of LPS. Leptin and BDNF were significantly higher, and neurotensin levels were significantly lower in D-IBS(+) than in controls. No differences were found in the frequency distribution of genotypes among the study groups. Conclusions Results from this study could be of some help in the characterization of the D-IBS and highlight the contribution of an altered intestinal barrier in the pathogenesis of this syndrome. Besides, a role could be ascribed to molecules secreted by the visceral adipose tissue that can impact on barrier functions.

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“…Results regarding adiponectin involvement in IBD pathogenesis are also divergent 12,23 . This adipokine is characterized by anti-inflammatory properties and its concentration decreases in obesity 24 .…”

Section: Discussionmentioning

confidence: 99%

“…Leptin is an adipokine secreted by adipocytes which stimulates the production of pro-inflammatory IL-1β and IL-6 in T cells 11 . Adiponectin is secreted from adipocytes and displays anti-inflammatory properties 12 . On the other hand, resistin is an adipokine upregulated in the mesenteric adipose tissue from CDpatients 11 which may act as an independent predictor of disease in CD 13 .…”

Section: Introductionmentioning

confidence: 99%

Serum adipokines as non-invasive biomarkers in Crohn’s disease

Moreno

Sanz-García

Fuente

et al. 2020

Sci Rep

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Adipose tissue secretes molecules that can promote activity in Crohn’s disease. We aimed to evaluate the role of serum adipokines as possible biomarkers in Crohn’s disease. Serum samples were obtained from 40 patients with endoscopically active or quiescent Crohn’s disease and 36 healthy controls. Serum leptin, ghrelin, resistin and adiponectin levels were analysed by Multiplex in a Luminex 200 system technology. Receiver Operating Characteristic curves were performed to evaluate the adipokines discriminatory capacity. A logistic regression adjusted by possible confounders (i.e. gender, age, BMI) was performed for those adipokines that showed an area under the curve > 0.7. No differences were found in age, gender or BMI among groups. Distribution for serum resistin was different among the three groups of study, and only this adipokine showed an area under the curve of 0.75 comparing actives patients and healthy control groups. Resistin median concentration was selected as a cut-off for a logistic regression analysis; odds ratio along its 95% confidence interval adjusted by gender, age, and BMI yielded a value of 5.46 (1.34–22.14) comparing actives patients and healthy controls. High concentration of serum resistin is probably associated to activity, being this association independent of gender, age or BMI.

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Are adipocytokines inflammatory or metabolic mediators in patients with inflammatory bowel disease?

Cited by 17 publications

References 40 publications

Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

Adipose Tissue-Derived Biomarkers of Intestinal Barrier Functions for the Characterization of Diarrhoea-Predominant IBS

Serum adipokines as non-invasive biomarkers in Crohn’s disease

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