scholarly journals Role of Overweight and Obesity in Gastrointestinal Disease

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 111 ◽  
Author(s):  
Sara Emerenziani ◽  
Michele Pier Luca Guarino ◽  
Laura Trillo Asensio ◽  
Annamaria Altomare ◽  
Mentore Ribolsi ◽  
...  
Keyword(s):  
Potential Role ◽  
Gastrointestinal Disease ◽  
Overweight And Obesity ◽  
Biological Mechanisms ◽  
Pathological Conditions ◽  
Severe Impairment ◽  
Prevalence Of Obesity ◽  
Inflammatory Bowel ◽  
Overall Mortality

The prevalence of obesity is increasing worldwide, leading to a severe impairment of overall health. Actually, obesity has been associated with several pathological conditions, causing an excess overall mortality. In particular, overweight and obesity are well known risk factors for a variety of gastrointestinal (GI) disorders i.e., functional GI disorders as well as, inflammatory bowel disease (IBD), pancreatitis, and GI cancer. The aim of the present review is to summarize the potential role of overweight and obesity in GI disease with particular focus on plausible biological mechanisms that could explain the association between obesity and GI disease based on the most recent evidence in the literature.

Obesity and inflammatory bowel disease

2021 ◽  
Vol 75 (1) ◽  
pp. 20-28
Author(s):  
Vladimír Teplan ◽  
Milan Lukáš
Keyword(s):  
Inflammatory Bowel Disease ◽  
Adipose Tissue ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Perioperative Complications ◽  
Overweight And Obesity ◽  
Special Role ◽  
Low Concentrations ◽  
Inflammatory Bowel

The incidence and prevalence of overweight and obesity has dramatically increased in the last decades and is generally considered to be global pandemics. The incidence of inflammatory bowel disease (IBD) is rising parallel with overweight and obesity. Contrary to a conventional believe, about 15–40% patients with IBD are obese, which can contribute to the development and course of IBD, especially in Crohn’s disease. Although the findings of some cohort studies are still conflicting, recent results indicate a special role of visceral adipose tissue and particularly mesenteric adipose tissue known as creeping fat, leading to intestinal inflammation. The involvement of altered adipocyte function and deregulated production of adipokines such as leptin and adiponectin has been suggested in the pathogenesis of IBD. The emerging role of Western diet and microbiota can also open new possibilities in IBD management. The effect of obesity on the IBD-related therapy remains to be studied. The finding that obesity results in suboptimal response to the therapy, potentially promoting rapid clearance of biologic agents and thus leading to their low concentrations, has a great importance. Obesity also makes IBD colorectal surgery technically challenging and might increase a risk of perioperative complications.

scholarly journals The application of omics techniques to understand the role of the gut microbiota in inflammatory bowel disease

2019 ◽  
Vol 12 ◽  
pp. 175628481882225 ◽  
Author(s):  
Jonathan P. Segal ◽  
Benjamin H. Mullish ◽  
Mohammed Nabil Quraishi ◽  
Animesh Acharjee ◽  
Horace R. T. Williams ◽  
...  
Keyword(s):  
Systems Biology ◽  
Gut Microbiota ◽  
Potential Role ◽  
Intestinal Inflammation ◽  
Clinical Care ◽  
Complex Interaction ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Compositional Changes

The aetiopathogenesis of inflammatory bowel diseases (IBD) involves the complex interaction between a patient’s genetic predisposition, environment, gut microbiota and immune system. Currently, however, it is not known if the distinctive perturbations of the gut microbiota that appear to accompany both Crohn’s disease and ulcerative colitis are the cause of, or the result of, the intestinal inflammation that characterizes IBD. With the utilization of novel systems biology technologies, we can now begin to understand not only details about compositional changes in the gut microbiota in IBD, but increasingly also the alterations in microbiota function that accompany these. Technologies such as metagenomics, metataxomics, metatranscriptomics, metaproteomics and metabonomics are therefore allowing us a deeper understanding of the role of the microbiota in IBD. Furthermore, the integration of these systems biology technologies through advancing computational and statistical techniques are beginning to understand the microbiome interactions that both contribute to health and diseased states in IBD. This review aims to explore how such systems biology technologies are advancing our understanding of the gut microbiota, and their potential role in delineating the aetiology, development and clinical care of IBD.

scholarly journals Manganese promotes the aggregation and prion-like cell-to-cell exosomal transmission of α-synuclein

2019 ◽  
Vol 12 (572) ◽  
pp. eaau4543 ◽  
Author(s):  
Dilshan S. Harischandra ◽  
Dharmin Rokad ◽  
Matthew L. Neal ◽  
Shivani Ghaisas ◽  
Sireesha Manne ◽  
...  
Keyword(s):  
Potential Role ◽  
Neuronal Model ◽  
Experimental Models ◽  
Bimolecular Fluorescence Complementation ◽  
Wild Type ◽  
Biological Mechanisms ◽  
Extracellular Medium ◽  
Cell To Cell Transfer ◽  
Serum Exosomes

The aggregation of α-synuclein (αSyn) is considered a key pathophysiological feature of certain neurodegenerative disorders, collectively termed synucleinopathies. Given that a prion-like, cell-to-cell transfer of misfolded αSyn has been recognized in the spreading of αSyn pathology in synucleinopathies, we investigated the biological mechanisms underlying the propagation of the disease with respect to environmental neurotoxic stress. Considering the potential role of the divalent metal manganese (Mn2+) in protein aggregation, we characterized its effect on αSyn misfolding and transmission in experimental models of Parkinson’s disease. In cultured dopaminergic neuronal cells stably expressing wild-type human αSyn, misfolded αSyn was secreted through exosomes into the extracellular medium upon Mn2+ exposure. These exosomes were endocytosed through caveolae into primary microglial cells, thereby mounting neuroinflammatory responses. Furthermore, Mn2+-elicited exosomes exerted a neurotoxic effect in a human dopaminergic neuronal model (LUHMES cells). Moreover, bimolecular fluorescence complementation (BiFC) analysis revealed that Mn2+ accelerated the cell-to-cell transmission of αSyn, resulting in dopaminergic neurotoxicity in a mouse model of Mn2+ exposure. Welders exposed to Mn2+ had increased misfolded αSyn content in their serum exosomes. Stereotaxically delivering αSyn-containing exosomes, isolated from Mn2+-treated αSyn-expressing cells, into the striatum initiated Parkinsonian-like pathological features in mice. Together, these results indicate that Mn2+ exposure promotes αSyn secretion in exosomal vesicles, which subsequently evokes proinflammatory and neurodegenerative responses in both cell culture and animal models.

scholarly journals P057 IL-17 regulates expression of chemotactic chemokines in human colonic subepithelial myofibroblasts

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S163-S163
Author(s):  
E Filidou ◽  
G Tarapatzi ◽  
M Boulkou ◽  
K Arvanitidis ◽  
S Vradelis ◽  
...  
Keyword(s):  
Potential Role ◽  
Cytokine Mrna ◽  
Chemokine Production ◽  
Intestinal Fibrosis ◽  
Basal Expression ◽  
Relapsing Remitting ◽  
Chemotactic Factors ◽  
Inflammatory Bowel ◽  
Colonic Biopsies

Abstract Background Crohn’s disease (CD) and ulcerative colitis (UC), the two main entities of inflammatory bowel disease (IBD), are characterised by chronic and relapsing/remitting inflammation of the gastrointestinal tract, and occasionally ultimately result in debilitating intestinal fibrosis. Apart from their key role in fibrosis, there is evidence that subepithelial myofibroblasts (SEMFs) participate in the IBD inflammatory cascade, as they express various pro-inflammatory cytokine receptors. We examined the effect of pro-inflammatory IL-17—the hallmark cytokine of T-lymphocytes differentiated to Th17—on the expression of lymphocyte-chemotactic chemokines in SEMFs. Methods SEMFs were isolated from endoscopically obtained colonic biopsies from healthy controls, set to culture and stimulated with 100 ng/ml IL-17 for 6 h. Total RNA was extracted and mRNA expression of CCL5, CXCL1 and CXCL11 was assessed with reverse transcription quantitative (RT-q) PCR. Changes in cytokine mRNA are provided as medians (IQR). Results Untreated SEMFs had a basal expression of chemokines of the CCL and CXCL family groups. So far, our study has shown that the IL-17 stimulation leads to a statistically significant upregulation of CCL and CXCL chemokines in SEMFs (p < 0.001). In detail, CCL5 was upregulated 5.7-fold (4.9–7.5), CXCL1 72.9-fold (63.1–90.7) and CXCL11 25.4-fold (17.3–37.3). Conclusion IL-17 induced the expression of chemotactic factors in SEMFs. Our results further support a potential role of SEMFs in the shaping of intestinal mucosal immunity by serving as immunological intermediates that respond to cytokines of adaptive immunity and amplify the recruitment of immune cells via chemokine production.

scholarly journals Compounds of the sphingomyelin-ceramide-glycosphingolipid pathways as secondary messenger molecules: new targets for novel therapies for fatty liver disease and insulin resistance

2016 ◽  
Vol 310 (11) ◽  
pp. G1102-G1117 ◽  
Author(s):  
Yaron Ilan
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Potential Role ◽  
Cell Organelles ◽  
Secondary Messenger ◽  
Pathological Conditions ◽  
Messenger Molecules

The compounds of sphingomyelin-ceramide-glycosphingolipid pathways have been studied as potential secondary messenger molecules in various systems, along with liver function and insulin resistance. Secondary messenger molecules act directly or indirectly to affect cell organelles and intercellular interactions. Their potential role in the pathogenesis of steatohepatitis and diabetes has been suggested. Data samples collected from patients with Gaucher's disease, who had high levels of glucocerebroside, support a role for compounds from these pathways as a messenger molecules in the pathogenesis of fatty liver disease and diabetes. The present review summarizes some of the recent data on the role of glycosphingolipid molecules as messenger molecules in various physiological and pathological conditions, more specifically including insulin resistance and fatty liver disease.

scholarly journals Evidence for a Potential Role of Metallothioneins in Inflammatory Bowel Diseases

2009 ◽  
Vol 2009 ◽  
pp. 1-9 ◽  
Author(s):  
Anouk Waeytens ◽  
Martine De Vos ◽  
Debby Laukens
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Potential Role ◽  
Current Knowledge ◽  
Zinc Homeostasis ◽  
Central Position ◽  
Small Proteins ◽  
Immune Mediated ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Inflammatory bowel diseases (IBDs) are a group of chronic, relapsing, immune-mediated disorders of the intestine, including Crohn's disease and ulcerative colitis. Recent studies underscore the importance of the damaged epithelial barrier and the dysregulated innate immune system in their pathogenesis. Metallothioneins (MTs) are a family of small proteins with a high and conserved cysteine content that are rapidly upregulated in response to an inflammatory stimulus. Herein, we review the current knowledge regarding the expression and potential role of MTs in IBD. MTs exert a central position in zinc homeostasis, modulate the activation of the transcription factor nuclear factor (NF)-B, and serve as antioxidants. In addition, MTs could be involved in IBD through their antiapoptotic effects or through specific immunomodulating extracellular effects. Reports on MT expression in IBD are contradictory but clearly demonstrate a deviant MT expression supporting the idea that these aberrations in IBD require further clarification.

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