Role of visceral fat in colonic inflammation

Paeschke, Anna; Erben, Ulrike; Kredel, Lea I.; Kühl, Anja A.; Siegmund, Britta

doi:10.1097/mog.0000000000000324

Cited by 32 publications

(14 citation statements)

References 67 publications

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“…In Crohn’s disease, the creeping fat surrounding the affected area was found to contribute to the overall inflammatory response 89 and to be associated with a structuring/fistulizing course of disease 90 . Similarly, surrounding visceral fat has been hypothesized to play a pathogenic role in complicated DD 91 . In this context, the clinically significant link that has recently been reported between visceral fat and the severity of the presentation of diverticulitis is of interest, with visceral to subcutaneous ratio likely representing a predictive value of more complicated disease 92 , in accordance with obesity as a risk factor for AD.…”

Section: Pathophysiology and Possible Underlying Biological Mechanismmentioning

confidence: 99%

Recent advances in understanding and managing diverticulitis

Severi

Carabotti²,

Cicenia

et al. 2018

F1000Res

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In the past few decades, the increasing socioeconomic burden of acute diverticulitis (AD) has become evident, and with the growth of the population age, this significant economic impact will likely continue to rise. Furthermore, recent evidence showed an increased rate of hospital admissions especially evident among women and younger individuals. The natural history and pathophysiology of this clinical condition is still to be fully defined, and efforts continue to be made in the identification of risk factors and the establishment of relative preventive strategies. The actual therapeutic strategies aimed to modulate gut microbiota, such as rifaximin or probiotics, or to reduce mucosal inflammation, such as mesalazine, present a relatively poor efficacy for both the prevention of the first AD episode (primary prevention) and its recurrence (secondary prevention). In the last few years, the main goal achieved has been in the management of AD in that uncomplicated AD can, to a larger extent, be managed in an outpatient setting with no or little supportive therapy, a strategy that will certainly impact on the health costs of this disease. The problem of AD recurrence remains a topic of debate. The aim of this review is to present updated evidence on AD epidemiology and relative open clinical questions and to analyze in detail predisposing and protective factors with an attempt to integrate their possible modes of action into the several pathogenic mechanisms that have been suggested to contribute to this multifactorial disease. A unifying hypothesis dealing with the colonic luminal and extra-luminal microenvironments separately is provided. Finally, evidence-based changes in therapeutic management will be summarized. Because of an ascertained multifactorial pathogenesis of uncomplicated and complicated AD, it is probable that a single ‘causa prima’ will not be identifiable, and a better stratification of patients could allow one to pursue tailored therapeutic algorithm strategies.

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Section: Pathophysiology and Possible Underlying Biological Mechanismmentioning

confidence: 99%

Recent advances in understanding and managing diverticulitis

Severi

Carabotti²,

Cicenia

et al. 2018

F1000Res

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“…Indeed, gut dysbiosis contributes to the impairment of intestinal permeability, favoring bacterial translocation [16]. This mechanism could explain the mesenteric adipose tissue expansion in CD [17,18].…”

Section: Introductionmentioning

confidence: 99%

Preventive Effect of Spontaneous Physical Activity on the Gut-Adipose Tissue in a Mouse Model That Mimics Crohn’s Disease Susceptibility

Maillard

Vazeille

Sauvanet

et al. 2019

Cells

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Crohn’s disease is characterized by abnormal ileal colonization by adherent-invasive E. coli (AIEC) and expansion of mesenteric adipose tissue. This study assessed the preventive effect of spontaneous physical activity (PA) on the gut-adipose tissue in a mouse model that mimics Crohn’s disease susceptibility. Thirty-five CEABAC10 male mice performed spontaneous PA (wheel group; n = 24) or not (controls; n = 11) for 12 weeks. At week 12, mice were orally challenged with the AIEC LF82 strain for 6 days. Body composition, glycaemic control, intestinal permeability, gut microbiota composition, and fecal short-chain fatty acids were assessed in both groups. Animals were fed a high fat/high sugar diet throughout the study. After exposure to AIEC, mesenteric adipose tissue weight was lower in the wheel group. Tight junction proteins expression increased with spontaneous PA, whereas systemic lipopolysaccharides were negatively correlated with the covered distance. Bifidobacterium and Lactobacillus decreased in controls, whereas Oscillospira and Ruminococcus increased in the wheel group. Fecal propionate and butyrate were also higher in the wheel group. In conclusion, spontaneous physical activity promotes healthy gut microbiota composition changes and increases short-chain fatty acids in CEABAC10 mice fed a Western diet and exposed to AIEC to mimic Crohn’s disease.

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“…Interestingly, adipose tissue also frequently covers the basolateral site of inflamed diverticula, thus locally reflecting the phenomenon seen in CD. This finding suggests that each inflamed diverticulum mechanistically reflects CD on a miniature scale [217].…”

Section: Diverticulosismentioning

confidence: 74%

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

Chang

Yang

2020

IJMS

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Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett’s esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.

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Role of visceral fat in colonic inflammation

Cited by 32 publications

References 67 publications

Recent advances in understanding and managing diverticulitis

Recent advances in understanding and managing diverticulitis

Preventive Effect of Spontaneous Physical Activity on the Gut-Adipose Tissue in a Mouse Model That Mimics Crohn’s Disease Susceptibility

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

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