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      Relationship of mesenteric panniculitis with visceral and subcutaneous adipose tissue

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          Abstract

          Background/aim

          Mesenteric panniculitis (MP) is an idiopathic benign disease characterized by fat necrosis, chronic inflammation, and fibrosis. The relationship between obesity and chronic low-grade inflammation has been reported. This study investigated the relationship of MP diagnosed using multidetector computed tomography (MDCT) with visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) areas.

          Materials and methods

          We retrospectively enrolled 104 patients with no radiological findings other than MP. Additionally, 76 individuals without any indicative radiological findings were included as controls. VAT and SAT were separately calculated (cm2) using a 3-dimensional workstation. The abdominal circumference was measured (cm).

          Results

          The mean abdominal circumference was 99.9 ± 7.9 cm, SAT was 195.3 ± 89.1 cm2, and VAT was 203.9 ± 72.8 cm2 in the MP group. The abdominal circumference, VAT, and SAT were significantly higher in the MP group than in the control group (P < 0.001). According to the receiver operating characteristic (ROC) analysis, cut-off level VAT and SAT were 167.5 cm2 (sensitivity 71%, specificity 69%) and 117.5 cm2 (sensitivity 78%, specificity 51 %), respectively.

          Conclusion

          Increased VAT and SAT were associated with MP, suggesting their role in the etiology of MP.

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          Most cited references14

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          CT evaluation of mesenteric panniculitis: prevalence and associated diseases.

          This study was undertaken to assess the prevalence of mesenteric panniculitis on CT and to describe its appearance and associated diseases. A total of 7620 consecutive abdominal CT examinations were prospectively evaluated for features common to mesenteric panniculitis such as a well-delineated inhomogeneous hyperattenuated fatty mass at the mesenteric root, envelopment of mesenteric vessels, and no evidence of invasion of the adjacent small-bowel loops that may be displaced. CT findings of mesenteric panniculitis were seen in 49 patients (0.6%). We found a female predominance. Mesenteric panniculitis coexisted with malignancy in 34 patients and with benign disorders in 11 patients. In the remaining four patients, mesenteric panniculitis, verified on histology, was considered to be responsible for the patients' clinical manifestations; no other abnormality was identified. Soft-tissue nodules (n = 39) and a fatty halo surrounding vessels and nodules (n = 42) were observed in most patients. Follow-up abdominal CT examinations in 29 of the 49 patients showed changes in only one patient. CT findings of mesenteric panniculitis may be seen in patients undergoing abdominal CT for various symptoms.
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            High-fat diet-induced obesity exacerbates inflammatory bowel disease in genetically susceptible Mdr1a-/- male mice.

            Obesity is a chronic inflammatory disease and a risk factor for disorders such as heart disease, diabetes, and cancer. A high-fat diet (HFD), a risk factor for obesity, has also been associated with inflammatory bowel disease (IBD). A proinflammatory state characterized by systemic and local increases in cytokine and chemokine levels are noted in both obesity and IBD, but it is unclear whether obesity is a risk factor for IBD. To examine any association between obesity and IBD, we chose FVB.129P2- Abcb1a(tm1Bor)N7 (Mdr1a(-/-)) mice, because this strain develops IBD spontaneously with age without a chemical or bacterial "trigger." In addition, its background strain, FVB, has been used for diet-induced obesity studies. Mdr1a(-/-) mice and wild-type (WT) mice were fed a HFD (∼60% calories from fat) or a low-fat diet (LFD; ∼11% calories from fat) for 12 wk. Obesity phenotypes examined included body weight measurements, glucose metabolism changes, and adiposity at termination of the study. IBD was determined by clinical signs, necropsy, and histopathology. We found that compared with those fed the LFD, both the Mdr1a(-/-) and WT mice fed the HFD had greater weight gains and elevated plasma leptin concentrations (P < 0.0001). When all mice were analyzed, weight gain was also associated with inflammation in mesenteric fat (R(2) = 0.5; P < 0.0001) and mesenteric lymph nodes (R(2) = 0.4; P < 0.0001). In contrast, the HFD was not associated with IBD in WT mice, whereas it exacerbated spontaneous IBD in Mdr1a(-/-) mice (P = 0.012; Fisher's exact test). Although a HFD and obesity were not associated with IBD in WT mice, our studies suggest that they are likely risk factors for IBD in a genetically susceptible host, such as Mdr1a(-/-) mice.
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              Obesity, visceral fat and Crohn's disease.

              Increasing evidence indicates that adipose tissue is an active endocrine organ involved in metabolic syndrome and regulation of inflammation. Visceral fat accumulation is a hallmark of both obesity and Crohn's disease. Here, we present recent data describing the immune properties of intra-abdominal adipose tissue that could link the innate immune response to obesity-related disorders and gut inflammation. Innate immune properties of adipocytes have become well characterized since recent studies described the Toll-like receptor (TLR) expression repertoire and specific TLR ligand responses of adipocytes. Adipokine secretion profiles have also been elucidated both in obese patients, when they may be involved in obesity-associated metabolic disease, and in Crohn's disease. Whereas mesenteric fat hypertrophy and fat wrapping of the bowel are characteristic of Crohn's disease, there exists a paucity of information concerning this important pathophysiological aspect. Our current classical animal models are of limited interest when investigating the role of mesenteric fat in gut inflammation. Recent new alternative disease paradigms could help to design more specific models for elucidating chronic transmural inflammation of the gut. Obesity and Crohn's disease share common features with the development of mesenteric fat that may be involved in gut inflammation. Further studies are required to clearly assess the origin and influence of intestinal fat deposits upon gut inflammation, notably during Crohn's disease development.
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                Author and article information

                Journal
                Turk J Med Sci
                Turk J Med Sci
                Turkish Journal of Medical Sciences
                The Scientific and Technological Research Council of Turkey
                1300-0144
                1303-6165
                2020
                13 February 2020
                : 50
                : 1
                : 44-48
                Affiliations
                [1 ] Department of Radiology, Faculty of Medicine, Afyonkarahisar Health Sciences University, Afyon Turkey
                Author notes
                * To whom correspondence should be addressed. E-mail: ozercigdem@ 123456gmail.com

                CONFLICT OF INTEREST:

                none declared

                Author information
                https://orcid.org/0000-0001-5345-1735
                https://orcid.org/0000-0002-0598-2037
                https://orcid.org/0000-0002-0675-3893
                https://orcid.org/0000-0001-5947-062X
                Article
                10.3906/sag-1908-138
                7080351
                31655530
                5107c76e-292f-490f-84c5-9f565c2446e3
                Copyright © 2019 The Author(s)

                This article is distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use and redistribution provided that the original author and source are credited.

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                Categories
                Article

                mesenteric panniculitis, fat tissue, multidetector computed tomography

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