For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
11
views
8
references
 Top references
cited by
0
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      1,227
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Serum sCD163 as a biomarker of adipose tissue inflammation in obstructive sleep apnoea patients: limits and perspectives

      letter
      Author(s): 1 , , 2 , 3 , 4
      Publication date (Electronic):
      Journal: The European Respiratory Journal
      Publisher: European Respiratory Society

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Recently, M urphy et al. [1] demonstrated, through a challenging animal, cellular and human translational approach, that intermittent hypoxia induces a pro-inflammatory activation of adipose tissue macrophages (ATMs), promoting insulin resistance. They confirmed that intermittent hypoxia lowers insulin-mediated glucose uptake in 3T3-L1 adipocytes, and evidenced the interrelationship between inflammation and insulin resistance in the adipose tissue of mice exposed to intermittent hypoxia. They then measured the concentration of serum soluble CD163 (sCD163), an assumed pro-inflammatory biomarker reflecting macrophage activation, in obstructive sleep apnoea (OSA) patients classified according to their BMI and apnoea/hypopnoea index (AHI). This is the first time serum sCD163 has been evaluated in OSA patients, and its association with AHI is promising. With the aim of enhancing its relevance in further studies, we wish to discuss the following points.

          Abstract

          Serum sCD163 as a biomarker of adipose tissue inflammation in OSA patients: limits and perspectives http://ow.ly/kgxL30d7RnE

          Related collections

          Most cited references8

          • Record: found
          • Abstract: found
          • Article: not found

          Intermittent hypoxia in obstructive sleep apnoea mediates insulin resistance through adipose tissue inflammation.

          Aoife M Murphy, Silke Ryan, Claire Arnaud … (2017)
          Obstructive sleep apnoea (OSA) is increasingly associated with insulin resistance. The underlying pathophysiology remains unclear but intermittent hypoxia (IH)-mediated inflammation and subsequent dysfunction of the adipose tissue has been hypothesised to play a key role.We tested this hypothesis employing a comprehensive translational approach using a murine IH model of lean and diet-induced obese mice, an innovative IH system for cell cultures and a tightly controlled patient cohort.IH led to the development of insulin resistance in mice, corrected for the degree of obesity, and reduced insulin-mediated glucose uptake in 3T3-L1 adipocytes, associated with inhibition of the insulin-signalling pathway and downregulation of insulin-receptor substrate-1 mRNA. Providing mechanistic insight, IH induced a pro-inflammatory phenotype of visceral adipose tissue in mice with pro-inflammatory M1 macrophage polarisation correlating with the severity of insulin resistance. Complimentary in vitro analysis demonstrated that IH led to M1 polarisation of THP1-derived macrophages. In subjects without comorbidities (n=186), OSA was independently associated with insulin resistance. Furthermore, we found an independent correlation of OSA severity with the M1 macrophage inflammatory marker sCD163.This study provides evidence that IH induces a pro-inflammatory phenotype of the adipose tissue, which may be a crucial link between OSA and the development of insulin resistance.
          Article 0 comments Cited 64 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Chronic liver injury during obstructive sleep apnea.

            Dominique Wendum, Raoul Poupon, Florence Tanné … (2005)
            Patients with obstructive sleep apnea (OSA) are at risk for the development of fatty liver as a result of being overweight. Several data suggest that OSA per se could be a risk factor of liver injury; ischemic hepatitis during OSA has been reported, and OSA is an independent risk factor for insulin resistance. Therefore, we investigated liver damage and potential mechanisms in 163 consecutive nondrinking patients with nocturnal polysomnographic recording for clinical suspicion of OSA. Serum levels of liver enzymes were measured in all patients. Liver biopsy was offered to patients with elevated liver enzymes. Intrahepatic hypoxia was assessed by the expression of vascular endothelial growth factor (VEGF) on liver biopsy specimens. Severe OSA (apnea-hypopnea index [AHI] > 50/hr) was seen in 27% of patients; 52% had moderate OSA (AHI 10-50/hr), and 21% had no OSA. Overall, 20% had elevated liver enzymes. Independent parameters associated with elevated liver enzymes were body mass index (BMI) (OR: 1.13; CI: 1.03-1.2) and severe OSA (OR: 5.9; CI: 1.2-29). Liver biopsy was performed in 18 of 32 patients with elevated liver enzymes and showed steatohepatitis in 12 cases, associated with fibrosis in 7 cases. Patients with severe OSA were more insulin-resistant according to homeostasis model assessment, had higher percentage of steatosis as well as scores of necrosis and fibrosis, despite similar BMI. Hepatic immunostaining used as an indirect marker of hypoxia was not different between patients with or without severe OSA. In conclusion, severe OSA is a risk factor for elevated liver enzymes and steatohepatitis independent of body weight. Promotion of insulin resistance is probably involved. Further studies are needed to determine whether hypoxia contributes directly to liver injury.
            Article 0 comments Cited 58 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Liver enzymes and histology in obese patients with obstructive sleep apnea.

              Eric Kallwitz, James Herdegen, James A. Madura … (2015)
              Recent studies have shown an association between obstructive sleep apnea (OSA) and elevated liver enzymes in patients with nonalcoholic fatty liver disease (NAFLD). The aim of the current study was to compare biochemical and histologic findings in patients with NAFLD as a function of OSA status. Subjects consisted of 85 patients who had a sleep study followed by a liver biopsy performed at the time of obesity surgery. The diagnosis of OSA was based on an apnea hypopnea index of >/=15. Demographic and laboratory data were collected retrospectively. Liver biopsies were systematically evaluated for features of NAFLD including degree of steatosis, inflammation, and fibrosis. All but one patient had histologic evidence of NAFLD and 51% of the study population had OSA. A higher proportion of patients with OSA had elevated alanine aminotransferase levels (13/39) compared with those without OSA (3/34) (P=0.01). Only 19% of subjects had fibrosis on liver biopsy and still fewer (5%) had bridging fibrosis or cirrhosis. There was a trend toward a higher prevalence of OSA in patients with evidence of progressive liver disease, as indicated by inflammation plus fibrosis (11/15), compared with those with inflammation alone (22/48) (P=0.06). In obese patients with NAFLD, OSA was associated with elevated alanine aminotransferase levels and a trend toward histologic evidence of progressive liver disease.
              Article 0 comments Cited 22 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Eur Respir J
                Journal ID (iso-abbrev): Eur. Respir. J
                Journal ID (publisher-id): ERJ
                Journal ID (hwp): erj
                Title: The European Respiratory Journal
                Publisher: European Respiratory Society
                ISSN (Print): 0903-1936
                ISSN (Electronic): 1399-3003
                Publication date Collection: August 2017
                Publication date (Electronic): 17 August 2017
                Volume: 50
                Issue: 2
                Electronic Location Identifier: 1701038
                Affiliations
                [1 ]Dept of Metabolic Biochemistry, La Pitié Salpêtrière-Charles Foix University Hospital (AP-HP), Paris, France
                [2 ]Service de biochimie et hormonologie, UF biomarqueurs inflammatoires et métaboliques, Hôpital Tenon, AP-HP, Paris, France
                [3 ]Inserm UMR S938, ICAN, CDR Saint-Antoine, Paris, France
                [4 ]Sorbonne Universités, UPMC Univ Paris 6, Paris, France
                Author notes
                Denis Monneret, Dept of Metabolic Biochemistry, La Pitié Salpêtrière-Charles Foix University Hospital (AP-HP), 47–83 Boulevard de l'Hôpital, 75013 Paris, France. E-mail: dmonneret2@ 123456gmail.com
                Article
                Publisher ID: ERJ-01038-2017
                DOI: 10.1183/13993003.01038-2017
                PMC ID: 5593341
                PubMed ID: 28818878
                SO-VID: 07d194bb-4bec-4fb2-b626-825d7202d474
                Copyright © Copyright ©ERS 2017
                History
                Date received : 22 May 2017
                Date accepted : 24 May 2017
                Related
                Categories
                Subject: Agora
                Subject: Correspondence
                Subject: 5

                ScienceOpen disciplines: Respiratory medicine
                Data availability:
                ScienceOpen disciplines: Respiratory medicine

                Comments

                Comment on this article