Macrophage Infiltration in Human Adipose Tissue

NCT ID: NCT00476658

Last Updated: 2011-12-07

Basic Information

• Recruitment Status: COMPLETED
• Total Enrollment: 200 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2007-01-31
• Study Completion Date: 2011-10-31

Brief Summary

Quantification of macrophage infiltration and characterization of macrophage phenotype in adipose tissue of 60 obese subjects and 20 non obese subjects

Detailed Description

Obesity results from a disequilibrium in energy balance and an inability to adapt to lifestyles which encourage increased energy intake and sedentariness. These last years, numerous studies contributed to show that obesity is the pathology of an organ, the white adipose tissue (AT), characterized by a low grade inflammation when it is enlarged. The fact that adipocytes secrete a number of inflammatory factors or "adipokines" has forced several groups to reassess the involvement of the AT in wide range of physiological and pathophysiological processes. Adipose tissue probably contributes to the links between obesity, inflammation and insulin-resistance. Our previous results based on transcriptomics studies, showed that genes encoding inflammatory molecules are mobilized in adipose tissue of obese subjects and that caloric restriction improves greatly inflammatory profile. Our preliminary studies on the morphology of adipose tissue lead us to observe a major infiltration of macrophages in morbidly obese subjects. This project is based on a clinical protocol performed in massively obese subjects (BMI>40 kg/m²), where drastic weight loss is achieved by gastric bypass. This project has several objectives. It will allow us to characterize the infiltration of macrophages in the subcutaneous adipose tissue of 60 obese subjects compared with 20 normal-weight subjects, to study the evolution during surgically-induced weight loss and to compare the infiltration observed in adipose tissue to that of other tissues (visceral adipose tissue, muscle, liver, bowel and stomach). This study will be not only quantitative (number of macrophages) but also qualitative by characterizing the phenotype of macrophages with transcriptomics and immunohistochemical approaches. We will analyze the relationships between morphological characteristics of adipose tissue and clinical and biochemical parameters related to insulin sensitivity. More generally, this project might lead us to go thoroughly into the knowledge of the link between obesity and associated comorbidities, particularly metabolic complications, and to consider novels therapeutic strategies.

Conditions

Obesity; Diabetes

Keywords

Obesity; macrophage infiltration; insulinoresistance; inflammation

Study Design

• Observational Model Type: COHORT
• Study Time Perspective: PROSPECTIVE

Eligibility Criteria

Inclusion Criteria

• Obese subjects group :

• Obesity with BMI> 40 kg/m² or obesity with BMI between 35 and 40 kg/M² with comorbidities (OAS, diabetes, hypertension etc…)
• Age: 18-60
• Non obese subjects group

• Abdominal surgery planned
• Age: 18-60

Exclusion Criteria

• Inflammatory disease
• cancer
• stroke
• Drugs (AINS)

• Minimum Eligible Age: 18 Years
• Maximum Eligible Age: 60 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

Assistance Publique - Hôpitaux de Paris

OTHER

Sponsor Role: lead

Responsible Party

Responsibility Role: SPONSOR

Principal Investigators

Christine POITOU-BERNERT, MD,PhD

Role: PRINCIPAL_INVESTIGATOR

Assistance Publique - Hôpitaux de Paris

Locations

APHP Hopital Hotel Dieu

Paris, , France

Countries

France

References

Bel Lassen P, Nori N, Bedossa P, Genser L, Aron-Wisnewsky J, Poitou C, Surabattula R, Juul Nielsen M, Asser Karsdal M, Julie Leeming D, Schuppan D, Clement K. Fibrogenesis Marker PRO-C3 Is Higher in Advanced Liver Fibrosis and Improves in Patients Undergoing Bariatric Surgery. J Clin Endocrinol Metab. 2022 Mar 24;107(4):e1356-e1366. doi: 10.1210/clinem/dgab897.

Reference Type: DERIVED

PMID: 34905051 (View on PubMed)

Sell H, Poitou C, Habich C, Bouillot JL, Eckel J, Clement K. Heat Shock Protein 60 in Obesity: Effect of Bariatric Surgery and its Relation to Inflammation and Cardiovascular Risk. Obesity (Silver Spring). 2017 Dec;25(12):2108-2114. doi: 10.1002/oby.22014. Epub 2017 Oct 11.

Reference Type: DERIVED

PMID: 29024428 (View on PubMed)

Reggio S, Rouault C, Poitou C, Bichet JC, Prifti E, Bouillot JL, Rizkalla S, Lacasa D, Tordjman J, Clement K. Increased Basement Membrane Components in Adipose Tissue During Obesity: Links With TGFbeta and Metabolic Phenotypes. J Clin Endocrinol Metab. 2016 Jun;101(6):2578-87. doi: 10.1210/jc.2015-4304. Epub 2016 Apr 6.

Reference Type: DERIVED

PMID: 27049236 (View on PubMed)

Poitou C, Dalmas E, Renovato M, Benhamo V, Hajduch F, Abdennour M, Kahn JF, Veyrie N, Rizkalla S, Fridman WH, Sautes-Fridman C, Clement K, Cremer I. CD14dimCD16+ and CD14+CD16+ monocytes in obesity and during weight loss: relationships with fat mass and subclinical atherosclerosis. Arterioscler Thromb Vasc Biol. 2011 Oct;31(10):2322-30. doi: 10.1161/ATVBAHA.111.230979. Epub 2011 Jul 28.

Reference Type: DERIVED

PMID: 21799175 (View on PubMed)

Dalmas E, Rouault C, Abdennour M, Rovere C, Rizkalla S, Bar-Hen A, Nahon JL, Bouillot JL, Guerre-Millo M, Clement K, Poitou C. Variations in circulating inflammatory factors are related to changes in calorie and carbohydrate intakes early in the course of surgery-induced weight reduction. Am J Clin Nutr. 2011 Aug;94(2):450-8. doi: 10.3945/ajcn.111.013771. Epub 2011 Jun 15.

Reference Type: DERIVED

PMID: 21677057 (View on PubMed)

Other Identifiers

P050318

Identifier Type: -

Identifier Source: org_study_id