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Inflammation Regulation in Obese Patients

NCT01561664 · Status: COMPLETED · Phase: NA · Type: INTERVENTIONAL · Enrollment: 30

Last updated 2015-09-18

No results posted yet for this study

Summary

Insulin resistance is one of the main mechanisms involved in metabolic diseases. inflammation has been implicated in its pathogenesis, due to innate immunity activation by free fatty acids, lipopolysaccharides (LPS) and lactate. Free fatty acids, LPS and lactate activate innate immunity in squelettal muscle and adipose tissue via Toll-like receptor 2/4, NFkB, IRF3 (Interferon Responsive Factor 3) and cytokines secretion (TNFa, IFN g, IL1b, IL6), chemokines secretion (MCP1) and leukotrienes (LTB4). Feed back mechanisms involved in TLR signaling pathways as RLI (ribonuclease L inhibitor)/ABCE1, have never been studied in inflammation due to obesity. RLI inhibits an endoribonuclease, RNase L, which has been recently implicated in TLR signaling The purpose of this study is to analyse the role of RLI and RNase L in TLR regulation, and its potential implication in the link between obesity, inflammation and insulin resistance in adipose tissue and squeletal muscle in humans.

Conditions

Interventions

OTHER

muscle and fat biopsy

muscle and fat biopsy

Sponsors & Collaborators

  • University Hospital, Montpellier

    lead OTHER

Principal Investigators

  • Jacques Mercier · University Hospital, Montpellier

Study Design

Allocation
NON_RANDOMIZED
Masking
NONE
Model
PARALLEL

Eligibility

Min Age
50 Years
Max Age
65 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2011-11-30
Primary Completion
2011-11-30
Completion
2013-12-31

Countries

  • France

Study Locations

More Related Trials

Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT01561664 on ClinicalTrials.gov