Inflammation Regulation in Obese Patients

The recruitment status of this study is unknown because the information has not been verified recently.
Verified March 2012 by University Hospital, Montpellier.
Recruitment status was  Recruiting
Sponsor:
Information provided by (Responsible Party):
University Hospital, Montpellier
ClinicalTrials.gov Identifier:
NCT01561664
First received: March 6, 2012
Last updated: March 21, 2012
Last verified: March 2012
  Purpose

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.


Condition Intervention
Obesity
Insulin Resistance
Other: muscle and fat biopsy

Study Type: Interventional
Study Design: Allocation: Non-Randomized
Intervention Model: Parallel Assignment
Masking: Open Label
Official Title: Relations Between Obesity and Insulin Resistance: Role of Inflammation Regulatory Mechanisms in Obese Patients Without Associated Comorbidity

Resource links provided by NLM:


Further study details as provided by University Hospital, Montpellier:

Primary Outcome Measures:
  • TLR regulation [ Time Frame: 2 years ] [ Designated as safety issue: No ]
    analyse the role of RLI and RNase L in TLR regulation, and its potential implication in the link between obesity, microinflammation and insulin resistance in adipose tissue and squelettal muscle in humans.


Estimated Enrollment: 30
Study Start Date: November 2011
Estimated Study Completion Date: November 2013
Primary Completion Date: November 2011 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Active Comparator: volunteers
not overweight Volunteers responding to the study criteria
Other: muscle and fat biopsy
muscle and fat biopsy
Experimental: overweight patients insulin sensitive
overweight patients insulin sensitive responding to the study criteria
Other: muscle and fat biopsy
muscle and fat biopsy
Experimental: overweight insulin resistant
overweight patients insulin resistant responding to the study criteria
Other: muscle and fat biopsy
muscle and fat biopsy

Detailed Description:

The investigators working hypothesis is that RNase L and RLI contribute to chronic inflammation regulation and to insulin response through TLR 4 pathway regulation in obesity. The investigators main purpose is to compare innate immunity activation pathway between insulin sensitive, insulin resistant obese patients and control patients. Insulin sensitive and insulin resistant obese patients will be distinguish thanks to the HOMA ir index. The investigators second objectives are to evaluate if the degree of inflammation in adipose tissue and squeletal muscle is correlated to insulin sensitivity measured by hyperinsulinemic euglycemic clamp and to characterise inflammatory pathway and regulation pathway. A special focus will be given to the leukotrienes and their potential role in insulin resistance pathogenesis. The investigators will have two approaches:- characterisation of subjects with normal weight, of obese insulin sensitive and obese insulin resistant through a metabolic evaluation, an inflammatory characterisation and a measure of insulin sensitivity at the systemic level, in adipose tissue and in squeletal muscle.- an in vitron approach with human myoblast and adipocytes culture, extracted from the investigators patients: characterisation of inflammation, innate immunity.

  Eligibility

Ages Eligible for Study:   50 Years to 65 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Criteria

Inclusion Criteria:

  • Age between 50 and 65 years old
  • Men/ menopausal women
  • BMI <25 kg/m2 for the control group, BMI >30 kg/m2 for the obese group
  • Non diabetic patients
  • HOMAIR <3 for the insulin sensitive obese group
  • Non smoking
  • Without any inflammatory disease
  • Without any first degrees relative with diabetes
  • Without any treatment that could interfere with insulin sensitivity
  • without any infection
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01561664

Contacts
Contact: Ariane Sultan, MCU-PH a-seddiki@chu-montpellier.fr

Locations
France
Montpellier University Hospital Recruiting
Montpellier, France, 34295
Principal Investigator: Ariane Sultan, MCU-PH         
Sponsors and Collaborators
University Hospital, Montpellier
Investigators
Study Chair: Jacques Mercier University Hospital, Montpellier
  More Information

No publications provided

Responsible Party: University Hospital, Montpellier
ClinicalTrials.gov Identifier: NCT01561664     History of Changes
Other Study ID Numbers: UF 8685
Study First Received: March 6, 2012
Last Updated: March 21, 2012
Health Authority: France: Afssaps - Agence française de sécurité sanitaire des produits de santé (Saint-Denis)

Keywords provided by University Hospital, Montpellier:
obesity
insulin resistance

Additional relevant MeSH terms:
Inflammation
Insulin Resistance
Obesity
Pathologic Processes
Hyperinsulinism
Glucose Metabolism Disorders
Metabolic Diseases
Overnutrition
Nutrition Disorders
Overweight
Body Weight
Signs and Symptoms
Insulin
Hypoglycemic Agents
Physiological Effects of Drugs
Pharmacologic Actions

ClinicalTrials.gov processed this record on July 22, 2014