This trial is active, not recruiting.

Condition obesity
Treatment cytokines assessed from fat tissue
Phase phase 3
Sponsor Vanderbilt University
Start date March 2006
End date November 2009
Trial size 120 participants
Trial identifier NCT00495599, 051215


The central hypothesis of our study is that metabolic and hemodynamic improvements following gastric bypass surgery are mediated by downregulation of inflammation-related adipokines produced by the intra-abdominal adipose tissue such as Visfatin.

United States No locations recruiting
Other Countries No locations recruiting

Study Design

Allocation non-randomized
Endpoint classification efficacy study
Intervention model single group assignment
Masking open label
Primary purpose diagnostic

Primary Outcomes

The primary endpoint of the study is change in mRNA levels of Visfatin.
time frame: Levels of Visfatin will be assayed from fat tissue taken before and after gastric bypass surgery or other laparoscopic surgery.

Eligibility Criteria

Male or female participants from 18 years up to 65 years old.

Inclusion Criteria: - Patients with a BMI < 35undergoing laparoscopic surgery; - Patients undergoing bariatric surgery with a BMI >35kg/m2; and - Those patients who have had gastric by-pass that require additional surgical procedures are eligible for this research protocol. Exclusion Criteria: - Unwilling to consent.

Additional Information

Official title Adipose Secretory Function in Patients Before & After Laparoscopic Surgery
Principal investigator Alfonso Torquati, M.D.
Description Central obesity represents a major risk for the development of type 2 diabetes and cardiovascular complications. Obesity is often associated with insulin resistance and abnormal production of inflammatory cytokines. Adipose tissue and especially omentum (adipocytes and resident macrophages) release several cytokines. Visfatin corresponds to a protein identified previously as pre-B cell colony-enhancing factor (PBEF), a 52-kilodalton cytokine expressed in lymphocytes. [1] Visfatin exerted insulin-mimetic effects in cultured cells and lowered plasma glucose levels in mice. Mice heterozygous for a targeted mutation in the visfatin gene had modestly higher levels of plasma glucose relative to wild-type littermates. Surprisingly, visfatin binds to and activates the insulin receptor. Adipose tissue protein and mRNA expression of Visfatin (PBEF) has not been investigated in a single study design with regard to the relationship to fat distribution, insulin resistance and other metabolic risk factors, especially in morbidly obese individual undergoing weight loss surgery. Therefore, we propose the following specific aims: Investigate the protein and mRNA expression of Visfatin (PBEF) in the peripheral (subcutaneous) and visceral (omentum) adipose tissues of morbidly obese subjects and their relationships to the changes in body composition, fat distribution, insulin sensitivity and time-dependent reversal of co-morbidities following gastric bypass surgery.
Trial information was received from ClinicalTrials.gov and was last updated in February 2008.
Information provided to ClinicalTrials.gov by Vanderbilt University.