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Insulin Resistance in Severely Obese Patients

This study has been completed.
Information provided by:
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Identifier:
First received: January 10, 2006
Last updated: March 17, 2010
Last verified: March 2010
This study aims to understand the biological processes that link obesity to diseases including insulin resistance and diabetes. Our approach involves studying the health of patient undergoing weight loss either via weight reduction surgery or by medically supervised liquid formula diets. Patients must be enrolled in a weight treatment program at Emory Bariatrics, Emory University, Atlanta GA, to be eligible for this study. This study does not cover the cost of treatment at Emory Bariatrics. The hypothesis is that decreases in adipose-tissue derived factors during weight loss will be related to improvement in insulin function.

Obesity Insulin Resistance Diabetes

Study Type: Observational
Study Design: Time Perspective: Prospective
Official Title: Insulin Resistance in Severely Obese Patients

Further study details as provided by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK):

Estimated Enrollment: 48
Study Start Date: September 2004
Detailed Description:
Severe obesity affects 4.7% of the U.S. population. A significant number of these individuals suffer from impaired glucose tolerance and type II diabetes due to insulin resistance (IR). Although it is generally accepted that the accumulation of intraabdominal (IA) fat increases the risk of developing IR, the mechanisms responsible for this phenomenon are not yet understood. In addition, the role of subcutaneous (SC) fat towards the etiology of IR - protective, inert or detrimental - is still under debate. This is because SC adipose tissue releases adipocytokines (IL-6, leptin, TNF- ) that have been demonstrated to impair insulin action. In individuals who are severely obese, hyperinsulinemia may induce an exaggerated production of adipocytokines from IA compared to SC fat stores. Our specific aims are: (1) to determine relative contribution of abdominal SC fat versus IA fat to systemic levels of IL-6, leptin and TNF- in lean and in severely obese individuals; (2) to determine the effects of systemic adipocytokine concentrations on whole body as well as tissue sensitivity to insulin. Hypothesis: (a) In the context of severe obesity, IA fat produces increased quantities of IL-6, leptin and TNF- compared to SC fat; (b) In severely obese patients undergoing weight loss, whole body and tissue IR can be predicted by changes in systemic adipocytokines. Methods: Adipose tissue content of IL-6, leptin and TNF- will be determined by ELISA in biopsies obtained from IA and SC fat stores in lean and severely obese patients. Computer tomography-determined areas of IA and SC fat will be related to changes in systemic adipocytokines at baseline and 6-mo following weight loss therapy. Changes in systemic IL-6, leptin and TNF- will be assessed from measurements made at baseline and following 6-mo weight loss. For this time period we will also determine changes in whole body (via IVGTT) and tissue sensitivity to insulin (via glucose uptake into muscle and fat). Relationships between systemic adipocytokines and IR will be assessed using uni- and multivariate correlation analysis. These novel studies will determine whether hypersecretion of adipocytokines by IA versus SC adipose tissue induces IR in patients with severe obesity.

Ages Eligible for Study:   18 Years to 65 Years   (Adult)
Sexes Eligible for Study:   Female
Accepts Healthy Volunteers:   No

Inclusion Criteria:

Enrolled in weight treatment program at Emory Bariatrics

Exclusion Criteria:

Male Smoker

  Contacts and Locations
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Please refer to this study by its identifier: NCT00275223

United States, Georgia
Emory University Hospital
Atlanta, Georgia, United States, 30322
Sponsors and Collaborators
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Principal Investigator: Nana Gletsu, Ph.D. Emory University
  More Information

Publications: Identifier: NCT00275223     History of Changes
Other Study ID Numbers: R03 DK67167 (completed)
Study First Received: January 10, 2006
Last Updated: March 17, 2010

Keywords provided by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK):
adipose tissue

Additional relevant MeSH terms:
Insulin Resistance
Glucose Metabolism Disorders
Metabolic Diseases processed this record on June 23, 2017