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Obesity, Weight Loss, and Cardiovascular Disease Risk

This study is enrolling participants by invitation only.
Sponsor:
Information provided by (Responsible Party):
Tracey McLaughlin, Stanford University
ClinicalTrials.gov Identifier:
NCT00186459
First received: September 13, 2005
Last updated: March 12, 2013
Last verified: March 2013

September 13, 2005
March 12, 2013
October 2000
Not Provided
Weight loss [ Designated as safety issue: No ]
1. Weight loss
Complete list of historical versions of study NCT00186459 on ClinicalTrials.gov Archive Site
  • Lipid/lipoprotein changes [ Designated as safety issue: No ]
  • Blood pressure changes [ Designated as safety issue: No ]
  • Insulin resistance changes [ Designated as safety issue: No ]
  • Endothelial function changes [ Designated as safety issue: No ]
  • 1. Lipid/lipoprotein changes
  • 2. Blood pressure changes
  • 3. Insulin resistance changes
  • 4. Endothelial function changes
Not Provided
Not Provided
 
Obesity, Weight Loss, and Cardiovascular Disease Risk
GCRC-CAP-Tracey McLaughlin, MD

The goal of the study is to define the roles played by resistance to insulin-mediated glucose disposal (insulin resistance) and circulating plasma insulin concentrations in: 1) ability to lose weight; 2) reduction of risk for coronary heart disease as a result of weight loss. We hypothesize that in the setting of caloric restriction, manipulating endogenous insulin concentrations will not alter ability of subjects to lose weight, but will lead to different reduction in CHD risk factors. To test this hypothesis, two parallel studs will be performed. First, obese insulin-resistant individuals will be randomized to one of two equally-hypocaloric diets that vary moderately in proportion of carbohydrate and mono/polyunsaturated fats (lower carbohydrate diet will be associated with greater reduction in endogenous insulin secretion). Second, diabetics treated with insulin secretagogues will be compared to diabetics treated with insulin sensitizers with respect to the same outcomes (secretagogues increase insulin secretion and insulin sensitizers decrease insulin concentrations). Endpoints include weight loss, change in insulin resistance, blood pressure, lipid and lipoproteins, markers of endothelial function, daylong insulin and glucose concentrations: these will be compared, in each of the parallel studies, between the group with insulin-stimulating intervention vs the group with the insulin-sparing intervention.

While obesity, insulin resistance, and diabetes are highly associated, it is not clear whether insulin resistance and compensatory hyperinsulinemia play important roles in the tendency to gain weight and/or inability to lose weight. The role of hyperinsulinemia in coronary heart disease (CHD)is also unclear. The specific aims of the proposed research are as follows:

  1. To compare insulin resistant versus insulin sensitive nondiabetic overweight individuals with respect to their ability to lose weight on a low calorie diet. CHD risk factors before and after weight loss will also be assessed to determine the degree to which insulin resistance is associated with CHD risk, as well as the impact that differences in insulin resistance have on the metabolic benefits of weight loss
  2. To determine if weight loss and its associated metabolic benefits vary as a function of the relative amounts of dietary fat and carbohydrate in hypocaloric diets. Because high carbohydrate diets increase insulin secretion, the relationship between dietary composition and change in circulating insulin concentrations will be analyzed with respect to both weight loss and CHD risk factors.
  3. To quantify and compare the improvement in glycemic control and CHD risk factors associated with weight loss in obese type 2 diabetics, while being treated with 1) an insulin secretagogue (sulfonylurea) or 2) an insulin sensitizer (thiazolidinedione). Manipulation of plasma insulin concentrations with these medications will provide a mechanism by which to evaluate the impact of circulating insulin concentrations on the described outcome measures.
  4. A subgroup of overweight/obese premenopausal women with PCOS will be studied using two diets in crossover design with regard to macronutrient effects on endogenous hyperinsulinism. For this subgroup age range will be 18-50 years, BMI 25-50 kg/m2.
  5. In order to increase our data and therefore increase our better understanding of fat cells and insulin resistance and changes in fat cells with weight loss we would like to increase our participant enrollment to 550 all to be enrolled at Stanford University Medical Center recruiting Bariatric participants:

Age for Bariatric patients 30-65 men and women BMI 27-no upper limit Currently we have completed all participants except the bariatric and post bariatric population and those with hypoglycemia following bariatric surgery.

The ethnic background of subjects reflects Stanford's patient population.

Interventional
Not Provided
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Prevention
Obesity
Behavioral: Hypocaloric diet of varying macronutrient composition
Not Provided
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Enrolling by invitation
550
Not Provided
Not Provided

Inclusion Criteria:

  • BMI 30-35
  • age 35-65
  • nondiabetic by fasting plasma glucose concentration
  • no active major organ diseases
  • insulin resistant or insulin sensitive

Exclusion Criteria:

  • anemia
  • pregnant
  • major organ disease
  • active malignancy
  • eating disorder
  • active psychiatric illness
  • chronic inflammatory conditions
Both
18 Years to 65 Years
Yes
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00186459
RR16071-01
Not Provided
Tracey McLaughlin, Stanford University
Stanford University
Not Provided
Principal Investigator: Dr Tracey Lynn McLaughlin Stanford University
Stanford University
March 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP