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Effect of Abdominal Obesity on Lipoprotein Metabolism

This study has been completed.
Sponsor:
Information provided by:
The University of Western Australia
ClinicalTrials.gov Identifier:
NCT00438061
First received: February 20, 2007
Last updated: February 23, 2007
Last verified: February 2007

February 20, 2007
February 23, 2007
January 1995
Not Provided
Primary: Fractional catabolic and production rates of LDL-apoB and HDL-apoA-I (before and after 16 week treatments)
Same as current
Complete list of historical versions of study NCT00438061 on ClinicalTrials.gov Archive Site
Secondary: Cholesterol; Triglyceride; LDL-cholesterol; Adipocytokines; Genetic polymorphism
Same as current
Not Provided
Not Provided
 
Effect of Abdominal Obesity on Lipoprotein Metabolism
Effect of Weight Loss on Lipoprotein Metabolism in Abdominal Obesity

Abdominal obesity is strongly associated with dyslipidemia, which may account for the associated increased risk of atherosclerosis and coronary disease. Weight reduction is suggested to be a preferred and effective first-line strategy to correct lipid abnormalities, particularly in overweight/obese subjects. This improvement may be related to the effect of reduction in abdominal fat mass on apoB and apoA-I metabolism, but this remains to be fully demonstrated.

Hypothesis: Reduction in abdominal fat mass by weight loss decreases apoB concentration and raises HDL-cholesterol chiefly by increasing LDL-apoB fractional catabolic rate (FCR), as well as decreasing HDL apoA-I, respectively.

We examined the mechanism of the effect of weight loss through dieting on LDL and HDL metabolism in abdominally obese men. LDL apoB-100 and HDL apoA-I kinetics were studied using a primed-constant infusion of 1-[13C]-leucine in a controlled, dietary intervention trial of 16 weeks duration in middle-aged, obese men with the metabolic syndrome. Isotopic enrichment in apoB and apoA-I was measured by gas chromatography-mass spectrometry and fractional turnover rates estimated using multi-compartmental modelling.

Interventional
Phase 3
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
  • Obesity
  • Dyslipidemia
  • Insulin Resistance
Behavioral: Weight loss by dietary restriction
Not Provided
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
40
December 1998
Not Provided

Inclusion Criteria:

  • Obesity was defined as a body mass index (BMI) >28kg/m2 and visceral visceral obesity (waist to hip ratio> 1.0 or waist circumference >100 cm)

Exclusion Criteria:

  • Diabetes mellitus,
  • Proteinuria,
  • Hypothyroidism,
  • Abnormal liver enzymes,
  • Major systemic illness,
  • A history of alcohol abuse,
  • A family history of hyperlipidemia or premature coronary artery disease or were taking medication known to affect lipid metabolism.
Male
18 Years to 65 Years
Yes
Contact information is only displayed when the study is recruiting subjects
Australia
 
NCT00438061
EC-256
Not Provided
Not Provided
The University of Western Australia
Not Provided
Principal Investigator: Dick C Chan, PhD The University of Western Australia
Study Chair: Gerald F Watts, MD The University of Western Australia
The University of Western Australia
February 2007

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