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Effect of Abdominal Obesity on Lipoprotein Metabolism

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

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.

Condition Intervention Phase
Insulin Resistance
Behavioral: Weight loss by dietary restriction
Phase 3

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
Official Title: Effect of Weight Loss on Lipoprotein Metabolism in Abdominal Obesity

Resource links provided by NLM:

Further study details as provided by The University of Western Australia:

Primary Outcome Measures:
  • Primary: Fractional catabolic and production rates of LDL-apoB and HDL-apoA-I (before and after 16 week treatments)

Secondary Outcome Measures:
  • Secondary: Cholesterol; Triglyceride; LDL-cholesterol; Adipocytokines; Genetic polymorphism

Estimated Enrollment: 40
Study Start Date: January 1995
Estimated Study Completion Date: December 1998
Detailed Description:
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.

Ages Eligible for Study:   18 Years to 65 Years   (Adult)
Sexes Eligible for Study:   Male
Accepts Healthy Volunteers:   Yes

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.
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Please refer to this study by its identifier: NCT00438061

Australia, Western Australia
Royal Perth Hospital
Perth, Western Australia, Australia, 6000
Sponsors and Collaborators
The University of Western Australia
Principal Investigator: Dick C Chan, PhD The University of Western Australia
Study Chair: Gerald F Watts, MD The University of Western Australia
  More Information Identifier: NCT00438061     History of Changes
Other Study ID Numbers: EC-256
Study First Received: February 20, 2007
Last Updated: February 23, 2007

Keywords provided by The University of Western Australia:
Lipoprotein metabolism
Cardiovascular disease

Additional relevant MeSH terms:
Insulin Resistance
Obesity, Abdominal
Nutrition Disorders
Body Weight
Signs and Symptoms
Glucose Metabolism Disorders
Metabolic Diseases
Lipid Metabolism Disorders processed this record on March 24, 2017