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.

Study Overview

• Status: Completed
• Conditions: Obesity; Insulin Resistance; Dyslipidemia
• Intervention / Treatment: Behavioral: Weight loss by dietary restriction

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.

• Study Type: Interventional
• Enrollment: 40
• Phase: Phase 3

Contacts and Locations

Study Locations

• Australia
  • Western Australia
    • Perth, Western Australia, Australia, 6000
      • Royal Perth Hospital

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 18 years to 65 years (Adult, Older Adult)
• Accepts Healthy Volunteers: Yes
• Genders Eligible for Study: Male

Description

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.

Study Plan

How is the study designed?

Design Details

• Primary Purpose: Treatment
• Allocation: Randomized
• Interventional Model: Parallel Assignment
• Masking: None (Open Label)

What is the study measuring?

Primary Outcome Measures

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

Secondary Outcome Measures

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

Collaborators and Investigators

• Sponsor: The University of Western Australia
• Investigators: Principal Investigator: Dick C Chan, PhD, The University of Western Australia; Study Chair: Gerald F Watts, MD, The University of Western Australia

Study record dates

Study Major Dates

• Study Start: January 1, 1995
• Study Completion: December 1, 1998

Study Registration Dates

• First Submitted: February 20, 2007
• First Submitted That Met QC Criteria: February 20, 2007
• First Posted (Estimate): February 21, 2007

Study Record Updates

• Last Update Posted (Estimate): February 26, 2007
• Last Update Submitted That Met QC Criteria: February 23, 2007
• Last Verified: February 1, 2007

More Information

Terms related to this study

• Keywords: Cardiovascular disease; Obesity; Lipoprotein metabolism
• Additional Relevant MeSH Terms: Glucose Metabolism Disorders; Metabolic Diseases; Overnutrition; Nutrition Disorders; Overweight; Body Weight; Hyperinsulinism; Lipid Metabolism Disorders; Obesity; Dyslipidemias; Insulin Resistance; Obesity, Abdominal
• Other Study ID Numbers: EC-256