Dyslipidemia, Insulin Resistance, Obesity
Conditions
Keywords
Lipoprotein metabolism, Cardiovascular disease, Obesity
Brief summary
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.
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.
Interventions
Sponsors
Study design
Eligibility
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.
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Primary: Fractional catabolic and production rates of LDL-apoB and HDL-apoA-I (before and after 16 week treatments) | — |
Secondary
| Measure | Time frame |
|---|---|
| Secondary: Cholesterol; Triglyceride; LDL-cholesterol; Adipocytokines; Genetic polymorphism | — |
Countries
Australia