Regulation of Lipoprotein Metabolism in Obese Men

Obesity Clinical Trial

Official title:

Effect of Atorvastatin and Fish Oils on Lipoprotein Metabolism in Visceral Obesity

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00392717
• Other study ID #: EC-576
• Status: Completed
• Phase: Phase 3
• First received: October 25, 2006
• Last updated: October 25, 2006
• Start date: February 1998
• Est. completion date: March 2002

Study information

• Verified date: October 2006
• Source: The University of Western Australia
• Contact: n/a
• Is FDA regulated: No
• Health authority: Australia: Human Research Ethics Committee
• Study type: Interventional

Clinical Trial Summary

Visceral obesity is strongly associated with dyslipidaemia (hypertriglyceridaemia, low HDL-cholesterol and mildly elevated LDL-cholesterol) and insulin resistance, key characteristics of metabolic syndrome (MetS). Recent evidence has clearly established that the risk of CVD is increased in subjects with the MetS. The precise reason for this remains unclear, but appears to be closely related with dyslipidaemia. Effective management of dyslipidaemia is important to reduce the risk of CVD in these subjects.

Hypothesis: Inhibition of hepatic cholesterol synthesis by statins and triglyceride synthesis by fish oils improve lipoprotein metabolism in visceral obese men.

Description:

The study employed a factorial study design, stable isotopy and mathematical modelling to examine the independent and combined effects of decreasing cholesterol substrate availability with atorvastatin and decreasing triglyceride substrate availability with fish oils on lipoprotien kinetics (apoB, apoA, apoC-III and chylomicron remnants) in insulin-resistant men with visceral obesity.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 48
• Est. completion date: March 2002
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Male
• Age group: 20 Years to 70 Years

Eligibility

Inclusion Criteria:

• Obesity was defined as a waist circumference >100 cm, waist:hip ratio >0.97 and BMI >29 kg/m2.

• Subjects were selected for having insulin-resistance, defined as a homostasis model assessment (HOMA) score (21) >5.1 (i.e. one SD above the mean for a reference population of 22 lean, normolipidemic healthy males of similar age).

• All subjects had plasma triglyceride >1.2 mmol/L and cholesterol >5.2 mmol/L at screening while consuming ad libitum, weight-maintaining diets

Exclusion Criteria:

• diabetes mellitus, apolipoprotein E2/E2 genotype, macroproteinuria, creatinemia, hypothyrodism, or abnormal liver enzymes.

• Subjects did not consume fish oil supplements or drank more than 30g alcohol/day.

• None reported a history of CVD, or was taking medication or other agents known to affect lipid metabolism.

Study Design

Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Factorial Assignment, Masking: Double-Blind, Primary Purpose: Treatment

Related Conditions & MeSH terms

• Dyslipidemia
• Dyslipidemias
• Insulin Resistance
• Obesity

Intervention

Drug:
• Atorvastatin

• Fish oils

Locations

Country	Name	City	State
Australia	Royal Perth Hospital	Perth	Western Australia

Sponsors (1)

Lead Sponsor	Collaborator
The University of Western Australia

Country where clinical trial is conducted

Australia, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Fractional catabolic rate of apoB, apoA, apoC-III and chylomicron remnants (before and after 6 week treatments)
Primary	Production rate of apoB, apoA, apoC-III and chylomicron remnants (before and after 6 week treatments)
Secondary	Cholesterol
Secondary	Triglyceride
Secondary	LDL-cholesterol
Secondary	Adipocytokines
Secondary	Genetic polymorphisms