N/A N=51 Randomized Single-blind Treatment

Obesity and Nonalcoholic Fatty Liver Disease

Non-alcoholic Fatty Liver Disease

Bottom Line

View on ClinicalTrials.gov: NCT00262964 ↗

Enrolled (actual)

Serious AEs

0.0%

Results posted

Jun 2010

Primary outcome: Primary: Hepatic Insulin Sensitivity Index (HISI) — 0.8; 1.4 [10000/(μmol/min)x(mU/L)] — p=<0.019

Study Design & Population

Study type: Interventional
Phase: N/A
Interventions: Niacin (Drug); fenofibrate (Drug); placebo (Drug)
Age: Adult · 18+ yrs
Sex: All
Sponsor: Washington University School of Medicine
Primary completion: Dec 2008

Outcome Measures

Outcome	Result	p-value
PRIMARY Hepatic Insulin Sensitivity Index (HISI)	0.8; 1.4	<0.019 sig
PRIMARY Percent Increase in Skeletal Muscle Insulin Sensitivity During Insulin Infusion.	173; 303	<0.001 sig
PRIMARY Adipose Tissue Insulin Sensitivity	66; 75	<0.002 sig
PRIMARY Hepatic Fat Content for Fenofibrate and Niacin Groups	23.2; 21.0; 23.6; 19.7	.301
PRIMARY Adipose Tissue Insulin Sensitivity in Fenofibrate and Niacin Groups	68; 63; 69; 35	.768
PRIMARY Change From Baseline in Skeletal Muscle Insulin Sensitivity	188; 183; 169; 142	.318
PRIMARY Change From Baseline in Hepatic Insulin Sensitivity Index	0.7; 0.8; 0.8; 0.5	.419
SECONDARY Very Low Density Lipoprotein - Triglyceride Production Rate	6.7; 3.8	<0.001 sig
SECONDARY Change From Baseline in Very Low Density Lipoprotein Apolipoprotein B Production Rate	0.5; 0.4; 0.4; 0.4	0.708
SECONDARY Change From Baseline in VLDL-Tg Clearance Rate	35; 34; 56; 52	.020 sig
SECONDARY Change From Baseline in VLDL-Tg Production Rate	6.4; 7.7; 6.0; 4.5	0.758
SECONDARY Change From Baseline in Very Low-density Lipoprotein Triglyceride Concentration	1.09; 1.04; 0.50; 0.64	.024 sig

Summary

The primary goal of this study is to provide a better understanding of: 1) the pathogenesis and pathophysiology of non-alcoholic fatty liver disease (NAFLD) in obese subjects, and 2) the effect of marked weight loss on the histologic and metabolic abnormalities associated with NAFLD. The following hypotheses will be tested: 1. obesity causes hepatic fat accumulation because of excessive fatty acid release from fat tissue and increased free fatty acid availability, 2. increased hepatic (liver) fat content causes insulin-resistant glucose (sugar) production by the liver and altered liver protein synthesis, 3. increased hepatic fat content causes increased lipid (fat) peroxidation, hepatic inflammation, necrosis and fibrosis, and 4. marked weight loss improves NAFLD once patients are weight stable.

Eligibility Criteria

Inclusion Criteria

All

18 - 45 years old
Class I obesity, i.e. Body Mass Index (BMI) between 30 and 45.
weight less than 300 lbs.

Exclusion Criteria

Active or previous infection with hepatitis B or C, as well as other liver disease.
History of alcohol abuse
Diabetes
Medications that cause liver damage or steatosis.
Women who are pregnant or lactating.

View full record on ClinicalTrials.gov →

Data sourced from ClinicalTrials.gov (NCT00262964). Outcome figures and adverse-event rates are extracted automatically from the registry's posted results and are provided for clinician reference, not as a substitute for the primary publication.