Faculty Collaboration Database

Alterations in fatty acid kinetics in obese adolescents with increased intrahepatic triglyceride content. Obesity (Silver Spring) 2009 Jan;17(1):25-9

Date

10/25/2008

Pubmed ID

18948971

Pubmed Central ID

PMC2649753

DOI

10.1038/oby.2008.494

Scopus ID

2-s2.0-57949116523 (requires institutional sign-in at Scopus site)   75 Citations

Abstract

OBJECTIVE: It has been hypothesized that excessive fatty acid availability contributes to steatosis and the metabolic abnormalities associated with nonalcoholic fatty liver disease (NAFLD). The purpose of this study was to evaluate whether adipose tissue lipolytic activity and the rate of fatty acid release into plasma are increased in obese adolescents with NAFLD.

METHODS: Palmitate kinetics were determined in obese adolescents with normal (n = 9; BMI = 37 +/- 2 kg/m(2); intrahepatic triglyceride (IHTG) <or=5.5% of liver volume) and increased (n = 9; BMI = 36 +/- 2 kg/m(2); IHTG >or= 10% of liver volume) IHTG content during the basal state (postabsorptive condition) and during physiological hyperinsulinemia (postprandial condition). Both groups were matched on body weight, BMI, percent body fat, age, sex, and Tanner stage. The hyperinsulinemic-euglycemic clamp procedure, in conjunction with a deuterated palmitate tracer infusion, was used to determine free-fatty acid (FFA) kinetics, and magnetic resonance spectroscopy was used to determine IHTG content.

RESULTS: The rate of whole-body palmitate release into plasma was greater in subjects with NAFLD than those with normal IHTG content during basal conditions, (87 +/- 7 vs. 127 +/- 13 micromol/min; P < 0.01) and during physiological hyperinsulinemia, (24 +/- 2 vs. 44 +/- 8 micromol/min; P < 0.01).

DISCUSSION: These results demonstrate that adipose tissue lipolytic activity is increased in obese adolescents with NAFLD and results in an increase in the rate of fatty acid release into plasma throughout the day. This continual excess in fatty acid flux supports the hypothesis that adipose insulin resistance is involved in the pathogenesis of steatosis and contributes to the metabolic complications associated with NAFLD.

Author List

Fabbrini E, deHaseth D, Deivanayagam S, Mohammed BS, Vitola BE, Klein S

Author

Bernadette Vitola MD, MPH Associate Professor in the Pediatrics department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Abdomen
Adipose Tissue
Adolescent
Body Composition
Body Mass Index
Fatty Liver
Female
Glucose Clamp Technique
Humans
Hyperinsulinism
Liver
Magnetic Resonance Imaging
Male
Obesity
Palmitic Acid
Skin
Triglycerides