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Plasminogen activator inhibitor-1 predicts quantity of hepatic steatosis independent of insulin resistance and body weight

  • Jeffrey R. Holzberg
  • , Ran Jin
  • , Ngoc Anh Le
  • , Thomas R. Ziegler
  • , Elizabeth M. Brunt
  • , Craig J. Mcclain
  • , Juna V. Konomi
  • , Gavin E. Arteel
  • , Miriam B. Vos

Research output: Contribution to journalArticlepeer-review

Abstract

Objective: The aim of the present study was to examine the association between plasminogen activator inhibitor-1 (PAI-1), an acute phase protein strongly associated with cardiovascular disease risk, and adiposity, insulin resistance, and inflammation among overweight and obese children with a wide range of hepatic steatosis. Methods: Plasma PAI-1 levels were measured in a prospectively recruited cohort of 39 overweight or obese children who underwent comprehensive anthropometric assessment and metabolic measurements. Hepatic steatosis was quantified using magnetic resonance spectroscopy and participants were divided into 3 groups based on whether they had normal hepatic steatosis (<5%), low hepatic steatosis (≥5%-10%), and high hepatic steatosis (>10%). Results: Plasma PAI-1 levels significantly increased across the severity of hepatic steatosis in overweight and obese children, and this association was independent of body mass index z score, visceral fat, insulin resistance, and inflammatory markers (P<0.05). Conclusion: Hepatic steatosis in children is positively associated with circulating levels of PAI-1 independent of body mass index, insulin resistance, and inflammatory markers. Further studies are needed to clarify the potential role of PAI-1 as a therapeutic target in pediatric nonalcoholic fatty liver disease.

Original languageEnglish
Pages (from-to)819-823
Number of pages5
JournalJournal of pediatric gastroenterology and nutrition
Volume62
Issue number6
DOIs
StatePublished - Jun 1 2016

Keywords

  • cardiovascular disease risk
  • children
  • insulin resistance
  • nonalcoholic fatty liver disease
  • plasminogen activator inhibitor-1

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