Steatohepatitis/Metabolic Liver Disease

You have full text access to this OnlineOpen article

Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease†

  1. Manal F. Abdelmalek1,‡,*,
  2. Ayako Suzuki1,
  3. Cynthia Guy2,
  4. Aynur Unalp-Arida3,
  5. Ryan Colvin3,
  6. Richard J. Johnson4,
  7. Anna Mae Diehl1,
  8. for the Nonalcoholic Steatohepatitis Clinical Research Network1

Article first published online: 28 JAN 2010

DOI: 10.1002/hep.23535

Issue

Hepatology

Hepatology

Volume 51, Issue 6, pages 1961–1971, June 2010

Additional Information

How to Cite

Abdelmalek, M. F., Suzuki, A., Guy, C., Unalp-Arida, A., Colvin, R., Johnson, R. J., Diehl, A. M. and for the Nonalcoholic Steatohepatitis Clinical Research Network (2010), Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease. Hepatology, 51: 1961–1971. doi: 10.1002/hep.23535

Author Information

  1. 1

    Division of Gastroenterology, Duke University, Durham, NC

  2. 2

    Department of Pathology, Duke University, Durham, NC

  3. 3

    NASH Clinical Research Network Data Coordinating Center, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD

  4. 4

    Division of Renal Diseases and Hypertension, University of Colorado, Denver, CO

  1. ‡

    fax: 919-684-8857

*Duke University Medical Center, Division of Gastroenterology, P.O. Box 3913, Durham, NC 27710

  1. †

    Potential conflict of interest: R.J.J.: Published a lay book “The Sugar Fix” that discusses the potential role of fructose in obesity and fatty liver and has a patent application on lowering uric acid to reduce fatty liver disease. All other authors have no conflict of interest.

  2. ‡

    fax: 919-684-8857

Publication History

  1. Issue published online: 23 MAY 2010
  2. Article first published online: 28 JAN 2010
  3. Accepted manuscript online: 28 JAN 2010 12:00AM EST
  4. Manuscript Accepted: 5 JAN 2010
  5. Manuscript Received: 29 SEP 2009

Funded by

  • The Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN)
  • National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Grant Numbers: U01DK061718, U01DK061728, U01DK061731, U01DK061732, U01DK061734, U01DK061737, U01DK061738, U01DK061730, U01DK061713
  • National Institute of Child Health and Human Development (NICHD)
  • General Clinical Research Centers or Clinical and Translational Science Awards in conduct of NASH CRN Studies. Grant Numbers: UL1RR024989, M01RR000750, M01RR00188, UL1RR02413101, M01RR000827, UL1RR02501401, M01RR000065, M01RR020359

SEARCH

SEARCH BY CITATION

ARTICLE TOOLS

View Full Article (HTML) Get PDF (209K)

Abstract

The rising incidence of obesity and diabetes coincides with a marked increase in fructose consumption. Fructose consumption is higher in individuals with nonalcoholic fatty liver disease (NAFLD) than in age-matched and body mass index (BMI)-matched controls. Because fructose elicits metabolic perturbations that may be hepatotoxic, we investigated the relationship between fructose consumption and disease severity in NAFLD. We studied 427 adults enrolled in the NASH Clinical Research Network for whom Block food questionnaire data were collected within 3 months of a liver biopsy. Fructose consumption was estimated based on reporting (frequency × amount) of Kool-aid, fruit juices, and nondietary soda intake, expressed as servings per week, and classified into none, minimum to moderate (<7 servings/week), and daily (≥7 servings/week). The association of fructose intake with metabolic and histological features of NAFLD was analyzed using multiple linear and ordinal logistic regression analyses with and without controlling for other confounding factors. Increased fructose consumption was univariately associated with decreased age (P < 0.0001), male sex (P < 0.0001), hypertriglyceridemia (P < 0.04), low high-density lipoprotein (HDL) cholesterol (<0.0001), decreased serum glucose (P < 0.001), increased calorie intake (P < 0.0001), and hyperuricemia (P < 0.0001). After controlling for age, sex, BMI, and total calorie intake, daily fructose consumption was associated with lower steatosis grade and higher fibrosis stage (P < 0.05 for each). In older adults (age ≥ 48 years), daily fructose consumption was associated with increased hepatic inflammation (P < 0.05) and hepatocyte ballooning (P = 0.05). Conclusion: In patients with NAFLD, daily fructose ingestion is associated with reduced hepatic steatosis but increased fibrosis. These results identify a readily modifiable environmental risk factor that may ameliorate disease progression in patients with NAFLD. HEPATOLOGY 2010

View Full Article (HTML) Get PDF (209K)