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Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease
Author(s) -
Abdelmalek Manal F.,
Suzuki Ayako,
Guy Cynthia,
UnalpArida Aynur,
Colvin Ryan,
Johnson Richard J.,
Diehl Anna Mae
Publication year - 2010
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.23535
Subject(s) - medicine , fructose , nonalcoholic fatty liver disease , fatty liver , endocrinology , diabetes mellitus , steatosis , gastroenterology , hypertriglyceridemia , hyperuricemia , body mass index , uric acid , cholesterol , disease , triglyceride , biology , food science
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. H EPATOLOGY 2010