PubMed ID:
20301112
Public Release Type:
Journal
Publication Year: 2010
Affiliation: Division of Gastroenterology, Duke University, Durham, NC 27710, USA. manal.abdelmalek@duke.edu
DOI:
https://doi.org/10.1002/hep.23535
Authors:
Hoofnagle J,
Vuppalanchi R,
Chalasani N,
Kleiner D,
Abdelmalek MF,
Abdelmalek MF,
Abrams S,
Ackermann S,
Aouizerat B,
Arceo D,
Bambha K,
Barlow S,
Bass NM,
Behling C,
Belt P,
Bhimalli P,
Boyett S,
Brancati FL,
Brunt EM,
Byam E,
Clark JM,
Clark L,
Coffey M,
Colvin R,
Colvin R,
Contos MJ,
Cummings OW,
Dasarathy S,
Derdoy J,
Diehl AM,
Diehl AM,
Donithan M,
Doo E,
Durelle J,
Espinosa D,
Everhart J,
Fairly LA,
Ferrell LD,
Filipowski D,
Fuchs M,
Gottfried M,
Grave GD,
Green M,
Guy C,
Guy C,
Hassanein T,
Hawkins C,
Hoffmann J,
Hollick R,
Huang TT,
Isaacson M,
Johnson RJ,
Jones A,
Killenberg P,
Kim W,
King D,
Klipsch A,
Kowdley KV,
Kwan S,
Lavine JE,
Lee L,
Liu YC,
Luketic VA,
Lydecker A,
Mann P,
McCullough A,
Mendoza S,
Merriman R,
Miriel L,
Mohan P,
Molleston J,
Mooney J,
Morris A,
Murray K,
Nair K,
Nelson J,
Nonalcoholic Steatohepatitis Clinical Research Network,
Pabst M,
Palomares Z,
Pan YP,
Pfeifer K,
Piercy D,
Ragozzino L,
Robuck PR,
Rosenthal M,
Rosenthal P,
Sandhu B,
Sanyal AJ,
Sargeant C,
Sargent R,
Saunders C,
Scheimann A,
Schwimmer JB,
Seeff L,
Selph K,
Siegner J,
Sirlin C,
Smith M,
Stager M,
Steel T,
Stein T,
Sternberg A,
Stewart S,
Subbarao G,
Suzuki A,
Tetri BA,
Thompson J,
Tonascia J,
Torbenson M,
Trinh V,
Unalp-Arida A,
Unalp-Arida A,
Van Natta M,
Wang C,
White M,
Wilson L,
Yates K,
Yeh M,
Young M
Studies:
Nonalcoholic Steatohepatitis Clinical Research Network
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 x 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 (> or =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 > or = 48 years), daily fructose consumption was associated with increased hepatic inflammation (P < 0.05) and hepatocyte ballooning (P = 0.05).