INCREASED FRUCTOSE CONSUMPTION IS ASSOCIATED WITH FIBROSIS SEVERITY IN PATIENTS WITH NAFLD

By M. Abdelmalek, A. Suzuki, C. Guy, A. Unalp-arida, R. Colvin, Richard J. Johnson, Anna Mae Diehl. Hepatology, 2010

734 citations recorded by the source corpus.

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

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/c6309fc9ccb3a2507cbbe9ac600f4fa1c9d121b6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology, Diabetes and Metabolism

1. M. Pinzani
2. Herbert Tilg
3. E. Tsochatzis
4. E. Buzzetti
5. A. Moschen

In Epidemiology

1. Herbert Tilg
2. M. Pinzani
3. A. Moschen
4. Shira Zelber-Sagi
5. E. Tsochatzis
6. A. Diehl
7. E. Buzzetti
8. G. Targher

In Pathology and Forensic Medicine

1. Shira Zelber-Sagi
2. M. Pinzani
3. Herbert Tilg

Citations in the corpus

• Role of Dietary Fructose and Hepatic de novo Lipogenesis in Fatty Liver Disease (2016, background): “Furthermore, increased fructose intake in humans has been linked with progression of liver disease to fibrosis [88], while fructose restriction leads to improvement in NAFLD [89–91].”
• Treatment of NAFLD with diet, physical activity and exercise. (2017, background): “In an observational study, fructose-containing soft drinks were also demonstrated to be associated with more severe fibrosis in NAFLD patients if consumed on a daily basis.(68) Taken together, these findings imply that, like alcohol, questions regarding SSB consumption should be part of the patient’”
• The severity of NAFLD is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota (2016, background): “Fructose has been associated with increased liver inflammation and fibrosis in NAFLD patients.((36)) Hence, Bacteroides-associated increases in deoxycholic acid, raffinose, and stachyose are predicted to promote NASH, whereas decreased SCFAs might be detrimental for NAFLD.”
• Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Daily fructose consumption is associated with increased hepatic inflammation and fibrosis in humans.(32) The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor sensing xenotoxicants such as dioxin.”
• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “In patients with NAFLD, daily fructose ingestion is associated with increased fibrosis [122] and it has been suggested that this”