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Fructose consumption as a risk factor for non-alcoholic fatty liver disease.
J Hepatol 2008; 48(6):993-9JH

Abstract

BACKGROUND/AIMS

While the rise in non-alcoholic fatty liver disease (NAFLD) parallels the increase in obesity and diabetes, a significant increase in dietary fructose consumption in industrialized countries has also occurred. The increased consumption of high fructose corn syrup, primarily in the form of soft drinks, is linked with complications of the insulin resistance syndrome. Furthermore, the hepatic metabolism of fructose favors de novo lipogenesis and ATP depletion. We hypothesize that increased fructose consumption contributes to the development of NAFLD.

METHODS

A dietary history and paired serum and liver tissue were obtained from patients with evidence of biopsy-proven NAFLD (n=49) without cirrhosis and controls (n=24) matched for gender, age (+/-5 years), and body mass index (+/-3 points).

RESULTS

Consumption of fructose in patients with NAFLD was nearly 2- to 3-fold higher than controls [365 kcal vs 170 kcal (p<0.05)]. In patients with NAFLD (n=6), hepatic mRNA expression of fructokinase (KHK), an important enzyme for fructose metabolism, and fatty acid synthase, an important enzyme for lipogenesis were increased (p=0.04 and p=0.02, respectively). In an AML hepatocyte cell line, fructose resulted in dose-dependent increase in KHK protein and activity.

CONCLUSIONS

The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption.

Authors+Show Affiliations

Division of Nephrology, University of Florida, Gainesville, FL, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18395287

Citation

Ouyang, Xiaosen, et al. "Fructose Consumption as a Risk Factor for Non-alcoholic Fatty Liver Disease." Journal of Hepatology, vol. 48, no. 6, 2008, pp. 993-9.
Ouyang X, Cirillo P, Sautin Y, et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol. 2008;48(6):993-9.
Ouyang, X., Cirillo, P., Sautin, Y., McCall, S., Bruchette, J. L., Diehl, A. M., ... Abdelmalek, M. F. (2008). Fructose consumption as a risk factor for non-alcoholic fatty liver disease. Journal of Hepatology, 48(6), pp. 993-9. doi:10.1016/j.jhep.2008.02.011.
Ouyang X, et al. Fructose Consumption as a Risk Factor for Non-alcoholic Fatty Liver Disease. J Hepatol. 2008;48(6):993-9. PubMed PMID: 18395287.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fructose consumption as a risk factor for non-alcoholic fatty liver disease. AU - Ouyang,Xiaosen, AU - Cirillo,Pietro, AU - Sautin,Yuri, AU - McCall,Shannon, AU - Bruchette,James L, AU - Diehl,Anna Mae, AU - Johnson,Richard J, AU - Abdelmalek,Manal F, Y1 - 2008/03/10/ PY - 2007/12/18/received PY - 2008/02/01/revised PY - 2008/02/01/accepted PY - 2008/4/9/pubmed PY - 2008/9/24/medline PY - 2008/4/9/entrez SP - 993 EP - 9 JF - Journal of hepatology JO - J. Hepatol. VL - 48 IS - 6 N2 - BACKGROUND/AIMS: While the rise in non-alcoholic fatty liver disease (NAFLD) parallels the increase in obesity and diabetes, a significant increase in dietary fructose consumption in industrialized countries has also occurred. The increased consumption of high fructose corn syrup, primarily in the form of soft drinks, is linked with complications of the insulin resistance syndrome. Furthermore, the hepatic metabolism of fructose favors de novo lipogenesis and ATP depletion. We hypothesize that increased fructose consumption contributes to the development of NAFLD. METHODS: A dietary history and paired serum and liver tissue were obtained from patients with evidence of biopsy-proven NAFLD (n=49) without cirrhosis and controls (n=24) matched for gender, age (+/-5 years), and body mass index (+/-3 points). RESULTS: Consumption of fructose in patients with NAFLD was nearly 2- to 3-fold higher than controls [365 kcal vs 170 kcal (p<0.05)]. In patients with NAFLD (n=6), hepatic mRNA expression of fructokinase (KHK), an important enzyme for fructose metabolism, and fatty acid synthase, an important enzyme for lipogenesis were increased (p=0.04 and p=0.02, respectively). In an AML hepatocyte cell line, fructose resulted in dose-dependent increase in KHK protein and activity. CONCLUSIONS: The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption. SN - 0168-8278 UR - https://www.unboundmedicine.com/medline/citation/18395287/Fructose_consumption_as_a_risk_factor_for_non_alcoholic_fatty_liver_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0168-8278(08)00164-5 DB - PRIME DP - Unbound Medicine ER -