In this issue, the review by Lustig, “Fructose: Metabolic, Hedonic, and Societal Parallels
with Ethanol” (
1
), contains a juxtaposition of information on metabolic, inflammatory, and hormonal
pathways from which the author suggests “parallelism” between fructose and ethanol.
The major premise of the review is that neither ethanol nor fructose provokes a satiety
signal (insulin or leptin), so feedback on the consumption of these nutrients is lacking,
leading to hedonic and societal consequences. The author further draws the parallel
between alcoholic fatty liver disease (AFLD) and nonalcoholic fatty liver disease
(NAFLD). He suggests the metabolic consequences of fructose and ethanol are also “parallel”
based on similarities in signaling pathways associated with the steatohepatitis that
results from excess intake of these nutrients. Similar arguments have been advanced
in another recently published review by Lustig's group (
2
).To read this article in full you will need to make a payment
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References
- Fructose: Metabolic, hedonic, and societal parallels with ethanol.J Am Diet Assoc. 2010; 110: 1307-1321
- The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome.Nat Rev Gastroenterol Hepatol. 2010; 7: 251-264
- Dietary fructose consumption among US children and adults: The Third National Health and Nutrition Examination Survey.Medscape J Med. 2008; 10: 160
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- Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Full Report.National Institutes of Health, Bethesda, MD2001 (NIH publication No. 01-3670)
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- Alcoholic fatty liver: Its pathogenesis and mechanism of progression to inflammation and fibrosis.Alcohol. 2004; 34: 9-19
- Folate deficiency, methionine metabolism, and alcoholic liver disease.Alcohol. 2002; 27: 169-172
- Elevated plasma homocysteine concentrations as a predictor of steatohepatitis in patients with non-alcoholic fatty liver disease.J Gastroenterol Hepatol. 2005; 20: 1448-1455
- Dietary sucrose is essential to the development of liver injury in the MCD model of steatohepatitis.J Lipid Res. 2009; 50: 2072-2082
- Mice deficient in cystathionine beta-synthase: Animal models for mild and severe homocyst(e)inemia.Proc Natl Acad Sci U S A. 1995; 92: 1585-1589
- De novo lipogenesis, lipid kinetics, and whole-body lipid balances in humans after acute alcohol consumption.Am J Clin Nutr. 1999; 70: 928-936
- Ethanol diversely alters palmitate, stearate, and oleate metabolism in the liver and pancreas of rats using the deuterium oxide single tracer.Pancreas. 2009; 38: e47-e52
- Alcoholism: Genes and mechanisms.Pharmacogenomics. 2004; 5: 1037-1048
Biography
L. O. Byerley is an associate professor, research, Department of Physiology, Louisiana State University Health Science Center, New Orleans.
Biography
W.-N. P. Lee is a professor, Department of Pediatrics, Endocrinology and Metabolism, Harbor-UCLA Medical Center, Torrance, CA.
Article info
Publication history
Accepted:
May 20,
2010
Identification
Copyright
© 2010 American Dietetic Association. Published by Elsevier Inc. All rights reserved.
