Literature DB >> 19626358

Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver.

Laura G Sánchez-Lozada1, Wei Mu, Carlos Roncal, Yuri Y Sautin, Manal Abdelmalek, Sirirat Reungjui, MyPhuong Le, Takahiko Nakagawa, Hui Y Lan, Xuequing Yu, Richard J Johnson.   

Abstract

BACKGROUND: There is evidence that disaccharide sucrose produce a greater increase in serum fructose and triglycerides (TGs) than the effect produced by their equivalent monosaccharides, suggesting that long-term exposure to sucrose or fructose + glucose could potentially result in different effects. AIM OF THE STUDY: We studied the chronic effects of a combination of free fructose and glucose relative to sucrose on rat liver.
METHODS: Rats were fed either a combination of 30% fructose and 30% glucose (FG) or 60% sucrose (S). Control rats were fed normal rat chow (C). All rats were pair fed and were followed for 4 months. After killing, blood chemistries and liver tissue were examined.
RESULTS: Both FG-fed- and S-fed rats developed early features of metabolic syndrome when compared with C. In addition, both diets induced hepatic alterations, including variable increases in hepatic TG accumulation and fatty liver, an increase in uric acid content in the liver, as well as an increase in hepatic levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) measured in liver homogenates.
CONCLUSIONS: Diets containing 30% of fructose either as free fructose and glucose, or as sucrose, induce metabolic syndrome, intrahepatic accumulation of uric acid and TGs, increased MCP-1 and TNF-alpha as well as fatty liver in rats. It will be relevant to determine clinically whether pharmacological reduction in uric acid levels might have a therapeutic advantage in the treatment of non-alcoholic fatty liver disease.

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Year:  2009        PMID: 19626358      PMCID: PMC2805058          DOI: 10.1007/s00394-009-0042-x

Source DB:  PubMed          Journal:  Eur J Nutr        ISSN: 1436-6207            Impact factor:   5.614


  45 in total

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2.  Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

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3.  Serum-fructose levels after sucrose or its constituent monosaccharides.

Authors:  I Macdonald; L J Turner
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Review 4.  Nonalcoholic steatohepatitis: definition and pathology.

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6.  Fasting insulin and uric acid levels but not indices of iron metabolism are independent predictors of non-alcoholic fatty liver disease. A case-control study.

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7.  Triglyceride concentrations: the disaccharide effect.

Authors:  R G Thompson; J T Hayford; J A Hendrix
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8.  Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

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Journal:  J Clin Invest       Date:  2009-04-20       Impact factor: 14.808

9.  Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects.

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10.  Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2.

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Review 2.  Fructose and sugar: A major mediator of non-alcoholic fatty liver disease.

Authors:  Thomas Jensen; Manal F Abdelmalek; Shelby Sullivan; Kristen J Nadeau; Melanie Green; Carlos Roncal; Takahiko Nakagawa; Masanari Kuwabara; Yuka Sato; Duk-Hee Kang; Dean R Tolan; Laura G Sanchez-Lozada; Hugo R Rosen; Miguel A Lanaspa; Anna Mae Diehl; Richard J Johnson
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5.  Ketohexokinase C blockade ameliorates fructose-induced metabolic dysfunction in fructose-sensitive mice.

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Review 9.  Fructose and cardiometabolic disorders: the controversy will, and must, continue.

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Review 10.  Animal Models of Fibrosis in Nonalcoholic Steatohepatitis: Do They Reflect Human Disease?

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