The role of fructose-enriched diets in mechanisms of nonalcoholic fatty liver disease

Nomura, Kyoko; Yamanouchi, Toshikazu

doi:10.1016/j.jnutbio.2011.09.006

Cited by 185 publications

(163 citation statements)

References 89 publications

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“…In humans, the increase of fructose consumption is strongly associated with a steady increase in obesity, insulin resistance, and other metabolic syndromes. 44,45 In addition, several studies in humans and mice suggest that fructose and glucose, the most common dietary sugars, are absorbed in distinct regions of the gastrointestinal tract and metabolized differently, 46,47 and that fructose and glucose affect brain activity and feeding behavior in a disparate manner. 48,49 Thus, it will be interesting to see whether this sugar-and a specific receptor for it-plays also a role in nutrient sensing in mammals.…”

Section: Corazonin Is the Likely Neurotransmitter In Gr43amentioning

confidence: 99%

Diverse roles for theDrosophilafructose sensor Gr43a

Miyamoto

Amrein

2013

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Section: Corazonin Is the Likely Neurotransmitter In Gr43amentioning

confidence: 99%

Diverse roles for theDrosophilafructose sensor Gr43a

Miyamoto

Amrein

2013

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“…Soft drink consumption was associated with NAFLD independent of metabolic syndrome [Abid et al, 2009] or in the absence of traditional risk factors, including obesity, diabetes or hyperlipidemia [Assy et al, 2008]. In fact, an increasing body of evidence indicates that fructose in the diet itself causes NAFLD [Nomura et al, 2012].…”

Section: Introductionmentioning

confidence: 99%

Rice Bran Oil and Pumpkin Seed Oil Alleviate Oxidative Injury and Fatty Liver in Rats Fed High Fructose Diet

Al‐Okbi¹,

Mohamed²,

Hamed³

et al. 2014

Pol. J. Food Nutr. Sci.

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Key words: fatty liver, non-alcoholic fatty liver with infl ammation, fructose, rice bran oil, pumpkin seed oil Nonalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease are increasing in adults and are likely to be increasing in children. The aim of the present research was to evaluate the protective effect of rice bran oil and pumpkin seed oil against high fructose diet (HFD) inducing nonalcoholic steatohepatitis (NASH). The results showed signifi cant elevation of plasma total and direct bilirubin, transaminases activities, total cholesterol (T-Ch), triglycerides (TG), low density lipoprotein-cholesterol (LDL-Ch), tumor necrosis factor- (TNF-) and malondialdehyde (MDA) with signifi cant increase in liver TG, T-Ch and MDA along with signifi cant reduction in plasma high density lipoprotein cholesterol (HDL-Ch) and increase in T-Ch/HDL-Ch in rats fed HFD compared to rats fed on balanced diet. Histopathology of liver of rats fed on HFD confi rmed the induction of NASH. Rice bran oil and pumpkin seed oil produced improvement in the biochemical parameters with different degrees. Pumpkin seed oil reversed all histopathological changes that occur in liver tissue which became comparable to normal in some rats. In conclusion, rats fed high fructose diet are a good model for studying NASH. Rice bran oil and pumpkin seed oil afford hepato protection against NASH in rat model.

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“…Interestingly, Lee et al (2009) showed that a low, noncytotoxic dose of H 2 O 2 dramatically increases the cytotoxicity of fructose and glyoxal, a fructose metabolite. Indeed, under normal circumstances, hepatocytes are highly resistant to H 2 O 2 , and fructose also exerts its cytotoxicity at fairly high concentrations (Nomura & Yamanouchi 2012). However, H 2 O 2 formation can be induced easily by mitochondrial stress brought about by an HFrD, thereby increasing the detrimental effects of fructose and its metabolites as cytotoxic endogenous toxins.…”

Section: Genes To Cells (2016) 21 1320-1332mentioning

confidence: 99%

Dietary fructose‐induced hepatocellular carcinoma development manifested in mice lacking apoptosis inhibitor of macrophage (AIM)

et al. 2016

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The consumption of fructose, including the use of high-fructose corn syrup as a sweetener, has increased continuously in recent decades. Although the involvement of fructose in the development of metabolic diseases has been emphasized recently, whether fructose intake increases susceptibility to steatosis-associated hepatocellular carcinoma (HCC) is unclear. Here, we investigated this issue using mice lacking a circulating protein, apoptosis inhibitor of macrophage (AIM, encoded by cd5l). AIM does not induce carcinogenesis of hepatocytes, but provokes necrotic death specifically in AIM-bound cancer cells through complement cascade activation, thereby preventing HCC tumor development in wild-type mice. When subjected to a high-fructose diet (HFrD), AIM-deficient (AIM -/-) mice showed liver steatosis and subsequent liver inflammation as well as fibrosis, but at much milder levels compared with mice fed a high-fat diet. However, AIM -/-mice were markedly susceptible to HCC tumor development, whereas no wild-type mice developed the disease. Systemic metabolic states, including obesity and insulin resistance, were similar in both types of mice after HFrD challenge, indicating no influence of AIM on HFrD-induced metabolic changes. Our results suggest that dietary fructose increases the risk for liver carcinogenesis and that individuals with low blood AIM levels may be susceptible to HCC under chronic fructose intake.

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The role of fructose-enriched diets in mechanisms of nonalcoholic fatty liver disease

Cited by 185 publications

References 89 publications

Diverse roles for theDrosophilafructose sensor Gr43a

Diverse roles for theDrosophilafructose sensor Gr43a

Rice Bran Oil and Pumpkin Seed Oil Alleviate Oxidative Injury and Fatty Liver in Rats Fed High Fructose Diet

Dietary fructose‐induced hepatocellular carcinoma development manifested in mice lacking apoptosis inhibitor of macrophage (AIM)

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