2019
DOI: 10.1007/s00018-019-03390-0
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Fructose-mediated effects on gene expression and epigenetic mechanisms associated with NAFLD pathogenesis

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Cited by 60 publications
(45 citation statements)
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References 112 publications
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“…In individuals at high-cardiovascular risk, the epigenetic signature associated with the consumption of fruit juice (rich in fructose) was enriched for pro-inflammatory pathways [16]. Consistently, compelling evidence supports the association of excessive fructose consumption with the presence of non-alcoholic fatty liver disease (NAFLD) involving alteration of transcriptomic and epigenetic mechanisms underlying lipid metabolism deregulation, increased liver fat accumulation, and inflammation [17]. Additionally, maternal low-dietary protein regulated miRNA expression targeting genes mapped to inflammatory-related pathways and metabolic health in offspring mice [18].…”
Section: Nutrition/dietary Bioactive Compoundsmentioning
confidence: 93%
“…In individuals at high-cardiovascular risk, the epigenetic signature associated with the consumption of fruit juice (rich in fructose) was enriched for pro-inflammatory pathways [16]. Consistently, compelling evidence supports the association of excessive fructose consumption with the presence of non-alcoholic fatty liver disease (NAFLD) involving alteration of transcriptomic and epigenetic mechanisms underlying lipid metabolism deregulation, increased liver fat accumulation, and inflammation [17]. Additionally, maternal low-dietary protein regulated miRNA expression targeting genes mapped to inflammatory-related pathways and metabolic health in offspring mice [18].…”
Section: Nutrition/dietary Bioactive Compoundsmentioning
confidence: 93%
“…We suspect that these effects of fructose intake are related to the respective nutritional status and gender of the test subjects. These effects persist in spite of fructose reduction, are passed on from mothers with high fructose consumption to their offspring and might influence the hepatic fat metabolism long before obesity and insulin resistance occur ( DiStefano 2020 ). An important regulator of cholesterol metabolism showed decreased gene expression in males from fructose-fed mothers.…”
Section: Association Of Fructose and Non-alcoholic Fatty Liver Diseasmentioning
confidence: 99%
“…Gene symbols (in alphabetical order) correspond to: Acaca , acetyl-CoA carboxylase-α; Acly , ATP citrate lyase; Acox1 , acyl-coenzyme A oxidase one; Aldob , aldolase B; Chrebp , carbohydratre response element-binding protein; Cpt1a , carnitine palmitoyltransferase 1 (isoform a); Elovl5 , elongation of very long chain fatty acids-like five; Elovl6 , elongation of very long chain fatty acids-like six; Fasn , fatty acid synthase; Fbp2 , fructose-1,6-bisphosphatase two; G6pc , glucose-6-phosphatase; Gpat , glycerol-3-phosphate acyltransferase (mitochondrial); Khk , ketohexokinase; Lipe/Lpl , lipase/lipoprotein lipase; Pdk3 , pyruvate dehydrogenase kinase, isoenzyme three; Pepck , phosphoenolpyruvate carboxykinase one; Pfk1 , phosphofructokinase (muscle type); Pklr , pyruvate kinase (liver and red blood cell); Ppara , peroxisome proliferation-activated receptor-α; Pparg , peroxisome proliferation-activated receptor-γ; Ppargc1a , peroxisome proliferation-activated receptor-γ coactivator 1-α; Scd , stearoyl-Coa desaturase; Sirt1 , sirtuin one; Slc2A5 , solute carrier family 2 (facilitated glucose/fructose transporter) member five; Srebp1c , sterol regulatory element-binding transcription factor 1 (isoform c). Adapted from ( DiStefano 2020 ).…”
Section: Association Of Fructose and Non-alcoholic Fatty Liver Diseasmentioning
confidence: 99%
“…The discrepancies between these studies may be attributed to the amount of fructose that was consumed, i.e., either moderate to high ( 5 ) or very low ( 13 ). Fructose can serve as a substrate for de novo lipogenesis and stimulate de novo lipogenesis via upregulation of transcription factors that enable the expression of genes involved in de novo lipogenesis, such as sterol regulatory element binding protein 1 (SREBP1), carbohydrate response element binding protein (ChREBP), and liver X receptor (LXR) ( 14 , 15 ). On the other hand, even at small (“catalytic”) amounts, fructose can also increase hepatic glucose disposal ( 16 , 17 ).…”
Section: Introductionmentioning
confidence: 99%