Long term nutritional intake and the risk for non-alcoholic fatty liver disease (NAFLD): A population based study

Zelber‐Sagi, Shira; Nitzan-Kaluski, Dorit; Goldsmith, Rebecca; Webb, Muriel; Blendis, Laurie; Halpern, Zamir; Oren, Ran

doi:10.1016/j.jhep.2007.06.020

Cited by 482 publications

(420 citation statements)

References 38 publications

(72 reference statements)

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“…Excessive consumption of simple sugars has been reported to promote the development of NAFLD in adults. A prospective association between dietary pattern, obesity, and metabolic complications has been reported by several studies in children (Johnson et al 2007a(Johnson et al , b, 2008Ambrosini et al 2012;Zelber-Sagi et al 2007). However, evidence relating dietary patterns to NAFLD is limited in the pediatric age.…”

Section: Introductionmentioning

confidence: 81%

Influence of dietary pattern, physical activity, and I148M PNPLA3 on steatosis severity in at-risk adolescents

Nobili

Liccardo

Bedogni³

et al. 2014

Genes Nutr

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Evidence relating dietary patterns to obesity and related disorders such as non-alcoholic fatty liver disease (NAFLD) is limited in pediatric age. Aim of this study was to analyze the association between dietary patterns, obesity and development of severe steatosis and the metabolic syndrome in a series of children and adolescents referred for suspected NAFLD, and the interaction with the rs738409 I148M PNPLA3 polymorphism. Two hundred patients (112 females) had completed a food frequency and demographic questionnaire. Nearly 58 % were obese, and 32 % were overweight. Mild, moderate, and severe fatty liver was present in 60 (30 %), 87 (44 %), and 51 (26 %) participants, respectively. A great proportion of overweight/obese children and adolescents reported a correct dietary pattern. At multivariate ordinal regression analysis considering demographic, anthropometric, genetic, and behavioral determinants, the major determinant of steatosis severity was PNPLA3 I148M genotype (p \ 0.0001), followed by older age (p = 0.017), higher waist circumference (p = 0.016), and less time spent practising physical exercise (p = 0.034). Furthermore, there was a significant interaction between PNPLA3 I148M and intake of sweetened beverages (p = 0.033) and of vegetables (p = 0.038).In conclusion, although dietary pattern was reportedly correct in at-risk overweight adolescents with NAFLD, we report a novel interaction between PNPLA3 I148M and dietary components with the severity of steatosis.

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Section: Introductionmentioning

confidence: 81%

Influence of dietary pattern, physical activity, and I148M PNPLA3 on steatosis severity in at-risk adolescents

Nobili

Liccardo

Bedogni³

et al. 2014

Genes Nutr

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“…Recently, it has been shown that a diet low in fructose might be beneficial with regard to reduction of liver fat content. 21,22 However, the exact mechanisms involved in sugar and particularly fructose-induced NAFLD are still poorly understood. Here, by feeding mice lacking the endotoxin receptor TLR-4 chronically with a moderate fructose-enhanced diet (e.g., 30% fructose in drinking solutions) we further tested the hypothesis that the endotoxin-induced activation of hepatic Kupffer cells resulting from intestinal bacterial overgrowth and increased intestinal permeability 13,14 is a key factor in the onset of fructose-induced NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

et al. 2009

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A link between dietary fructose intake, gut-derived endotoxemia, and nonalcoholic fatty liver disease (NAFLD) has been suggested by the results of human and animal studies. To further investigate the role of gut-derived endotoxin in the onset of fructose-induced NAFLD, Toll-like receptor (TLR-) 4-mutant (C3H/HeJ) mice and wildtype (C3H/HouJ) mice were either fed plain water or water enriched with 30% fructose for 8 weeks. Hepatic steatosis, plasma alanine aminotransferase (ALT), and markers of insulin resistance as well as portal endotoxin levels were determined. Hepatic levels of myeloid differentiation factor 88 (MyD88), interferon regulatory factor (IRF) 3 and 7, and tumor necrosis factor alpha (TNF␣) as well as markers of lipid peroxidation were assessed. Chronic intake of 30% fructose solution caused a significant increase in hepatic steatosis and plasma ALT levels in wildtype animals in comparison to water controls. In fructose-fed TLR-4 mutant mice, hepatic triglyceride accumulation was significantly reduced by Ϸ40% in comparison to fructose-fed wildtype mice and plasma ALT levels were at the level of water-fed controls. No difference in portal endotoxin concentration between fructose-fed wildtype and TLR-4-mutant animals was detected. In contrast, hepatic lipid peroxidation, MyD88, and TNF␣ levels were significantly decreased in fructose-fed TLR-4-mutant mice in comparison to fructose-fed wildtype mice, whereas IRF3 and IRF7 expression remained unchanged. Markers of insulin resistance (e.g., plasma TNF␣, retinol binding protein 4, and hepatic phospho-AKT) were only altered in fructose-fed wildtype animals. Conclusion: Taken together, these data further support the hypothesis that in mice the onset of fructose-induced NAFLD is associated with intestinal bacterial overgrowth and increased intestinal permeability, subsequently leading to an endotoxin-dependent activation of hepatic Kupffer cells.

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“…Fructose and high-fructose corn syrup, a common soft drink sweetener, in particular, have been independently connected to the risk and severity of NAFLD in population-based studies and in a randomised crossover trial [115][116][117][118][119].…”

Section: Implications For Future Researchmentioning

confidence: 99%

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

et al. 2012

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Aims/hypothesis Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH): NAFLD causes an increased risk of cardiovascular disease, diabetes and liverrelated complications (the latter confined to NASH). The effect of proposed treatments on liver disease, glucose metabolism and cardiovascular risk in NAFLD is unknown. We reviewed the evidence for the management of liver disease and cardiometabolic risk in NAFLD. Methods Publications through November 2011 were systematically reviewed by two authors. Outcomes evaluated though standard methods were: histological/radiological/biochemical features of NAFLD, variables of glucose metabolism and cardiovascular risk factors. Seventy-eight randomised trials were included (38 in NASH, 40 in NAFLD): 41% assessed post-treatment histology, 71% assessed glucose metabolism and 88% assessed cardiovascular risk factors. Lifestyle intervention, thiazolidinediones, metformin and antioxidants were most extensively evaluated. Results Lifestyle-induced weight loss was safe and improved cardio-metabolic risk profile; a weight loss ≥7% improved histological disease activity, but was achieved by <50%

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Long term nutritional intake and the risk for non-alcoholic fatty liver disease (NAFLD): A population based study

Cited by 482 publications

References 38 publications

Influence of dietary pattern, physical activity, and I148M PNPLA3 on steatosis severity in at-risk adolescents

Influence of dietary pattern, physical activity, and I148M PNPLA3 on steatosis severity in at-risk adolescents

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

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