| Study |
Hepatic Disorder and Sample Size |
Variables |
Results |
| Kanerva et al. [55] |
N=1611, 663 diagnosed with NAFLD by the algorithm Fatty Liver Index (FLI) and 511 by the NAFLD Fat Liver Score |
Algorithm for definition of NAFLD, food frequency questionnaire, anthropometry, factors of MS |
Subjects in the highest quartile of 28-44% fructose intake (range: 29.2-88.0 g/d) had smaller waist circumference values and lower risk of NAFLD assessed by using the FLI and NAFLD liver fat score. Association persisted aftermodel adjusted for lifestyle and variables related to food consumption. |
| Volynets et al. [53] |
20 NAFLD by ultrassonography (3 NASH) vs. 10 healthy controls |
Food frequency questionnaire |
NAFLD group had increased consumption of protein carbohydrates, sucrose, fructose and glucose. PAI-1, endotoxin, and ALT plasma levels were positively related to total protein and carbohydrate intake. |
| Abdelmalek et al.[43] |
427 with biopsy proven NAFLD |
Food frequency questionnaire, liver biopsy, biochemical tests |
Group with daily consumption of industrialized beverages had higher triglyceride levels, fasting plasma glucose, total calories, proteins, carbohydrates and lipids compared to those who consumed moderately. Model adjusted for sex, age, BMI and total caloric intake showed that daily consumption of industrialized beverages was associated with a decrease in the degree of steatosis (OR = 0.4, CI 0.4-0.9; p = 0.02) and an increase in the degree of fibrosis (OR = 2.6, CI 1,4- 5; p = 0.004). |
| Abid et al. [36] |
31 NAFLD with risk factors for metabolic syndrome (DM, obesity and hypertriglyceridemia), 29 NAFLD without risk factors for metabolic syndrome and 30 controls |
Food record, HFCS consumption, ultrasound, HOMA, triglycerides |
NAFLD with MS: increased HOMA (8.3 ± 8 vs. 3.7 ± 3.7 vs. 1.7 ± 0.5; p = 0.001) and triglycerides (208 ± 69 vs. 142 ± 64 vs. 108 ± 34; p = 0.001). Logistic regression demonstrated a strong association between consumption of industrialized beverages and hepatic fat (OR = 2; CI 95% = 1-5 p = 0.03). |
| Ouyang et al. [41] |
49 NAFLDvs.
24 controls |
Consumption on HFCS, triglycerides, cholesterol, uric acid, fructokinase, fattyacidsynthase |
NAFLD group: increased consumption of HFCS (365kcal / day vs. 190kcal / day, p<0.05) and higher triglycerides, cholesterol and uric acid. Expression of frutoquinase enzymes and fatty acid synthase were increased in NAFLD compared to samples from controls without steatosis. |
| Assy et al.[52] |
31 NAFLD without classic risk factors of the disease (DM, obesity, dyslipidemia and hypertension) and 30 controls |
Food record, ultrasound |
NAFLD group: increased consumption of industrialized beverages compared to controls (80% vs. 20%, p = 0.001); higher consumption of added sugar in g/day (75.6 ± 8.4 vs. 33.6 ± 12.6; p = 0.001. Correlation between consumption of processed drinks and fatty liver infiltrate (r=0.63; p<0.01). |
| Toshimitsu et al.[54] |
28 NASHvs.
18 steatosis |
Three diet recalls |
NASH group: increased consumption of carbohydrates (20-39 ys and 40-59 ys) compared to simple steatosis (56 ± 9 vs. 47 ± 13, p<0.05) (58 ± 9 vs. 49 ± 12, p<0.05). |
| Thuy et al.[57] |
12 nondiabetic NAFLD and
6 healthy controls |
Diet, endotoxin, TLR4,
PAI-1 plasma and liver |
NAFLD group: higher consumption of fructose (p<0.05; plasma levels of endotoxin (p<0.05), PAI-1 (p<0.05), hepatic TLR4 (p<0.05) and PAI-1 mRNA expression (p<0.05). PAI-1 concentrations correlated with endotoxin levels and with hepatic TLR4 mRNA expression. Hepatic mRNA expression of PAI-1 correlated with dietary intakes of carbohydrates, fructose, glucose and sucrose |
| Vos et al.[63] |
149 children (110 boys, 79 girls) biopsy proven NAFLD |
Sugar sweetened beverage per week, food questionnaire, demographic, anthropometric, clinical, laboratory and histology data |
Sugar sweetened beverage consumption was low without correlation with histology hepatic. Uric acid was increased in NASH group (p=0.008). Median consumption of vitamin E was lower in children with higher grade of steatosis. |
| Jin et al.[61] |
9 NAFLD (7 NASH, 1 steatosis, 2 NASH with fibrosis) and 10 controls without NAFLD |
Intervention: balanced meal added to 1) a sweetened beverage with fructose (FB); or 2) a drink sweetened with glucose (GB). |
NAFLD group: increase in triglycerides after FB compared to GB both NAFLD and control groups.For all subjects, high-density lipoprotein cholesterol declined in the postprandial and overnight hours with FB, but not with GB (p=0.0006). Non sterified fatty acids were significantly higher in NAFLD. |