Non-alcoholic Fatty Liver Risk Research Articles

Sugar-Sweetened Beverages and Artificially Sweetened Beverages Consumption and the Risk of Nonalcoholic Fatty Liver (NAFLD) and Nonalcoholic Steatohepatitis (NASH).

Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are fast becoming the most common chronic liver disease and are often preventable with healthy dietary habits and weight management. Sugar-sweetened beverage (SSB) consumption is associated with obesity and NAFLD. However, the impact of different types of SSBs, including artificially sweetened beverages (ASBs), is not clear after controlling for total sugar intake and total caloric intake. The aim of this study was to examine the association between the consumption of different SSBs and the risk of NAFLD and NASH in US adults. The representativeness of 3739 US adults aged ≥20 years old who had completed 24 h dietary recall interviews and measurements, including dietary, SSBs, smoking, physical activity, and liver stiffness measurements, were selected from the National Health and Nutrition Examination Survey 2017-2020 surveys. Chi-square tests, t-tests, and weighted logistic regression models were utilized for analyses. The prevalence of NASH was 20.5%, and that of NAFLD (defined without NASH) was 32.7% of US. adults. We observed a higher prevalence of NASH/NAFLD in men, Mexican-Americans, individuals with sugar intake from SSBs, light-moderate alcohol use, lower physical activity levels, higher energy intake, obesity, and medical comorbidities. Heavy sugar consumption through SSBs was significantly associated with NAFLD (aOR = 1.60, 95% CI = 1.05-2.45). In addition, the intake of ASBs only (compared to the non-SSB category) was significantly associated with NAFLD (aOR = 1.78, 95% CI = 1.04-3.05), after adjusting for demographic, risk behaviors, and body mass index. A higher sugar intake from SSBs and exclusive ASB intake are both associated with the risk of NAFLD.

1379-P: Adding Salt to Foods and Risk of Severe Nonalcoholic Fatty Liver

Background: High sodium intake is associated with insulin resistance, obesity, and metabolic syndrome, whereas very few studies have assessed the association of sodium intake with risk of nonalcoholic fatty liver disease (NAFLD). We recently found that the frequency of adding salt to foods could reflect a person’s long-term salt taste preference and sodium intake and was significantly related to life expectancy and cardiovascular disease risk. In this study, we aimed to evaluate the association between the frequency of adding salt to foods and liver proton density fat fraction (PDFF, a magnetic resonance imaging-based measure to assess liver fat content) and severe NAFLD risk. Methods: A total of 494,240 participants from UK biobank, who were free of NAFLD at baseline (2006-2010) were analyzed in this study. Of the above participants, 9816 participants have MRI-PDFF data, measured in 2014. Generalized linear models were used to evaluated association between the frequency of adding salt to foods with liver-PDFF; Cox proportional hazards models were used to estimate the association between the frequency of adding salt to foods and severe NAFLD risk. Results: During a median of 11 years of follow-up, 5,294 severe NAFLD cases were documented. Compared with participants who Never/Rarely added salt to foods, the adjusted Hazard Ratios (95% confidence interval) were 1.11 (1.04, 1.18), 1.27 (1.17, 1.37), and 1.45 (1.30, 1.62) across the groups of Sometimes, Usually, and Always, respectively (P-trend<0.001). The liver-PDFF values were 4.7 % (95% CI, 3.9, 5.5), 5.1% (4.3, 5.9), 5.2% (4.4, 6.0) and 5.5% (4.5-6.4) in the groups of Never/Rarely, Sometimes, Usually, and Always added salt to foods, respectively (P-trend<0.001). In sensitivity analyses, we replaced the frequency of adding salt to foods with estimated 24-hour urinary sodium extraction and found similar significant associations. Conclusions: Our findings indicate that high sodium intake is associated with higher risk of severe NAFLD. Disclosure H. Ma: None. X. Wang: None. X. Li: None. Y. Heianza: None. L. Qi: None.

The nonalcoholic fatty liver risk in prediction of unfavorable outcome after stroke: A nationwide registry analysis

Few researches have looked at the relationship between nonalcoholic fatty liver disease (NAFLD) at the time of admission and the long-term outcomes of patients suffering from acute ischemic stroke (AIS). We aimed to probe the relationship between NAFLD risk evaluated by NAFLD indices and long-term endpoints, along with the prognostic value of merging NAFLD indices with established risk markers for the prognosis of AIS patients. The fatty liver index (FLI) and the Hepatic steatosis index (HSI) were used to evaluate NAFLD risk in the Third China National Stroke Registry (CNSR-III), a large, prospective, national, multicenter cohort registry study. NAFLD was defined as FLI ≥35 for males and FLI ≥ 20 for females, as well as HSI>36. Death or major disability (modified Rankin Scale score ≥3) were the primary outcomes following the beginning of a stroke. On patient outcomes, the prognostic performance of two objective NAFLD parameters was evaluated. NAFLD was detected in 32.10-51.90% of AIS patients. After 1-year, 14.5% of the participants had died or suffered a severe outcome. After controlling for known risk factors, NAFLD was associated with a modest probability of adverse outcome (odds ratio,0.72[95% CI, 0.61-0.86] for FLI; odds ratio,0.68[95% CI, 0.55-0.85] for HSI). The inclusion of the two NAFLD indicators in the conventional prediction model was justified by the integrated discrimination index, continuing to increase the model's overall predictive value for long-term adverse outcomes. NAFLD risk was linked to a lower risk of long-term death or major disability in people with AIS. The predictive value of objective NAFLD after AIS was demonstrated in our study.

Association Between Serum Vitamin C and Non-alcoholic Fatty Liver Disease: A Cross-sectional Study.

The association between vitamin C and the risk of developing non-alcoholic fatty liver disease remains controversial. The aim of the present study is to examine any correlation between serum vitamin C and the risk of non-alcoholic fatty liver disease. Our study enrolled 3374 participants aged ≥ 20 years from the National Health and Nutritional Survey (2003-2006). Nonalcoholic fatty liver disease was defined as the US Fatty Liver Index ≥ 30 in the absence of other chronic liver disease. Multivariate logistic regression and the fitted smoothing curves were adopted for analyzing the correlation between serum vitamin C levels and the risk of developing non-alcoholic fatty liver disease. After adjusting for all the covariates, it was discovered that serum vitamin C was negatively correlated with the risk of nonalcoholic fatty liver disease (odds ratio: 0.664, 95% CI: 0.512-0.860, P = .002). Through smooth curve fitting, it was further noticed that the relationship between serum vitamin C and the risk of non-alcoholic fatty liver disease was non-linear. The inflection point was 0.92, and to its left, a negative correlation was seen between vitamin C and non-alcoholic fatty liver disease (odds ratio: 0.451, 95% CI: 0.288- 0.706, P = .001). To the right of the inflection point, however, the correlation between vitamin C and non-alcoholic fatty liver disease was not found to be significant. The correlation was non-linear between serum vitamin C levels and the risk of developing non-alcoholic fatty liver disease. Serum vitamin C was negatively correlated with the risk of non-alcoholic fatty liver disease when its level was less than 0.92 mg/dL.

Serum 25-hydroxyvitamin D levels and the risk of non-alcoholic fatty liver: A two-sample Mendelian randomization study.

Accumulated studies have shown that low expression of 25-hydroxyvitamin D [25(OH)D] was significantly associated with the risk of non-alcoholic fatty liver disease (NAFLD). However, the exact causality is still unknown. The aim of this study was to investigate whether levels of 25(OH)D are associated with risk of NAFLD, using a two-sample Mendelian randomization (MR). Data from a recent large vitamin D genome-wide association study (GWAS) on 417,580 Europeans were utilized, and the largest published histology-based NAFLD GWAS study (1,483 cases and 17,781 healthy controls) for genetic variants predicted to cause NAFLD were searched. All genetic datasets for the MR analyses were obtained using publicly available summary statistics based on individuals of European ancestry from the MR-Base and NHGRI-EBI GWAS Catalog database. Inverse-variance weighted (IVW) MR approach was used to estimate causal effects in the main analysis, complemented by 4 additional methods to control for pleiotropy. Sensitivity analyses were conducted to verify whether heterogeneity and pleiotropy can bias the MR results. The MR analysis did not provide strong evidence for the causal association of circulating 25(OH)D with NAFLD by IVW method (OR = 0.746, 95%CI 0.517-1.078; P = 0.119). The results were consistent using four other MR methods. Sensitivity analysis using all different analytical approaches yielded similar results. There was no evidence for pleiotropy (MR-Egger intercept: -0.0003758, P = 0.970). The replication process also showed consistent results using IVW method (P = 0.710). This study indicates that serum 25(OH)D levels did not possess an obvious effect on the risk of NAFLD. The associations in previous studies may be due to residual confounding or reverse causation.

Short sleep duration and the risk of nonalcoholic fatty liver disease/metabolic associated fatty liver disease: a systematic review and meta-analysis.

It is unclear whetheror not nonalcoholic fatty liver disease (NAFLD)/metabolic dysfunction-associated fatty liver disease (MAFLD) is related to short sleep duration. A meta-analysis was conducted to determine if inadequate sleep time increased the risk of NAFLD/MAFLD. A comprehensive systematic literature review was conducted in the Embase, PubMed, and Cochrane Library databases from inception to August 1, 2022. Studies examining the correlation between inadequate sleep time and the risk of NAFLD/MAFLD were included. We pooled the odds ratios (ORs) and 95% confidence intervals (CIs) using a random-effects model. This meta-analysis included fifteen studies involving a total of 261,554 participants. In the pooled analysis, short sleep duration was found to be strongly correlated with an increased risk of NAFLD/MAFLD (OR, 1.15; 95% CI, 1.04-1.28; P = 0.01), with a moderate degree of heterogeneity between studies (I2 = 71.92%, Q = 49.87, P < 0.01). The sensitivity analysis suggested that the primary outcome was robust, and there was no significant publication bias. This meta-analysis indicates that inadequate sleep duration is strongly correlated with an elevated risk of NAFLD/MAFLD. The findings suggest that obtaining an adequate amount of sleep may be useful for preventing NAFLD/MAFLD, which is especially important given the low rate of response to pharmacotherapy.

Relationship Between PEMT Gene rs7946 Polymorphism and Nutritional Choline Status in Association With Nonalcoholic Fatty Liver Risk

ObjectivesPhosphatidylethanolamine N-methyltransferase (PEMT) rs7946 genetic polymorphism and nutritional choline status on nonalcoholic fatty liver (NAFL) risk have not been well elucidated. The aims of the study were to investigate the choline-polymorphic relationship on NAFL risk.MethodsThe study recruited 253 patients with metabolic disorders from one regional hospital in 2020. By abdominal ultrasound diagnosis, 99 patients with hepatic steatosis (HS) and 99 age- and sex-matched controls without HS were included for the study. Habitual dietary choline intakes were assessed using validated quantitative FFQ by a face-to-face interview. PEMT rs7946 (V175M, G to A substitution) polymorphism, blood choline concentrations and metabolic disorders factors were analyzed for their interaction with HS risk.ResultsGenetic distribution of PEMT rs7946 polymorphism significantly differed in controls (GG: 48%, GA, 32%, AA, 20%) and in the HS cases (GG: 69%, GA: 26%, AA: 5%) (p = 0.003). Higher values of body mass index (BMI), serum triglycerides (TG), insulin resistance (HOMO-IR), alanine aminotransferase and lower levels of HDL were associated with HS cases. Plasma free choline levels were significantly higher in HS cases (median:12.4 μM, quartile range (9.9–14.8)) than in controls (median: 10.6 μM, quartile range (9.3–12.8)) (p = 0.001). The daily dietary intake of total choline and the choline derivatives did not differ between the two groups. After adjustment of age, gender, BMI, energy consumption, fiber intake, and blood metabolic markers (TG, LDL, HDL and HOMA-IR), odds ratios of HS were 7-fold increase (OR: 7.6, 95% CI: 2.3–24.4) for patients with PEMT rs7946 GG genotype of high plasma choline level (> median levels: 11.6 μM) as compared with GA/AA genotype of plasma choline level lower than 11.6 μM.ConclusionsThe PEMT rs7946 GG genotype in combination with high plasma choline levels was associated with increased risks of hepatic fat accumulation in patients with metabolic disorders.Funding SourcesThe Ministry of Health and Welfare-affiliated Taipei Hospital. The Ministration of Science and Technology, Taiwan, ROC.

Positive association of nap duration with risk of non-alcoholic fatty liver disease in an occupational population in Guangdong Province, China: a cross-sectional study

BackgroundA lack of sleep or disorder in sleep–wake cycles has been associated with metabolic impairments. However, few studies have investigated the association between daytime napping duration and the risk of non-alcoholic fatty liver disease. This study aimed to investigate the association of daytime napping duration with the risk of non-alcoholic fatty liver disease in a Chinese population.MethodsThis cross-sectional study analyzed data from the Health Management Center of Nanfang Hospital, Guangdong Province. A total of 3363 participants aged 20–79 years were recruited and admitted from January 20, 2018, to October 16, 2020. Non-alcoholic fatty liver disease was diagnosed using abdominal ultrasonography. The outcome was the association between daytime sleep duration and the risk of non-alcoholic fatty liver disease.ResultsCompared with non-nappers, long daytime nappers (≥ 60 min) were associated with a higher risk of non-alcoholic fatty liver disease in the crude model (odds ratio 2.138; 95% confidence interval 1.88–2.61, P < 0.05) and in the multivariable adjustment model (odds ratio 2.211; 95% confidence interval 1.042–4.690, P < 0.05) after adjusting for demographic, educational, and metabolic risk factors. The association was moderately enhanced with additional adjustments for night sleep duration and socioeconomic or other factors (odds ratio 2.253; 95% confidence interval 1.061–4.786, P = 0.035).ConclusionIn this cross-sectional study, daytime napping duration of ≥ 60 min was positively associated with the risk of non-alcoholic fatty liver disease in an occupational population of Guangdong Province after multivariable adjustment.

Copy number variation in the CES1 gene and the risk of non-alcoholic fatty liver in a Chinese Han population

A recent genome-wide copy number variations (CNVs) scan identified a 16q12.2 deletion that included the carboxylesterase 1 (CES1) gene, which is important in the metabolism of fatty acids and cholesterol. We aimed to investigate whether CES1 CNVs was associated with susceptibility to non-alcoholic fatty liver disease (NAFLD) in a Chinese Han population. A case–control study was conducted among 303 patients diagnosed with NAFLD and 303 age (± 5) and sex-matched controls from the Affiliated Nanping First Hospital of Fujian Medical University in China. The copy numbers of CES1 were measured using TaqMan quantitative real-time polymerase chain reaction (qPCR) and serum CES1 was measured using enzyme-linked immunosorbent assays. The Chi-squared test and a logistic regression model were used to evaluate the association between CES1 CNVs and NAFLD susceptibility. The distribution of CES1 CNVs showed a higher frequency of CNVs loss (< 2) among patients; however, the difference was not significant (P = 0.05). After controlling for other known or suspected risk factors for NAFLD, CES1 CNVs loss was significantly associated with greater risk of NAFLD (adjusted OR = 2.75, 95% CI 1.30–5.85, P = 0.01); while CES1 CNVs gain (> 2) was not. There was a suggestion of an association between increased CES1 serum protein levels and CNVs losses among cases, although this was not statistically significant (P = 0.07). Copy number losses (< 2) of CES1 contribute to susceptibility to NAFLD in the Chinese Han population.

Assessment of the association between body composition and risk of non-alcoholic fatty liver.

Non-alcoholic fatty liver disease (NAFLD) is defined as the condition of fat accumulation in the liver. This cross-sectional study aimed to investigate the relationship between body composition and fatty liver and determine of cut-off point for predicting NAFLD. Samples were selected from the nutrition clinic from 2016 to 2017 in Tehran, Iran. The liver steatosis was calculated using the CAP score through the FiroScan™ and body composition was measured using the dual-energy X-ray absorptiometry scan method. A total of 2160 patients participated in this study, 745 (34.5%) subjects had NAFLD. We found that fat-free tissue was inversely and fat tissue was directly correlated with the risk of NAFLD in almost all factors and the risk of developing NAFLD increases if the total fat exceeds 32.23% and 26.73% in women and men and abdominal fat exceeds 21.42% and 13.76% in women and men, respectively. Finally, we realized that the total fat percent had the highest AUC (0.932 for men and 0.917 for women) to predict the risk of NAFLD. Overall, the likelihood of NAFLD development rose significantly with increasing the amount of total fat and abdominal fat from the cut-off point level.

Harnessing Muscle-Liver Crosstalk to Treat Nonalcoholic Steatohepatitis.

Non-alcoholic fatty liver disease (NAFLD) has reached epidemic proportions, affecting an estimated one-quarter of the world’s adult population. Multiple organ systems have been implicated in the pathophysiology of NAFLD; however, the role of skeletal muscle has until recently been largely overlooked. A growing body of evidence places skeletal muscle—via its impact on insulin resistance and systemic inflammation—and the muscle-liver axis at the center of the NAFLD pathogenic cascade. Population-based studies suggest that sarcopenia is an effect-modifier across the NAFLD spectrum in that it is tightly linked to an increased risk of non-alcoholic fatty liver, non-alcoholic steatohepatitis (NASH), and advanced liver fibrosis, all independent of obesity and insulin resistance. Longitudinal studies suggest that increases in skeletal muscle mass over time may both reduce the incidence of NAFLD and improve preexisting NAFLD. Adverse muscle composition, comprising both low muscle volume and high muscle fat infiltration (myosteatosis), is highly prevalent in patients with NAFLD. The risk of functional disability conferred by low muscle volume in NAFLD is further exacerbated by the presence of myosteatosis, which is twice as common in NAFLD as in other chronic liver diseases. Crosstalk between muscle and liver is influenced by several factors, including obesity, physical inactivity, ectopic fat deposition, oxidative stress, and proinflammatory mediators. In this perspective review, we discuss key pathophysiological processes driving sarcopenia in NAFLD: anabolic resistance, insulin resistance, metabolic inflexibility and systemic inflammation. Interventions that modify muscle quantity (mass), muscle quality (fat), and physical function by simultaneously engaging multiple targets and pathways implicated in muscle-liver crosstalk may be required to address the multifactorial pathogenesis of NAFLD/NASH and provide effective and durable therapies.

The evaluation value of transient elastography for liver characteristics in obese children

Objective: To evaluate the feasibility of transient elastography (FibroTouch) in obese children and to investigate the liver characteristics of obese children based on FibroTouch. Methods: Children (5-18 years of age) from the Guangzhou Women and Children's Medical Center were examined by FibroTouch. The fat attenuation parameter (FAP) was used to assess liver fat deposition, and liver stiffness measurement (LSM) was used to assess liver fibrosis. The children were divided into obesity group (n=67) and non-obesity group (n=139). The FAP, LSM, and their influencing factors were analysed in the obese group. Results: The total effective rate of FibroTouch in non-sedated children aged 5-18 years (n=229) was 97.8%. The FAP value 259.4 (235.9-275.5) dB/m in obese children was significantly higher than that in the control group 178.1 (168.7-195.6) dB/m, (Z=-10.586, P<0.001). The LSM value in obese children 5.9 (4.5-7.5) kPa was significantly higher than that in non-obese children 3.2 (2.3-4.1) kPa, (Z=-8.832, P<0.001). The proportion of liver fibrosis in obese group was 30%, and that of nonalcoholic fatty liver was 65.7%. Logistic regression analysis showed that BMI percentile (≥ 95%) was an independent factor for significant liver fibrosis (OR=1.267, 95%CI: 1.056-1.519, P=0.011) and nonalcoholic fatty liver disease (OR=1.248, 95%CI: 1.007-1.546, P=0.043). Conclusions: FibroTouch can be successfully applied to obese children. Fibrotouch can accurately evaluate the liver fibrosis and fat attenuation parameters in obese children. Obese children have higher FAP and LSM, which increase the risk of non-alcoholic fatty liver and liver fibrosis.

A Nomogram Model Based on Noninvasive Bioindicators to Predict 3-Year Risk of Nonalcoholic Fatty Liver in Nonobese Mainland Chinese: A Prospective Cohort Study.

The purpose of this study is to establish and validate an accurate and personalized nonalcoholic fatty liver disease (NAFLD) prediction model based on the nonobese population in China. This study is a secondary analysis of a prospective study. We included 6,155 nonobese adults without NAFLD at baseline, with a median follow-up of 2.3 years. Univariate and multivariate Cox regression analyses were used to determine independent predictors. The least absolute shrinkage and selection operator (LASSO) regression analysis was used to optimize the selection of variables. Based on the results of multivariate analysis, a prediction model was established. Harrell's consistency index (C-index) and area under the curve (AUC) were used to determine the discrimination of the proposed model. The goodness of fit of the calibration model was tested, and the clinical application value of the model was evaluated by decision curve analysis (DCA). The participants were randomly divided into a training cohort (n = 4,605) and a validation cohort (n = 1,550). Finally, seven of the variables (HDL-c, BMI, GGT, ALT, TB, DBIL, and TG) were included in the prediction model. In the training cohort, the C-index and AUC value of this prediction model were 0.832 (95% confidence interval (CI), 0.820-0.844) and 0.861 (95% CI, 0.849-0.873), respectively. In the validation cohort, the C-index and AUC values of this prediction model were 0.829 (95% CI, 0.806-0.852) and 0.859 (95% CI, 0.841-0.877), respectively. The calibration plots demonstrated good agreement between the estimated probability and the actual observation. DCA demonstrated a clinically effective predictive model. Our nomogram can be used as a simple, reasonable, economical, and widely used tool to predict the 3-year risk of NAFLD in nonobese populations in China, which is helpful for timely intervention and reducing the incidence of NAFLD.

Lard-Blended Vegetable Oil Diet Reduces Risk of Nonalcoholic Fatty Liver: A Novel Discovery of Traditional Chinese Dietary Pattern

Our previous work has suggested that the traditional Chinese dietary pattern, blending lard with vegetable oil, could reduce abnormal fat accumulation in adipose tissue. As the morbidity of nonalcoholic fatty liver disease (NAFLD) in China were far lower than which in Western countries was observed, we proposed that whether the lard-blended vegetable oil diet was involved in decrease of NAFLD? The aim of the current study is to answer this question. Mice fed with a mixture of lard and vegetable oil (sunflower oil and soybean oil), particularly a mixture of lard and soybean oil, showed lower body weight, body fat rate, triglyceride and free fatty acid levels in serum and liver compared to lard diet, sunflower oil diet or soybean oil diet separately. Further analysis indicated that the expression of hormone-sensitive lipase and activation of the AMPK pathway contribute to these observed phenotypes, and insulin resistance of mixed oil diet was ameliorated compared to lard, circulating insulin content of mixed oil diet elevated properly compared to vegetable oil. Conclusion: moderate lard intake blended lard with vegetable oil especially soybean oil — has the potential to reduce the risk of nonalcoholic fatty liver via AMPK pathway activation and insulin resistance amelioration.These results indicate that the traditional dietary pattern may be responsible for the lower morbidity of NAFLD in China. Funding Statement: This research was funded by the National Key R&D Program of China [grant no. 2016YDF0501200]. Declaration of Interests: The authors declare that they have no conflicts of interest. Ethics Approval Statement: This study was performed in strict accordance with the European Community (Directive 2010/63/EU) for the care and use of laboratory animals. All the experimental protocols were approved by the Ethics Committee of Hunan Agricultural University, China (No. 43321543).

Fast Food Consumption and the Risk of Non-Alcoholic Fatty Liver in Adults: A Community-Based Case-Control Study

Fast Food Consumption and the Risk of Non-Alcoholic Fatty Liver in Adults: A Community-Based Case-Control Study

Epidemiological modifiers of non-alcoholic fatty liver disease: Focus on high-risk groups

An improved understanding of non-alcoholic fatty liver disease epidemiology would lead to identification of individuals at high risk of developing chronic liver disease and extra-hepatic complications, thus contributing to more effective case finding of non-alcoholic fatty liver disease among selected groups.We aimed to illustrate the epidemiology of non-alcoholic fatty liver disease in high-risk groups, which were identified based on existing literature. To this end, PubMed was searched to retrieve original articles published until May 2015 using relevant and pertinent keywords “nonalcoholic fatty liver disease” and “diabetes”, “obesity”, “hyperlipidaemia”, “familial heterozygous hypobetalipoproteinaemia”, “hypertension”, “metabolic syndrome”, “ethnicity”, “family history” or “genetic polymorphisms”.We found that age, sex and ethnicity are major physiological modifiers of the risk of non-alcoholic fatty liver disease, along with belonging to “non-alcoholic fatty liver disease families” and carrying risk alleles for selected genetic polymorphisms. Metabolic syndrome, diabetes, obesity, mixed hyperlipidaemia and hypocholesterolaemia due to familial hypobetalipoproteinaemia are the major metabolic modifiers of non-alcoholic fatty liver disease risk. Compared with these metabolic conditions, however, arterial hypertension appears to carry a relatively more modest risk of non-alcoholic fatty liver disease.A better understanding of the epidemiology of non-alcoholic fatty liver disease may result in a more liberal policy of case finding among high-risk groups.

Higher Dietary Choline Intake Is Associated with Lower Risk of Nonalcoholic Fatty Liver in Normal-Weight Chinese Women

Background: Choline deficiency has been shown to induce liver fat accumulation in both rodent and human studies. However, it is unclear whether dietary choline intake is related to fatty liver in the general population.Objective: We examined the association between choline intake and nonalcoholic fatty liver.Methods: Participants included 56,195 Chinese women and men, 40–75 y of age, with no or negligible alcohol consumption and with no history of hepatitis, cardiovascular disease, or cancer. All participants reported undergoing liver ultrasonography. Fatty liver was defined by self-report of a physician diagnosis. Habitual dietary intakes were assessed via validated food-frequency questionnaires.Results: The average total choline intakes were 289 ± 85 mg/d in women and 318 ± 92 mg/d in men. Major food sources were eggs, soy foods, red meat, fish, and vegetables. A higher choline intake was associated with lower risk of fatty liver; after adjustment for sociodemographic characteristics, lifestyle factors, and other dietary intakes, the ORs (95% CIs) for the highest vs. the lowest quintiles of choline intake were 0.68 (0.59, 0.79) in women and 0.75 (0.60, 0.93) in men (both P-trend < 0.01). The inverse association was attenuated after further adjustment for history of metabolic disease and, in particular, BMI. The corresponding ORs (95% CIs) were 0.88 (0.75, 1.03) in women (P-trend = 0.05) and 0.85 (0.68, 1.06) in men (P-trend = 0.09). Stratified analyses suggested a potential effect modification by obesity status in women; the OR (95% CI) across extreme quintiles was 0.72 (0.57, 0.91) in normal-weight women vs. 1.05 (0.84, 1.31) in overweight or obese women (P-trend = 0.007 vs. 0.99, P-interaction < 0.0001).Conclusion: Higher dietary choline intake may be associated with lower risk of nonalcoholic fatty liver only in normal-weight Chinese women.

Statin therapy is associated with a reduced risk of non-alcoholic fatty liver in overweight individuals.

Non-alcoholic fatty liver or hepatic steatosis is considered the hepatic manifestation of the metabolic syndrome. Statins are often used by patients with metabolic syndrome, but their effect in steatosis is not well established. To study the association between statins and the presence of steatosis. In the population-based Rotterdam Study, 2578 subjects underwent liver ultrasonography and had prescription data available. In a cross-sectional design, we investigated the effect of current, past, and duration of statin use. Logistic regression analyses were adjusted for age, sex, and other known risk factors. The prevalence of steatosis was 35.3%. We identified 631 current and 359 past statin users. In multivariable analyses, current statin use >2 years was associated with a significantly lower steatosis prevalence [OR 0.43, 95% CI 0.19-0.96]. Stratification by mean body mass index showed that this association was stronger in patients with body mass index ≥ 27.5 [OR 0.30, 95% CI 0.11-0.81 for current use >2 years], while in patients with body mass index <27.5 the association was non-significant. Within the Rotterdam study, in patients with body mass index ≥ 27.5 current use of statins for >2 years was associated with a lower prevalence of steatosis.

Relationship between hematocrit and the risk of nonalcoholic fatty liver disease: A follow-up observation for five years

Objective To investigate the relationship between hematocrit(HCT) and the risk of nonalcoholic fatty liver disease.Methods A community-based health examination survey in individuals who were randomly selected from residents living in the urban area of Xuzhou was carried out in 2006.2 798 subjects without nonalcoholic fatty liver disease were included in the present study.Subjects were divided into two groups according to HCT level,group A (HCT ≤ 0.49 L/L) and group B (HCT ＞ 0.49 L/L).Serum alanine aminotransferase,aspartate aminotransferase,triglycerides,total cholesterol,high density lipoprotein-cholesterol,low density lipoproteincholesterol,fasting plasma glucose,and imaging examinations were determined.Results The prevalence of nonalcoholic fatty liver disease was higher in group B than that in group A (26.5％ vs 15.9％,P＜0.01),and the difference was statistically significant.Logistic regression showed that the incidence of nonalcoholic fatty liver disease was increased along with elevated levels of HCT.Conclusions HCT is found to be correlated with the prevalence of nonalcoholic fatty liver disease. Key words: Nonalcoholic fatty liver disease ; Hematocrit ; Incidence

Significance of high sensitivity C-reactive protein level for predicting risk of nonalcoholic fatty liver in type 2 diabetes mellitus patients

To investigate the significance of high sensitivity C-reactive protein (hsCRP) levels in serum for detecting type 2 diabetes mellitus (T2DM) patients at risk of developing nonalcoholic fatty liver (NAFLD). Individuals with T2DM (n = 9489) were recruited from the Kailuan Company between 2006 and 2007 for the first phase of this community-based prospective cohort study. For the second phase of the study, the original cohort was recruited for follow-up (at two years from each subject's original enrollment date (baseline)). The total followed-up subjects (n = 2802; 2344 males, 458 females, 22-88 years old) were categorized into quartiles according to baseline measurements of serum hsCRP levels (less than or equal to 0.30, > 0.30-0.60, > 0.60-1.92 and > 1.92 mg/L) and used to determine the relationship between change in incidence rates of NAFLD and predictive value of baseline serum hsCRP levels by logistic regression analysis. Twenty-nine percent (n = 813) of the followed-up subjects developed NAFLD. The incidence (%) of NAFLD at the two-year follow-up had increased in conjunction with the level of serum hsCRP detected at baseline (quartile 1: 22.5%, 2: 27.3%, 3: 32.1%, and 4: 34.3%; all, P less than 0.01). It was found that the subjects in the highest quartile had an increased risk of NAFLD (odds ratio (OR) = 1.80, 95% confidence interval (CI): 1.42-2.28, P less than 0.01), as compared with those in the lowest quartile. Moreover, when the regression model was adjusted for baseline factors of age, sex, triglycerides, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, fasting serum glucose, and body mass index, the risk of NAFLD remained significantly higher for the highest quartile (vs. the lowest quartile; OR = 1.49, 95% CI: 1.16-1.91, P less than 0.01). Serum hsCRP levels may be predictive of development of NAFLD in individuals with type 2 diabetes mellitus. The risk of NAFLD increases in parallel with increasing levels of serum hsCRP.