Understanding Of Nonalcoholic Fatty Liver Disease Research Articles

Knowledge, Attitudes, and Determinants of Nonalcoholic Fatty Liver Disease Among Adults in Jazan Province: A Cross-Sectional Study.

Background Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease globally, with its prevalence rising worldwide. This study aimed to evaluate the knowledge, attitudes, and determinants related to NAFLD among adults in Jazan, Saudi Arabia. Methods A cross-sectional study was conducted using a validated online questionnaire distributed to 540 participants in Jazan Province. Data analysis involved descriptive and comparative statistics to assess knowledge, attitudes, and influencing factors related to NAFLD. Results The majority of participants (244, 45.2%) demonstrated poor knowledge about NAFLD, while 226 (41.9%) had fair knowledge. Notably, individuals aged 40-49, males, healthcare workers, those with obesity and diabetes mellitus, and those with a family history of NAFLD showed significantly higher levels of knowledge (p < 0.05). Regarding attitudes, most participants (64.4%) exhibited a positive attitude toward NAFLD, 28.3% had a satisfactory attitude, and only 7% demonstrated a poor attitude. Conclusion The findings highlight the need for targeted educational interventions and public awareness campaigns to enhance the general public's understanding of NAFLD. Providing accurate and up-to-date information about the disease, its consequences, and preventive measures is crucial for improving awareness and knowledge.

Nurses' Knowledge of Nonalcoholic Fatty Liver Disease: A Cross-sectional Study

General Background: Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver conditions, including simple steatosis, cirrhosis, liver cancer, and non-alcoholic steatohepatitis (NASH). Specific Background: Given the increasing prevalence of NAFLD, understanding healthcare professionals' knowledge about this condition is crucial for effective patient care and management. Knowledge Gap: However, there is limited research assessing nurses' knowledge regarding NAFLD, particularly in the context of Basrah City Center Hospitals. Aims: This study aimed to evaluate nurses' knowledge of NAFLD and investigate its relationship with demographic characteristics such as gender, age, years of experience, and departmental affiliation. Results: A cross-sectional survey involving 150 nurses revealed that 57.3% possessed high levels of knowledge regarding NAFLD, while 34% had moderate knowledge. Notably, a significant correlation was found between nurses working at Al-Shifaa Hospital and their knowledge levels. The majority of participants were female (64.7%) and aged 20-30 (72%), with a predominant educational background from Nursing Institutes (39.3%) and fewer than five years of experience (56%). Novelty: This study is pioneering in assessing the knowledge of NAFLD among nurses in Basrah, highlighting specific areas of strength and weakness in their understanding. Implications: The study highlights the need for targeted educational interventions to improve nurses' understanding of NAFLD, leading to improved patient care and outcomes in liver disease management. practice. Highlights: Increasing NAFLD prevalence necessitates enhanced healthcare provider awareness. Nurses showed significant knowledge levels about NAFLD. Knowledge varies significantly by hospital affiliation. Keywords: Non-alcoholic fatty liver disease, nurses' knowledge, Basrah City, cross-sectional study, healthcare education.

Harnessing polarity-dependent fluorescent probe for lipid droplet metabolism dissection and in vivo nonalcoholic fatty liver disease diagnosis

Nonalcoholic fatty liver disease (NAFLD) has emerged as a prevalent chronic liver condition worldwide. The dysregulated metabolism of lipid droplets (LDs) in cells is physiologically and pathologically linked to NAFLD. The development of fluorescent probes for imaging LD metabolism holds promise for noninvasive diagnosis and understanding of NAFLD. However, the development of such probes is challenging, and their in vivo diagnostic potential remains largely unexplored. Here, we present the synthesis of ZP-1, a bright fluorophore serving as a specific probe for LDs. ZP-1 possesses a donor-acceptor electronic structure with intramolecular charge transfer characteristics and shows polarity-dependent emission. In highly polar solvents, such as water, ZP-1 exhibits minimal fluorescence, while in low-polarity solvents, it displays strong fluorescence. This property enables high-specificity LD detection with excellent imaging contrast. Attributed to its high photostability and pH stability, ZP-1 effectively visualizes LD metabolism in live cells via real-time imaging, encompassing processes such as growth, migration, fusion, and fission. Moreover, we demonstrate in vivo diagnosis of NAFLD in a mouse model, providing rich information regarding LD morphology, numbers, volumes, and tissue structures. This work introduces ZP-1 as a valuable tool for NAFLD diagnosis and research, facilitating noninvasive assessment and improved understanding of the disease.

Fructose aggravates copper-deficiency-induced non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD), is the most common cause of chronic liver disease, affecting 24% of the global population. Accumulating evidence demonstrates that copper deficiency (CuD) is implicated in the development of NAFLD, besides, high fructose consumption by promoting inflammation contributes to NAFLD. However, how CuD and/or fructose (Fru) causes NAFLD is not clearly delineated. The present study aims to investigate the role of CuD and/or fructose supplement on hepatic steatosis and hepatic injury. We established a CuD rat model by feeding weaning male Sprague-Dawley rats for 4 weeks with CuD diet. Fructose was supplemented in drinking water. We found the promoting role of CuD or Fructose (Fru) in the progress of NAFLD, which was aggravated by combination of the two. Furthermore, we presented the alteration of hepatic lipid profiles (including content, composition, and saturation), especially ceramide (Cer), cardiolipin (CL), phosphatidylcholine (PC) and phosphatidylethanolamine (PE) was closely associated with CuD and/or Fru fed induced-NAFLD in rat models. In conclusion, insufficient copper intake or excessive fructose supplement resulted in adverse effects on the hepatic lipid profile, and fructose supplement causes a further hepatic injury in CuD-induced NAFLD, which illuminated a better understanding of NAFLD.

Nonalcoholic Fatty Liver Disease: Focus on New Biomarkers and Lifestyle Interventions.

Nonalcoholic fatty liver disease (NAFLD) is considered a hepatic manifestation of metabolic syndrome, characterized from pathological changes in lipid and carbohydrate metabolism. Its main characteristics are excessive lipid accumulation and oxidative stress, which create a lipotoxic environment in hepatocytes leading to liver injury. Recently, many studies have focused on the identification of the genetic and epigenetic modifications that also contribute to NAFLD pathogenesis and their prognostic implications. The present review is aimed to discuss on cellular and metabolic alterations associated with NAFLD, which can be helpful to identify new noninvasive biomarkers. The identification of accumulated lipids in the cell membranes, as well as circulating cytokeratins and exosomes, provides new insights in understanding of NAFLD. This review also suggests that lifestyle modifications remain the main prevention and/or treatment for NAFLD.

Major royal jelly proteins prevents NAFLD by improving mitochondrial function and lipid accumulation through activating the AMPK / SIRT3 pathway in vitro.

Nonalcoholic fatty liver disease (NAFLD) is a metabolic syndrome, whose main characteristics are excessive lipid accumulation and oxidative stress. Major royal jelly proteins (MRJPs) is a kind of water-soluble protein, which is abundant in royal jelly (RJ). The aim of this study was to evaluate the effect of MRJPs on lipid accumulation and oxidative stress of liver cells. Here, we first optimized the conditions for extracting MRJPs from RJ and identified the extraction effect and product by SDS-PAGE. Then, we used oleic acid (OA) of 1.0mM to induce hepatocytes for 24 hr to establish a stable cell models of lipid accumulation, and we found that pre-administration (24 hr) of MRJPs (0.2, 0.5, and 1.0g/L) could significantly reduce the lipid drop content and triglyceride level in the model cells, and simultaneously reduce the alanine aminotransferase and aspertate aminotransferase levels in the cell culture supernatant. In addition, pre-incubation (24 hr) with MRJPs (0.2, 0.5, and 1.0g/L) could restore superoxide dismutase (SOD) level and mitochondrial membrane potential as compared with OA group. Furthermore, MRJPs administration significantly upregulated the expression of Silent Information Regulator 2 Associated Protein 3, mitochondrial superoxide dismutase (SOD2), and cytochrome c oxidase subunit IV in OA-treated HepG2 cells. The study for the first time provides evidences on the lipid-lowering effect of MRJPs at the cellular level, which can further provide support for the development and application of polypeptide drugs in the future, and can also provide a choice for the prevention and treatment of liver metabolic diseases represented by NAFLD. PRACTICAL APPLICATION: Our study proved that MRJPs had substantial preventing effect on OA-induced lipid accumulation and mitochondrial dysfunction in HepG2 cells. This research can further provide theoretical support for the development and application of peptide drugs in the future. Besides, it can not only further broaden our understanding of NAFLD and other diseases, but also provide ideas for research on oxidative stress and lipid accumulation in the body.

Network Modeling Approaches and Applications to Unravelling Non-Alcoholic Fatty Liver Disease.

Non-alcoholic fatty liver disease (NAFLD) is a progressive condition of the liver encompassing a range of pathologies including steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma. Research into this disease is imperative due to its rapid growth in prevalence, economic burden, and current lack of FDA approved therapies. NAFLD involves a highly complex etiology that calls for multi-tissue multi-omics network approaches to uncover the pathogenic genes and processes, diagnostic biomarkers, and potential therapeutic strategies. In this review, we first present a basic overview of disease pathogenesis, risk factors, and remaining knowledge gaps, followed by discussions of the need and concepts of multi-tissue multi-omics approaches, various network methodologies and application examples in NAFLD research. We highlight the findings that have been uncovered thus far including novel biomarkers, genes, and biological pathways involved in different stages of NAFLD, molecular connections between NAFLD and its comorbidities, mechanisms underpinning sex differences, and druggable targets. Lastly, we outline the future directions of implementing network approaches to further improve our understanding of NAFLD in order to guide diagnosis and therapeutics.

1190 Does Nonalcoholic Fatty Liver Disease Increase the Risk for Acute Ischemic Bowel Disease?

INTRODUCTION: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States. It has been reported in the literature that NAFLD increases the risk for cardiovascular disease, but a possible association between NAFLD and acute ischemic bowel disease (AIBD) has not been studied. Our aim in this study is to evaluate if NAFLD is an independent risk factor for AIBD. METHODS: Using data from the National Inpatient Sample (NIS) database between 2002 and 2014, we identified patients who were diagnosed with NAFLD and AIBD using appropriate ICD 9 coding. The control group was the patients who did not have a diagnosis of NAFLD. We then performed multivariate logistic regression analysis for the association between NAFLD and AIBD RESULTS: The total population was comprised of 101,137,143 patients, of which 365,701 (0.36%) were diagnosed with NAFLD and 133,201 (0.13%) were diagnosed with AIBD. Patients in the NAFLD group were older (53 vs 48), less likely to be females (57.7% vs 58.4%) and African American (9.3% vs 14.3%) (P &lt; 0.0001 for all). In addition, NAFLD patients had more tobacco use (13.9% vs 9.5%), alcohol (7.1% vs 3.4%), obesity (26.2% vs 6.9%) and diabetes mellitus (DM) with or without complications (5.6% vs 3.2%) and (30.7% vs 14.1%) respectively. Furthermore, individuals in the NAFLD group had less comorbid chronic obstructive pulmonary disease (COPD) (9.5% vs 10.9%), congestive heart failure (CHF) (5.5% vs 6.5%), cardiovascular atherosclerosis (13.8% vs 17%) and atrial fibrillation (AFib) (5.8% vs 8.8%) (P &lt; 0.0001 for all). Both groups had similar prevalence of major cardiovascular surgery (0.1%) (P &gt; 0.05). Using Multivariate logistic regression, and after adjusting for potential cofounding factors including: (age, gender, race, obesity, COPD, CHF, DM, tobacco use, cardiovascular atherosclerosis, AFib and a history of major cardiovascular surgery), NAFLD group had a statistically significant higher rate of AIBD (Odds Ratio [OR], 2.11, 95% confidence interval [CI], 2.02-2.20, P &lt; 0.0001) compared with the non-NAFLD group. CONCLUSION: Based on our analysis, patients in the NAFLD group were twice more likely to have AIBD. To our knowledge, this the first study that evaluated the risk for AIBD in NAFLD patients. This finding adds to our understanding of NAFLD as multisystem disease and highlights the importance of controlling the risk factors associated with NAFLD.

Comparative study of liver injury induced by high-fat methionine- and choline-deficient diet in ICR mice originating from three different sources

Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease worldwide. It is characterized by the accumulation of lipids without alcohol intake and often progresses to non-alcoholic steatohepatitis (NASH), liver fibrosis, and end-stage liver diseases such as cirrhosis or cancer. Although animal models have greatly contributed to the understanding of NAFLD, studies on the disease progression in humans are still limited. In this study, we used the recently reported high-fat L-methionine-defined and choline-deficient (HFMCD) diet to rapidly induce NASH and compared the responses to HFMCD in ICR mice from three different countries: Korea (supplied by the National Institute of Food and Drug Safety Evaluation), USA, and Japan during 6 weeks. Feeding HFMCD did not cause significant differences in weight gain in comparison with mice fed control diet. Relative weight of the liver increased gradually, while the relative weight of the kidneys remained unchanged. The parameters of liver injury (serum activities of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase) increased rapidly from 1 week and remained elevated for as long as 6 weeks. Histopathological analysis showed that the accumulation of hepatic lipids induced by HFMCD was prominent at 1 week after diet supplementation and increased further at 6 weeks. Inflammatory markers were significantly increased in a time-dependent manner by HFMCD. The mRNA levels of TNF-α and IL-6 were elevated approximately 15-fold relative to control diet and that of IL-1β was increased more than 20-folds at 6 week after the onset of HFMCD intake. In addition, mRNA expression of fibrosis markers such as α-SMA, TGFβ1, and Col1a1 were also significantly increased at 6 week. In summary, the responses of Korl:ICR mice by intake of HFMCD diet were similar to those of ICR mice from other sources, which suggests that Korl:ICR mice is also a useful resource to study the pathogenesis of diet-induced NAFLD.

SAT-109 tiRNA-5 Reflects the Severity of Mitochondrial Oxidative Stress in Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is a chronic metabolic disease with complicated mechanisms among which disturbance of mitochondria function weighs a lot. Overexpression of CypD, the initial factor in mitochondrial permeability transition pore, led to mitochondrial stress triggered hepatic TG accumulation. tRNA fragments (tRFs) are non-coding RNAs produced by precise cleavage of tRNA and divided into subtypes including tiRNA-5, tiRNA-3, tRF-5, tRF-3 and tRF-1. It is reported that tRFs, especially tiRNA-5 associated with stress. However, whether tRFs connect with NAFLD is unclear. To solve the problem, CypD overexpression models were constructed by injecting mouse AdPPIF virus to 8-weeks male C57BL/6 mice as study group (CH, n=6). Control group (WT, n=6) was established by injecting empty vector virus (AdEGFP). Then tRFs in liver were detected by high-throughput sequencing. Proportion of tRFs in CH was 40.8% higher vs WT. A connection might exist between CypD and tRFs. To validate this speculation, CypD knockdown mice were established as study group and 8-weeks male C57BL/6 as control. Then both groups were fed with 60 kcal% fat diet for 4 weeks or 8 weeks and named as CKO4, CWT4, CKO8 or CWT8 (n=6). Sequencing showed that proportion of tRFs in CKO4 and CKO8 was 42.7% and 31.2% lower vs control respectively, consistent with the speculation. Therefore, bioinformatics analysis was used to explore further. Pie plot based on proportion of each tRFs subtype showed that over 90% tRFs were tRF-5 and tiRNA-5. tiRNA-5 was 38.5% higher in CH vs WT, 27.4% lower in CKO4 vs CWT4 and 36.0% lower in CKO8 vs CWT8, indicating a connection between tiRNA-5 and CypD. Integration of pathological sections, metabolic index and more analysis were done for futher study. PCA and Venn diagram described the difference on the whole while absolute value of Pearson correlation coefficient (CH vs WT=0.84, CKO4 vs CWT4=0.93, CKO8 vs CWT8=0.73) and Scatter plot (CH vs WT =0.69, CKO4 vs CWT4=0.85, CKO8 vs CWT8=0.66) reflected the similarity between study and control group. These data indicated a connection between tRF and the severity of NAFLD assessed by pathology and metabolism index. Finally, a cutoff of fold change ≥ 1.5 was employed to identify the differentially expressed tRFs and most of those were tiRNA-5 as speculated. qRT-PCR was conducted for validation, among which fold change of AS-tDR-000666 (GlyGCC derived tiRNA-5) was significative (CH vs WT=4.29, CKO4 vs CWT4=0.22, CKO8 vs CWT8=0.05). It might be a potential biomarker related with severity of NAFLD. Because the CypD-change-induced mitochondrial oxidative stress was the direct mechanism triggering NAFLD in mouse models above, we could conclude that mitochondrial oxidative stress in NAFLD changed the profile of tRFs and tiRNA-5 had the potential to reflect the severity of mitochondrial oxidative stress in NAFLD. This study provided a new understanding of NAFLD.

Co-Morbidities as a Predictor for Progression of Non-Alcoholic Fatty Liver Disease

Introduction: Greater than 64 million people in the US have Non-alcoholic fatty liver disease (NAFLD), constituting an economic burden of more than $100 billion annually in healthcare costs. Though metabolic syndrome is a major risk factor, there remains uncertainty about the natural history of disease and the interplay of major comorbidities. A better understanding of the progression from NAFLD to nonalcoholic steatohepatitis (NASH) and cirrhosis has major implications for healthcare cost, screening recommendations, evaluation and treatment. Methods: Retrospective review of outpatients between 2008 and 2016 using ICD-9 and ICD-10 codes. Over 500 patients with NAFLD were identified. Those without liver biopsy or incomplete data were excluded. Biopsies were categorized based on the NAFLD activity score (NAS) which is the unweighted sum of the grade of steatosis, lobular inflammation and hepatocellular ballooning. NAS score of 0-2 was classified as non-NASH, 3-4 as borderline steatohepatitis and 5-8 as NASH. Patients with cirrhosis were excluded as NAS is not an accurate representation of severity of liver disease in this population and cirrhotics tend to have low NAS. Chi-square was used for categorical values and analysis of variance (ANOVA) was used for numerical values. Results: 114 patients were available for review. 60.5% were female, mean age (SD): 54 (12), and 82.4% Caucasian. There was no statistical difference in age, gender, BMI or ethnicity among the three groups. Final analysis revealed a distribution of non-NASH, borderline steatohepatitis and NASH in 8 (70%), 59 (51.7%) and 47 (41.2%), respectively. Polycystic ovarian syndrome (PCOS) and Coronary Artery Disease (CAD) were seen in 4.4% and 1.8% of the population. NAFLD patients with CAD, gallstone disease, obstructive sleep apnea (OSA) and PCOS were more likely to have borderline steatohepatitis or NASH (p < 0.05). Conclusion: Our data suggests that gallstone disease, CAD, OSA, and PCOS, all diseases related to obesity, may have implications in predicting risk for progression of NAFLD to NASH. Evolving our understanding of NAFLD will help mitigate disease progression to fibrosis and cirrhosis, and to target patients at higher risk for developing NASH. NAFLD is a major cause of chronic liver disease worldwide, and its clinical and economic burden will continue to grow with parallel increases in rates of obesity and metabolic syndrome. Further evaluation with a larger dataset, at multiple institutions, is warranted to validate our results.

A systematic review of the present and future of non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the Western world. Ongoing research has furthered our understanding of NAFLD, the nature of progression of this disease, and its impact on morbidity and mortality. An active form of NAFLD is non-alcoholic steatohepatitis (NASH); it is the most severe subtype, without any current recommended therapies, according to the European Medicines Agency. The development of new therapies presents challenges, notably due to the slow progression of NASH and the clinically relevant endpoints.Correlating new data with effective treatment regimens is an emerging challenge, which will increase our understanding of the factors affecting the NAFLD course. This can enable more appropriate non-invasive prognostic assessments, which can focus on specifically at-risk NAFLD populations for tailored individual treatment. This review article aims to highlight the current developments in the field of NAFLD: pathogenesis, epidemiology, diagnosis, clinical features, and available treatment, including novel targets and therapies.

The Association between Non-Alcoholic Fatty Liver Disease and Cardiovascular Risk in Children.

The rising prevalence of childhood obesity in the past decades has made Non-Alcoholic Fatty Liver Disease (NAFLD) the most common cause of pediatric chronic liver disease worldwide. Currently, a growing body of evidence links NAFLD with cardiovascular disease (CVD) even at an early age. Data on the pediatric population have shown that NAFLD could represent an independent risk factor not only for cardiovascular events but also for early subclinical abnormalities in myocardial structure and function. Briefly, we review the current knowledge regarding the relationship between pediatric NAFLD and cardiovascular risk in an attempt to clarify our understanding of NAFLD as a possible cardiovascular risk factor in childhood.

Oxidative Stress as a Critical Factor in Nonalcoholic Fatty Liver Disease Pathogenesis.

Nonalcoholic fatty liver disease (NAFLD), characterized by liver triacylglycerol build-up, has been growing in the global world in concert with the raised prevalence of cardiometabolic disorders, including obesity, diabetes, and hyperlipemia. Redox imbalance has been suggested to be highly relevant to NAFLD pathogenesis. Recent Advances: As a major health problem, NAFLD progresses to the more severe nonalcoholic steatohepatitis (NASH) condition and predisposes susceptible individuals to liver and cardiovascular disease. Although NAFLD represents the predominant cause of chronic liver disorders, the mechanisms of its development and progression remain incompletely understood, even if various scientific groups ascribed them to the occurrence of insulin resistance, dyslipidemia, inflammation, and apoptosis. Nevertheless, oxidative stress (OxS) more and more appears as the most important pathological event during NAFLD development and the hallmark between simple steatosis and NASH manifestation. The purpose of this article is to summarize recent developments in the understanding of NAFLD, essentially focusing on OxS as a major pathogenetic mechanism. Various attempts to translate reactive oxygen species (ROS) scavenging by antioxidants into experimental and clinical studies have yielded mostly encouraging results. Although augmented concentrations of ROS and faulty antioxidant defense have been associated to NAFLD and related complications, mechanisms of action and proofs of principle should be highlighted to support the causative role of OxS and to translate its concept into the clinic. Antioxid. Redox Signal. 26, 519-541.

Concepts and Treatment Approaches in Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) affects up to 30% of adults and is the most common liver disease in Western nations. NAFLD is associated with central adiposity, insulin resistance, type 2 diabetes mellitus, hyperlipidemia, and cardiovascular disease. It encompasses the entire spectrum of fatty liver diseases from simple steatosis to nonalcoholic steatohepatitis (NASH) with lobular/portal inflammation, hepatocellular necrosis, and fibrosis. Of those who develop NASH, 15–25% will progress to end stage liver disease and hepatocellular carcinoma over 10–20 years. Its pathogenesis is complex, and involves a state of lipid accumulation due to increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, and increased incidence of de novo lipogenesis. Plasma aminotransferases and liver ultrasound are helpful in the diagnosis of NAFLD/NASH, but a liver biopsy is often required for definitive diagnosis. Many new plasma biomarkers and imaging techniques are now available that should improve the ability to diagnose NAFLD noninvasively Due to its complexity and extrahepatic complications, treatment of NAFLD requires a multidisciplinary approach with excellent preventative care, management, and treatment. This review will evaluate our current understanding of NAFLD, with a focus on existing therapeutic approaches and potential pharmacological developments.

Nonalcoholic fatty liver disease in children

Nonalcoholic fatty liver disease (NAFLD) has become the most common cause of liver disease in children from the developed world. The purpose of this review is to provide both a focused overview of pediatric NAFLD as well as a summary of the most recent advancements in the field. Pediatric NAFLD is an underdiagnosed condition which can result in significant liver injury including cirrhosis. Although liver biopsy remains the standard for diagnosis and monitoring disease activity, several noninvasive biomarkers and imaging techniques hold significant promise. Dietary constituents, the intestinal bacterial flora, and sex hormones have been implicated as modulators of disease activity. NAFLD predisposition runs strongly in families and an allele in the PNPLA3 gene has shown a strong association with liver steatosis and hepatic inflammation. Treatment for pediatric NAFLD remains diet and exercise, but vitamin E may be a helpful adjunct. Pediatric NAFLD shares many features with its adult counterpart but is a distinct entity which requires independent investigation. Our understanding of NAFLD in terms of epidemiology and risk factors has improved considerably but significantly more investigation is required to unravel its pathophysiology and identify novel therapeutic targets.