Changes In Non-alcoholic Fatty Liver Disease Research Articles

Trimethylamine-N-oxide, a New Risk Factor for Non-alcoholic Fatty Liver Disease Changes the Expression of miRNA-34a, and miRNA-122 in the Fatty Liver Cell Model.

Non-alcoholic fatty liver disease is a multifactorial disorder with complicated pathophysiology ranging from simple steatosis to steatohepatitis and liver fibrosis. Trimethylamine-N-oxide (TMAO) production is believed to be correlated with choline deficiency. This study investigated the expression of miRNA-34a, miRNA-122, and miRNA-192 in the fatty liver cell model treated with different concentrations of TMAO. A fatty liver cell model was developed by exposing HepG2 cells to a mixture of palmitate and oleate in a ratio of 1:2 at a final concentration of 1200μM for 24h. The confirmed fatty liver cells were treated with 37.5, 75, 150, and 300μM of TMAO for 24h. RT-qPCR was used to quantify the expression of microRNAs in a cellular model. The cellular expression of all microRNAs was significantly higher in treated fatty liver cells compared to normal HepG2 cells (P < 0.05). Only 75 and 150µM of TMAO significantly increased the expression of miRNA-34a and miRNA-122 compared to both fatty and normal control cells (P < 0.05). Our results provided an experimental documentation for the potential effect of TMAO to change the expression of miR-34a and miR-22 as a mechanism for contributing to the pathogenesis of non-alcoholic fatty liver disease.

Correlation between metabolic, liver profile, dietary habits and ultrasound scan determined non-alcoholic fatty liver disease changes in children aged 6-18 years with body mass index

Introduction: Non-alcoholic fatty liver disease (NAFLD) is the commonest cause of liver disease worldwide and this is linked to the change in lifestyle and rise in prevalence of overweight and obesity among children.  Objectives: To study the correlation between metabolic, liver profile, dietary habits and ultrasound scan determined NAFLD changes in children aged 6–18 years old with their body mass index (BMI). Method: A tertiary care hospital based comparative, prospective study was conducted on 159 children aged 6-18 years at Indira Gandhi Medical College and Hospital, Shimla, India over a period of one year. Children presenting to the outpatient department (OPD) were assigned to two groups based on their BMI, group I with BMI of ≤85th centile and group II with BMI >85th centile. Those with acute and chronic liver ailments and on drugs like vitamin E, statins or antihypertensives were excluded. These were subjected to venepuncture for estimating fasting blood sugar (FBS), liver function tests (LFTs) and complete lipid profile. Ultrasound scan was done to look for NAFLD changes. Results: Children in group II had increased incidence of dyslipidaemia 93.7% vs 41.2%, deranged LFTs 49.4% vs 12.5%, increased FBS 10.1% vs 2.5% and NAFLD 40.5% vs 2.5% when compared to children in group I. Conclusions: BMI and dietary habits have an important bearing on occurrence of NAFLD in children aged 6–18 years old. Sri Lanka Journal of Child Health , 2018; 47 (2): 125-128

Serum metabolites in non-alcoholic fatty-liver disease development or reversion; a targeted metabolomic approach within the PREDIMED trial

Background Limited prospective studies have examined changes in non-alcoholic fatty-liver disease (NAFLD) related serum-metabolites and none the effects of NAFLD-reversion. We aimed to evaluate whether perturbations in metabolites indicate predisposition to NAFLD development and to assess the effects of NAFLD reversion on metabolite profiles.MethodsA targeted liquid-chromatography tandem mass-spectrometry metabolic profiling (n = 453 metabolites) approach was applied, using serum from 45 subjects of the PREDIMED study, at baseline and after a median 3.8-year follow-up. NAFLD was determined using the hepatic steatosis index; with three groups classified and studied: Group 1, not characterized as NAFLD cases during the follow-up (n = 15); Group 2, characterized as NAFLD during the follow-up (n = 15); Group 3, characterized as NAFLD-reversion during the follow-up (n = 15).ResultsAt baseline, significantly lower storage and transport lipids (triacylglycerols and cholesteryl esters), several monoetherglycerophosphocholines, acylglycerophosphocholines, ceramides and ceramide to sphingomyelin ratio (P < 0.05), were found; whereas a higher L-cystine to L-glutamate ratio (P < 0.05) was observed, in group 2 as compared to group 1.P-ether acylglycerophosphocholines, ceramides and sphingolipids were significantly different betweengroup 3 and group 1 (P < 0.05). Higher 16:1n-7 to 16:0, and 18:0 to16:0 ratio (P < 0.05), while lower 18:1n-9 to 18:0, 16:0 to 18:2n-6, and 18:3n-6 to 18:2n-6 ratio (P < 0.05) were observed in the final, compared to baseline values, in groups 2 and 3.ConclusionThe rearrangement of lipid biosynthesis and serum transport may indicate predisposition to NAFLD development. Despite an expected reduction of hepatic lipotoxicity and improved hepatic function in the participants of the study characterized as NAFLD-reversing, the side effects of NAFLD in serum metabolic profiles remained present.Trial registrationThe trial is registered at ISRCTN35739639. Registration date: 5th October 2005.

Structural changes in the liver in metabolic syndrome

Scientifically proven close relationship of nonalcoholic fatty liver disease with development of metabolic syndrome and its individual components involves the conclusion that the target organ in metabolic symptom, even regardless of the severity of obesity, the liver occupies a dominant position, as the body undergoes the first characteristic of non-alcoholic fatty liver disease changes, involving violation of metabolism in the body. Dislipoproteinemia plays an important role in the formation of metabolic syndrome in obesity and other obesity-associated diseases. Altered liver function are the root cause of violations of processes of lipid metabolism and, consequently, abnormal functioning of the liver may be a separate, additional and independent risk factor for development of dyslipidemia and obesity as the main component of the metabolic syndrome.