scholarly journals Newborn and childhood differential DNA methylation and liver fat in school-age children

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Madelon L. Geurtsen ◽  
Vincent W. V. Jaddoe ◽  
Lucas A. Salas ◽  
Susana Santos ◽  
Janine F. Felix
Keyword(s):  
Dna Methylation ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
School Age Children ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation ◽  
Fat Fraction ◽  
Alcoholic Fatty Liver Disease

Abstract Background Non-alcoholic fatty liver disease is the most common chronic liver disease in children in western countries. Adverse early-life exposures are associated with higher liver fat percentages in children. Differential DNA methylation may underlie these associations. We aimed to identify differential DNA methylation in newborns and children associated with liver fat accumulation in childhood. We also examined whether DNA methylation at 22 cytosine-phosphate-guanine sites (CpGs) associated with adult non-alcoholic fatty liver disease is associated with liver fat in children. Within a population-based prospective cohort study, we analyzed epigenome-wide DNA methylation data of 785 newborns and 344 10-year-old children in relation to liver fat fraction at 10 years. DNA methylation was measured using the Infinium HumanMethylation450 BeadChip (Illumina). We measured liver fat fraction by Magnetic Resonance Imaging. Associations of single CpG DNA methylation at the two-time points with liver fat accumulation were analyzed using robust linear regression models. We also analyzed differentially methylation regions using the dmrff package. We looked-up associations of 22 known adult CpGs at both ages with liver fat at 10 years. Results The median liver fat fraction was 2.0% (95% range 1.3, 5.1). No single CpGs and no differentially methylated regions were associated with liver fat accumulation. None of the 22 known adult CpGs were associated with liver fat in children. Conclusions DNA methylation at birth and in childhood was not associated with liver fat accumulation in 10-year-old children in this study. This may be due to modest sample sizes or DNA methylation changes being a consequence rather than a determinant of liver fat.

MO457PREVALENCE OF NON-ALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH CHRONIC KIDNEY DISEASE: A CASE-CONTROL STUDY

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Therese Adrian ◽  
Mads Hornum ◽  
Ida Maria Hjelm Soerensen ◽  
Ellen Linnea Freese Ballegaard ◽  
Susanne Bro ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Liver Disease ◽  
Kidney Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
Hounsfield Units ◽  
Alcoholic Fatty Liver ◽  
Fat Fraction ◽  
Alcoholic Fatty Liver Disease

Abstract Background and Aims Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease and is characterised by hepatic accumulation of lipids. NAFLD represents a wide spectrum ranging from mild steatosis over non-alcoholic steatohepatitis with and without fibrosis to overt cirrhosis. Patients with NAFLD have a high risk of developing cardiovascular disease and chronic kidney disease (CKD). So far, there is scarce evidence of the prevalence of NAFLD among patients with CKD. The aim of this study was to investigate the prevalence of moderate to severe steatosis in a cohort with patients with different stages of CKD not on dialysis. Method A total of 291 patients from the Copenhagen Chronic Kidney Disease Study were included. For comparison, 866 participants with normal kidney function from the Copenhagen General Population Study were identified as controls. Blood samples, clinical demographics, information about smoking and alcohol were collected. Hepatic liver fat fraction was evaluated in all participants by computed tomography (CT). Liver attenuation density <48 Hounsfield Units was used as cut-off value for moderate to severe steatosis corresponding to 10% liver fat after transformation of the CT attenuation. Results The prevalence of moderate to severe steatosis was 7.9% and 10.7% among patients with CKD and controls, respectively. Data of the continuous Hounsfield Units showed lower values among patients with CKD compared with the control group. No significant association between liver fat fraction and CKD stage was found. Pooled data from both cohorts showed that adjusted odds ratios (OR) for steatosis were strongly significant among persons with diabetes (OR 3.1, 95% confidence interval (CI) 1.6-5.9), overweight (OR 14.8, 95% CI 4.6-47.9) and obesity (OR 42.0, 95% CI 12.9-136.6), respectively. Conclusion In the present cohort of 291 patients with CKD, kidney function was not associated with the prevalence of hepatic steatosis as assessed by CT scan.

scholarly journals Bilirubin Nanoparticles Reduce Diet-Induced Hepatic Steatosis, Improve Fat Utilization, and Increase Plasma β-Hydroxybutyrate

2020 ◽  
Vol 11 ◽  
Author(s):  
Terry D. Hinds ◽  
Justin F. Creeden ◽  
Darren M. Gordon ◽  
Donald F. Stec ◽  
Matthew C. Donald ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation ◽  
Fat Utilization ◽  
Hepatic Fat ◽  
Alcoholic Fatty Liver Disease

The inverse relationship of plasma bilirubin levels with liver fat accumulation has prompted the possibility of bilirubin as a therapeutic for non-alcoholic fatty liver disease. Here, we used diet-induced obese mice with non-alcoholic fatty liver disease treated with pegylated bilirubin (bilirubin nanoparticles) or vehicle control to determine the impact on hepatic lipid accumulation. The bilirubin nanoparticles significantly reduced hepatic fat, triglyceride accumulation, de novo lipogenesis, and serum levels of liver dysfunction marker aspartate transaminase and ApoB100 containing very-low-density lipoprotein. The bilirubin nanoparticles improved liver function and activated the hepatic β-oxidation pathway by increasing PPARα and acyl-coenzyme A oxidase 1. The bilirubin nanoparticles also significantly elevated plasma levels of the ketone β-hydroxybutyrate and lowered liver fat accumulation. This study demonstrates that bilirubin nanoparticles induce hepatic fat utilization, raise plasma ketones, and reduce hepatic steatosis, opening new therapeutic avenues for NAFLD.

scholarly journals The Impact of Macronutrient Intake on Non-alcoholic Fatty Liver Disease (NAFLD): Too Much Fat, Too Much Carbohydrate, or Just Too Many Calories?

2021 ◽  
Vol 8 ◽  
Author(s):  
Theresa Hydes ◽  
Uazman Alam ◽  
Daniel J. Cuthbertson
Keyword(s):  
Physical Activity ◽  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Lipid Storage ◽  
Liver Fat ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is a growing epidemic, in parallel with the obesity crisis, rapidly becoming one of the commonest causes of chronic liver disease worldwide. Diet and physical activity are important determinants of liver fat accumulation related to insulin resistance, dysfunctional adipose tissue, and secondary impaired lipid storage and/or increased lipolysis. While it is evident that a hypercaloric diet (an overconsumption of calories) promotes liver fat accumulation, it is also clear that the macronutrient composition can modulate this risk. A number of other baseline factors modify the overfeeding response, which may be genetic or environmental. Although it is difficult to disentangle the effects of excess calories vs. specifically the individual effects of excessive carbohydrates and/or fats, isocaloric, and hypercaloric dietary intervention studies have been implemented to provide insight into the effects of different macronutrients, sub-types and their relative balance, on the regulation of liver fat. What has emerged is that different types of fat and carbohydrates differentially influence liver fat accumulation, even when diets are isocaloric. Furthermore, distinct molecular and metabolic pathways mediate the effects of carbohydrates and fat intake on hepatic steatosis. Fat accumulation appears to act through impairments in lipid storage and/or increased lipolysis, whereas carbohydrate consumption has been shown to promote liver fat accumulation through de novo lipogenesis. Effects differ dependent upon carbohydrate and fat type. Saturated fat and fructose induce the greatest increase in intrahepatic triglycerides (IHTG), insulin resistance, and harmful ceramides compared with unsaturated fats, which have been found to be protective. Decreased intake of saturated fats and avoidance of added sugars are therefore the two most important dietary interventions that can lead to a reduction in IHTG and potentially the associated risk of developing type 2 diabetes. A healthy and balanced diet and regular physical activity must remain the cornerstones of effective lifestyle intervention to prevent the development and progression of NAFLD. Considering the sub-type of each macronutrient, in addition to the quantity, are critical determinants of liver health.

scholarly journals Relationship between Muscle Mass and Non-Alcoholic Fatty Liver Disease

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 122
Author(s):  
Jun-Hyuk Lee ◽  
Hye-Sun Lee ◽  
Byoung-Kwon Lee ◽  
Yu-Jin Kwon ◽  
Ji-Won Lee
Keyword(s):  
Skeletal Muscle ◽  
Risk Factor ◽  
Liver Disease ◽  
Fatty Liver ◽  
Muscle Mass ◽  
Fatty Liver Disease ◽  
Skeletal Muscle Mass ◽  
Liver Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Although sarcopenia is known to be a risk factor for non-alcoholic fatty liver disease (NAFLD), whether NAFLD is a risk factor for the development of sarcopenia is not clear. We investigated relationships between NAFLD and low skeletal muscle mass index (LSMI) using three different datasets. Participants were classified into LSMI and normal groups. LSMI was defined as a body mass index (BMI)-adjusted appendicular skeletal muscle mass <0.789 in men and <0.512 in women or as the sex-specific lowest quintile of BMI-adjusted total skeletal muscle mass. NAFLD was determined according to NAFLD liver fat score or abdominal ultrasonography. The NAFLD groups showed a higher hazard ratios (HRs) with 95% confidence intervals (CIs) for LSMI than the normal groups (HRs = 1.21, 95% CIs = 1.05–1.40). The LSMI groups also showed a higher HRs with 95% CIs for NAFLD than normal groups (HRs = 1.56, 95% CIs = 1.38–1.78). Participants with NAFLD had consistently less skeletal muscle mass over 12 years of follow-up. In conclusion, LSMI and NAFLD showed a relationship. Maintaining muscle mass should be emphasized in the management of NAFLD.

scholarly journals Magnesium Intake Is Inversely Associated with the Risk of Non-Alcoholic Fatty Liver Disease Among American Young adults

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1446-1446
Author(s):  
Liping Lu ◽  
Cheng Chen ◽  
Yuexia Li ◽  
Lisa Vanwagner ◽  
Wenzhi Guo ◽  
...  
Keyword(s):  
Young Adults ◽  
Liver Disease ◽  
Coronary Artery ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Lower Risk ◽  
Liver Fat ◽  
Inverse Association ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Abstract Objectives To examine magnesium (Mg) intake from diet and supplements during young adulthood in relation to risk of non-alcoholic fatty liver disease (NAFLD) in midlife. Methods A total of 2712 black and white American adults aged 18 to 30 years were recruited in the Coronary Artery Risk Development in Young Adult (CARDIA) study in 1985–1986 (baseline) with 8 additional examinations during 25 years thereafter. Mg intake was assessed at baseline and exam years 7 and 20 using the CARDIA diet history questionnaires. Computed tomography (CT) scanning was performed at exam year 25 (2010–2011) to ascertain NAFLD cases, which was defined as liver attenuation (LA) ≤51 Hounsfield units after exclusion for other causes of liver fat. Logistic regression was used to examine the association between cumulative average Mg intake and the risk of NAFLD. Results At exam year 25, 638 NAFLD cases were documented. An inverse association between total Mg intake (from diet and supplements) and NAFLD risk was observed after adjustment sociodemographics, major lifestyle factors, dietary quality, and clinical measurements (body mass index, blood pressure, lipid profiles, and fasting insulin). Compared with participants in the lowest quintile of Mg intake, those in the highest quintile had a 54% lower risk of NAFLD [multivariable-adjusted odds ratio = 0.46, 95% confidence interval = (0.25, 0.87), P for trend = 0.0498]. Consistently, there was an inverse association between whole grain consumption (a major food source of magnesium) and NAFLD risk. Conclusions This study suggests that higher intake of Mg throughout adulthood is associated with a lower risk of NAFLD in middle age. Funding Sources The Coronary Artery Risk Development in Young Adults Study is supported by grants from the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the University of Alabama at Birmingham, Northwestern University, University of Minnesota, and Kaiser Foundation Research Institute.This study is also partially supported by the NIH grants and NHLBI.

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