New Perspectives on Genetic Prediction for Pediatric Metabolic Associated Fatty Liver Disease

Lin, Yu‐Cheng; Wu, Chi-Chien; Ni, Yen‐Hsuan

doi:10.3389/fped.2020.603654

Cited by 24 publications

(28 citation statements)

References 150 publications

(111 reference statements)

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“…For what concerns the pediatric population affected by NAFLD, the OS mechanisms seem to be influenced also by other polymorphisms rarely seen in adult-onset forms [370]. Various genes are involved, such as the G protein-coupled receptor 120 (GPR120) [371], uridine-5 diphosphoglucuronosyltransferase 1A1 (UGT1A1) [372,373], heme oxygenase-1 (HO-1) [374], PPAR gamma coactivator 1-alpha (PPARGC1A) [375,376], cannabinoid receptor type 2 (CB2) [370], and beta-Klotho rs17618244 gene variant (KLB) [362].…”

Section: Other Genetic Variantsmentioning

confidence: 99%

Oxidative Stress in Non-Alcoholic Fatty Liver Disease

Smirne

Croce

Benedetto

et al. 2022

Livers

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Non-alcoholic fatty liver disease (NAFLD) is a challenging disease caused by multiple factors, which may partly explain why it still remains an orphan of adequate therapies. This review highlights the interaction between oxidative stress (OS) and disturbed lipid metabolism. Several reactive oxygen species generators, including those produced in the gastrointestinal tract, contribute to the lipotoxic hepatic (and extrahepatic) damage by fatty acids and a great variety of their biologically active metabolites in a “multiple parallel-hit model”. This leads to inflammation and fibrogenesis and contributes to NAFLD progression. The alterations of the oxidant/antioxidant balance affect also metabolism-related organelles, leading to lipid peroxidation, mitochondrial dysfunction, and endoplasmic reticulum stress. This OS-induced damage is at least partially counteracted by the physiological antioxidant response. Therefore, modulation of this defense system emerges as an interesting target to prevent NAFLD development and progression. For instance, probiotics, prebiotics, diet, and fecal microbiota transplantation represent new therapeutic approaches targeting the gut microbiota dysbiosis. The OS and its counter-regulation are under the influence of individual genetic and epigenetic factors as well. In the near future, precision medicine taking into consideration genetic or environmental epigenetic risk factors, coupled with new OS biomarkers, will likely assist in noninvasive diagnosis and monitoring of NAFLD progression and in further personalizing treatments.

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Section: Other Genetic Variantsmentioning

confidence: 99%

Oxidative Stress in Non-Alcoholic Fatty Liver Disease

Smirne

Croce

Benedetto

et al. 2022

Livers

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“…43 Children with NAFLD have a much longer disease course; therefore, they are more reliable to complications. 44 Measures aimed at reducing adolescent obesity, maternal pre-pregnancy obesity, and gestational weight gain could lead to a lower risk of NAFLD in adolescent boys. 45 NAFLD in other special populations:…”

Section: Nafld In Pediatric Populationsmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease: Current Global Burden

et al. 2022

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The map and global disease burden of chronic liver diseases are markedly changing, with non-alcoholic fatty liver disease (NAFLD) becoming the most common cause of liver affection coinciding with the current epidemics of obesity, type 2 diabetes, and metabolic syndrome. Understanding the incidence and prevalence of NAFLD is critical because of its linkage to a significant economic burden of hospitalization and changing patterns in consequences such as liver transplantation. Moreover, the long-term average healthcare expenses of NAFLD patients have exceeded those of other liver diseases. To lessen the imminent burden of NAFLD, immediate actions to raise worldwide awareness and address metabolic risk factors are required. This review summarizes key data about the global disease burden of NAFLD, modifiable and non-modifiable risk factors, and current preventive approaches.

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“…Different genes encode proteins involved in the regulation of lipid metabolism in the liver. Over the past two decades, sequence variations in various genetic loci, including PNPLA3 , TM6SF2 , GCKR , MBOAT7 , and HSD17B13 , have been shown to increase NAFLD susceptibility [ 19 ]. These genes can be used in clinical risk stratification and personalized therapy.…”

Section: Geneticsmentioning

confidence: 99%