ArticleWorld journal of hepatology2015
Understanding the pathophysiological mechanisms in the pediatric non-alcoholic fatty liver disease: The role of genetics.
Article in World journal of hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.
- Association between PNPLA3 rs738409 polymorphism and nonalcoholic fatty liver disease: a systematic review and meta-analysis.BMC endocrine disorders · 2021Pooled it
- Pooled it
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Childhood Obesity: A Multisystem Challenge Linking Hypertension, NAFLD, and Sleep Apnea.Medical sciences (Basel, Switzerland) · 2026Review
- Phytochemical Analysis and Anti-Lipid Accumulation Effects of Pulsed Electric Field (PEF)-Processed Black Rice and Green Tea Extracts in Oleic Acid-Induced Hepatocytes.Food science & nutrition · 2025Article
- A new perspective on non-invasive diagnosis of non- alcoholic fatty liver disease: evidence integration of inflammatory and metabolic biomarkers based on a scoping review.Frontiers in endocrinology · 2025Article
- Protective effects and mechanisms of Lizhong decoction against non-alcoholic fatty liver disease in a rat model.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- Advances in pediatric non-alcoholic fatty liver disease: From genetics to lipidomics.World journal of clinical pediatrics · 2022Review
- Review
- Pediatric obesity-related non-alcoholic fatty liver disease: waist-to-height ratio best anthropometrical predictor.Pediatric research · 2021Article
- [Concern about liver disease in children].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021Article
- Transmembrane 6 superfamily member 2 167K allele improves renal function in children with obesity.Pediatric research · 2020Article
- Fructose and Uric Acid: Major Mediators of Cardiovascular Disease Risk Starting at Pediatric Age.International journal of molecular sciences · 2020Review
- Diet as moderator in the association of adiposity with inflammatory biomarkers among adolescents in the HELENA study.European journal of nutrition · 2019Article
- Diet as a moderator in the association of sedentary behaviors with inflammatory biomarkers among adolescents in the HELENA study.European journal of nutrition · 2019Article
- Pediatric non-alcoholic fatty liver disease: current perspectives on diagnosis and management.Pediatric health, medicine and therapeutics · 2019Article
- Current status of imaging in nonalcoholic fatty liver disease.World journal of hepatology · 2018Review
- Polymorphisms in FFAR4 (GPR120) Gene Modulate Insulin Levels and Sensitivity after Fish Oil Supplementation.Journal of personalized medicine · 2017Article
- The Association between Non-Alcoholic Fatty Liver Disease and Cardiovascular Risk in Children.Children (Basel, Switzerland) · 2017Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Classically, the non-alcoholic fatty liver disease (NAFLD) physiopathology and progression has been summarized in the two hits hypothesis. The first hit is represented by the action of hyperinsulinemia and insulin resistance, accompanying obesity, that leads to liver steatosis increasing the absolute non esterified fatty acids uptake in the liver and the esterification to form triacylglycerol. The oxidative stress is involved in the second hit leading to the progression to nonalcoholic steatohepatitis (NASH) because of its harmful action on steatosic hepatocytes. However, at the present time, the two hits hypothesis needs to be updated because of the discover of genetic polymorphisms involved both in the liver fat accumulation and progression to NASH that make more intriguing understanding the NAFLD pathophysiological mechanisms. In this editorial, we want to underline the role of PNPLA3 I148M, GPR120 R270H and TM6SF2 E167K in the pediatric NAFLD development because they add new pieces to the comprehension of the NAFLD pathophysiological puzzle. The PNPLA3 I148M polymorphism encodes for an abnormal protein which predisposes to intrahepatic triglycerides accumulation both for a loss-of-function of its triglyceride hydrolase activity and for a gain-of-function of its lipogenic activity. Therefore, it is involved in the first hit, such as TM6SF2 E167K polymorphisms that lead to intrahepatic fat accumulation through a reduced very low density lipoprotein secretion. On the other hand, the GPR120 R270H variant, reducing the anti-inflammatory action of the GPR120 receptor expressed by Kuppfer cells, is involved in the second hit leading to the liver injury.
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