ReviewNature reviews. Gastroenterology & hepatology2017
Developmental origins of NAFLD: a womb with a clue.
Review in Nature reviews. Gastroenterology & hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
126 citing papers in PubMed, 238 citations in OpenAlex.
- Mechanisms of postpartum metabolic dysfunction-associated steatotic liver disease in women with a history of gestational diabetes mellitus.Endocrine connections · 2026Review
- MASLD In Children - A Distinct Phenotype?Current obesity reports · 2026Review
- Liver function indicators as risk factors of pediatric metabolic (dysfunction)-associated fatty liver disease: a systematic review and meta-analysis.Translational pediatrics · 2026Article
- Maternal Programming with a Cafeteria Diet Leads to Glucose Intolerance, Increased Insulinemia, Inflammation, and Intestinal Dysbiosis in Rat Offspring.Preventive nutrition and food science · 2026Article
- Dimethyl fumarate therapy in a Western diet pregnancy model: a pilot study in guinea pigs.PeerJ · 2026Article
- Gut microbiota and pediatric metabolic dysfunction-associated steatotic liver disease: clinical evidence and therapeutic implications.Frontiers in pediatrics · 2026Review
- Persistent perinatal protein malnutrition and post-weaning high-fat diet induce metabolic syndrome and hepatic UCP2 overexpression in IUGR offspring.Frontiers in nutrition · 2026Article
- Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD.EBioMedicine · 2026Article
- Metabolic dysfunction‑associated steatotic liver disease: Pathogenesis, model and treatment (Review).International journal of molecular medicine · 2025Review
- Activating nuclear receptor subfamily 2 group F member 2 in adipocyte stem cells rescues beige adipocyte metabolism impaired by excess early-life omega-6 fatty acids.Clinical nutrition (Edinburgh, Scotland) · 2025Article
- Hepatocyte reporter cells and integrated metabolomic and transcriptomic analyses reveal insights into hepatocyte changes in offspring of pregnancies with obesity.Scientific reports · 2025Article
- Ganoapplanilactone C fromAntioxidants (Basel, Switzerland) · 2025Article
- Oral Microbiota Dysbiosis in Firefighters and the Potential Contributing Environmental and Lifestyle Factors Based on a Case-Control Study.Microorganisms · 2025Article
- Metabolic dysfunction-associated steatotic liver disease and pregnancy.The Journal of clinical investigation · 2025Review
- Hypoxic pregnancy promotes fibrosis and increases stress metabolites in the ovine fetal liver.The Journal of physiology · 2025Article
- Maternal Western Diet Programmes Bile Acid Dysregulation and Hepatic Fibrosis in Fetal and Juvenile Macaques.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Maternal western-style diet alters Kupffer cell proportion leading to metabolic dysfunction-associated steatotic liver disease when challenged with western diet in adulthood.Frontiers in immunology · 2025Article
- Serum adropin is unaltered in adolescents with histology-confirmed steatotic liver disease.Journal of pediatric gastroenterology and nutrition · 2025Article
- Investigation of Active Components ofInternational journal of molecular sciences · 2024Article
- Pediatric metabolic (dysfunction)-associated fatty liver disease: current insights and future perspectives.Hepatology international · 2024Review
66 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Changes in the maternal environment leading to an altered intrauterine milieu can result in subtle insults to the fetus, promoting increased lifetime disease risk and/or disease acceleration in childhood and later in life. Particularly worrisome is that the prevalence of NAFLD is rapidly increasing among children and adults, and is being diagnosed at increasingly younger ages, pointing towards an early-life origin. A wealth of evidence, in humans and non-human primates, suggests that maternal nutrition affects the placenta and fetal tissues, leading to persistent changes in hepatic metabolism, mitochondrial function, the intestinal microbiota, liver macrophage activation and susceptibility to NASH postnatally. Deleterious exposures in utero include fetal hypoxia, increased nutrient supply, inflammation and altered gut microbiota that might produce metabolic clues, including fatty acids, metabolites, endotoxins, bile acids and cytokines, which prime the infant liver for NAFLD in a persistent manner and increase susceptibility to NASH. Mechanistic links to early disease pathways might involve shifts in lipid metabolism, mitochondrial dysfunction, pioneering gut microorganisms, macrophage programming and epigenetic changes that alter the liver microenvironment, favouring liver injury. In this Review, we discuss how maternal, fetal, neonatal and infant exposures provide developmental clues and mechanisms to help explain NAFLD acceleration and increased disease prevalence. Mechanisms identified in clinical and preclinical models suggest important opportunities for prevention and intervention that could slow down the growing epidemic of NAFLD in the next generation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.