ArticleAmerican journal of obstetrics and gynecology2012
Nutrient sensor-mediated programmed nonalcoholic fatty liver disease in low birthweight offspring.
Article in American journal of obstetrics and gynecology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
- Nutrition and Developmental Origins of Kidney Disease.Nutrients · 2023Review
- Liver disease in obesity and underweight: the two sides of the coin. A narrative review.Eating and weight disorders : EWD · 2021Review
- MiR-199a-5p regulates sirtuin1 and PI3K in the rat hippocampus with intrauterine growth restriction.Scientific reports · 2018Article
- Effects of dimethylglycine sodium salt supplementation on growth performance, hepatic antioxidant capacity, and mitochondria-related gene expression in weanling piglets born with low birth weight1.Journal of animal science · 2018Article
- Mitochondrial role in the neonatal predisposition to developing nonalcoholic fatty liver disease.The Journal of clinical investigation · 2018Review
- Growth hormone reverses dyslipidemia in adult offspring after maternal undernutrition.Scientific reports · 2017Article
- Developmental origins of NAFLD: a womb with a clue.Nature reviews. Gastroenterology & hepatology · 2017Review
- Undernourishment in utero Primes Hepatic Steatosis in Adult Mice Offspring on an Obesogenic Diet; Involvement of Endoplasmic Reticulum Stress.Scientific reports · 2015Article
- Early developmental conditioning of later health and disease: physiology or pathophysiology?Physiological reviews · 2014Review
- Nutritional models of foetal programming and nutrigenomic and epigenomic dysregulations of fatty acid metabolism in the liver and heart.Pflugers Archiv : European journal of physiology · 2014Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveWe hypothesized that gestationally programmed nonalcoholic fatty liver disease in low-birthweight offspring is mediated through nutrient sensors nicotinamide adenine dinucleotide+-dependent histone deacetylase (SIRT1) and AMP-activated protein kinase (AMPK). STUDY
designPregnant dams received ad libitum food or were 50% food restricted from pregnancy days 10-21 to produce control and low-birthweight newborn offspring, respectively. All pups were nursed by control dams and weaned to ad libitum feed. We determined hepatic SIRT1 and AMPK activities and protein expression of lipid targets in low-birthweight and control fetuses, newborns, and adult offspring (3 months).
resultsLow-birthweight fetuses demonstrated increased prenatal hepatic SIRT1 activity, although with increased lipogenesis. After birth, low-birthweight newborn offspring undergo postnatal suppression of hepatic SIRT1 and AMPK activities in conjunction with increased lipogenesis, decreased lipolysis, and increased fat stores.
conclusionThese findings suggest that undernutrition stress in utero may program hepatic nutrient sensors to perceive normal postnatal nutrition as a state of nutrient excess with the induction of hepatic lipid storage.
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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.