ArticlePLoS biology2020
Maternal obesity-induced endoplasmic reticulum stress causes metabolic alterations and abnormal hypothalamic development in the offspring.
Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 70 citations in OpenAlex.
- Thermal challenge and food intake: Mutual regulatory mechanisms.Neural regeneration research · 2026Article
- Maternal Nutrition and Hypothalamic Programming of Offspring Metabolic Health.The Journal of nutrition · 2026Review
- Early-life programming of hypothalamic circuits by maternal obesity: implications for neuroendocrine disorders.Reviews in endocrine & metabolic disorders · 2026Review
- A high-fat, high-sugar diet impairs maternal metabolism throughout pregnancy and lactation in mice.The Journal of physiology · 2026Article
- Hypothalamic endoplasmic reticulum stress drives pubertal precocity due to early-onset obesity in female rodents.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Impact of long-term maternal high-fat, high-sugar feeding on gastric vagal afferent responses and feeding behaviour in mouse offspring.Experimental physiology · 2026Article
- Maternal high-fat diet exposure is associated with altered hypothalamic microglial development and reduced early postnatal TGFβ1 signaling in male offspring.Frontiers in endocrinology · 2026Article
- Maternal Obesity in Pregnancy: Risk Factor for Neurodevelopmental Outcomes in Offspring.Journal of neurochemistry · 2025Review
- Oxytocin neurons drive melanocortin circuit maturation via vesicle release during a neonatal critical period.PLoS biology · 2025Article
- The long-term impact of obesity in pregnancy on offspring hypothalamic feeding pathways.Royal Society open science · 2025Review
- Neurodevelopmental Pathways from Maternal Obesity to Offspring Outcomes: An Umbrella Review of Cognitive and Behavioral Consequences Across Development.Healthcare (Basel, Switzerland) · 2025Review
- Environmental adversity, endoplasmic reticulum stress, and neurogenesis.Neurotoxicology · 2025Review
- Maternal Nutritional Environment and the Development of the Melanocortin System.Comprehensive Physiology · 2025Review
- Investigation of a mouse model of Prader-Willi Syndrome with combined disruption of Necdin and Magel2.JCI insight · 2025Article
- Pregnancy and a high-fat, high-sugar diet each attenuate mechanosensitivity of murine gastric vagal afferents, with no additive effects.The Journal of physiology · 2025Article
- Intermittent Fasting Improves Social Interaction and Decreases Inflammatory Markers in Cortex and Hippocampus.Molecular neurobiology · 2025Article
- Update on Hypothalamic Inflammation and Gliosis: Expanding Evidence of Relevance Beyond Obesity.Current obesity reports · 2025Review
- Upregulation of Xbp1 in NPY/AgRP neurons reverses diet-induced obesity and ameliorates leptin and insulin resistance.Neuropeptides · 2024Article
- Acute elevated dietary fat alone is not sufficient to decrease AgRP projections in the paraventricular nucleus of the hypothalamus in mice.Scientific reports · 2024Article
- Therapeutic targeting of white adipose tissue metabolic dysfunction in obesity: mechanisms and opportunities.MedComm · 2024Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The steady increase in the prevalence of obesity and associated type II diabetes mellitus is a major health concern, particularly among children. Maternal obesity represents a risk factor that contributes to metabolic perturbations in the offspring. Endoplasmic reticulum (ER) stress has emerged as a critical mechanism involved in leptin resistance and type 2 diabetes in adult individuals. Here, we used a mouse model of maternal obesity to investigate the importance of early life ER stress in the nutritional programming of this metabolic disease. Offspring of obese dams developed glucose intolerance and displayed increased body weight, adiposity, and food intake. Moreover, maternal obesity disrupted the development of melanocortin circuits associated with neonatal hyperleptinemia and leptin resistance. ER stress-related genes were up-regulated in the hypothalamus of neonates born to obese mothers. Neonatal treatment with the ER stress-relieving drug tauroursodeoxycholic acid improved metabolic and neurodevelopmental deficits and reversed leptin resistance in the offspring of obese dams.
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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.