ReviewBiomedicines2023
The Impact of Maternal Obesity on Adipose Progenitor Cells.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Biopsychosocial and Environmental Factors That Impact Brain-Gut-Microbiome Interactions in Obesity.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2026Pooled it
- Histone Modifications: Decoding the Epigenetic Basis of Economic Traits in Livestock and Poultry.Genes · 2026Review
- Cross-Generational Integration of Exercise and Nutritional Encoding in Offspring Adipose Genomics.International journal of molecular sciences · 2026Review
- Gestational diabetes mellitus-induced adipokine dysregulation and links to metabolic programming risks.Frontiers in endocrinology · 2026Observational
- Implications of adipocyte dysfunction in pediatric obesity: a narrative review.Pediatric endocrinology, diabetes, and metabolism · 2026Review
- Maternal obesity alters adipogenic potential and mitochondrial maximal respiration in infant mesenchymal stem cells.Frontiers in endocrinology · 2026Article
- Maternal high-fat diet-induced obesity in offspring: Unraveling adipose tissue dysfunction mediated by increased heat shock proteins.The international journal of biochemistry & cell biology · 2025Article
- White Adipocyte Stem Cell Expansion Through Infant Formula Feeding: New Insights into Epigenetic Programming Explaining the Early Protein Hypothesis of Obesity.International journal of molecular sciences · 2025Review
- The unrevealed links: periodontal health, human milk composition, and infant gut microbiome dynamics.Primary health care research & development · 2024Review
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 3 institutions in 2 countries.
Funding
Abstract
The concept of Developmental Origin of Health and Disease (DOHaD) postulates that adult-onset metabolic disorders may originate from suboptimal conditions during critical embryonic and fetal programming windows. In particular, nutritional disturbance during key developmental stages may program the set point of adiposity and its associated metabolic diseases later in life. Numerous studies in mammals have reported that maternal obesity and the resulting accelerated growth in neonates may affect adipocyte development, resulting in persistent alterations in adipose tissue plasticity (i.e., adipocyte proliferation and storage) and adipocyte function (i.e., insulin resistance, impaired adipokine secretion, reduced thermogenesis, and higher inflammation) in a sex- and depot-specific manner. Over recent years, adipose progenitor cells (APCs) have been shown to play a crucial role in adipose tissue plasticity, essential for its development, maintenance, and expansion. In this review, we aim to provide insights into the developmental timeline of lineage commitment and differentiation of APCs and their role in predisposing individuals to obesity and metabolic diseases. We present data supporting the possible implication of dysregulated APCs and aberrant perinatal adipogenesis through epigenetic mechanisms as a primary mechanism responsible for long-lasting adipose tissue dysfunction in offspring born to obese mothers.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.