ArticleBMC medicine2025
Insulin resistance as a potential driving force of parental obesity-induced adverse metabolic programming mechanisms in children with obesity.
Article in BMC medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Independent and synergistic effects of maternal and paternal obesogenic diets on offspring early-life outcomes in the rat.Experimental physiology · 2026Article
- Obesity and insulin resistance trigger the early onset of adolescent-like sexually dimorphic metabotypes in middle childhood.Cardiovascular diabetology · 2026Article
- Selected Nutraceuticals in Metabolic Syndrome: Molecular Mechanisms and Clinical Implications.Biomedicines · 2026Review
- Insulin resistance: mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundParental obesity has been identified as one of the most important early risk factors for childhood obesity, but molecular mechanisms driving this greater predisposition remain to be elucidated.
methodsIn this study, we recruited a cohort comprising children with obesity (body mass index over two z-scores above the age/sex-adjusted mean of the Spanish reference population, age range: 6-12 years), born to parents with obesity (N = 18) or without obesity (N = 41), as well as matched healthy controls (N = 26). Plasma and erythrocyte samples were collected for comprehensive biochemical and metabolomics analyses, this latter by applying high-throughput liquid chromatography-mass spectrometry. Then, a combination of multivariate and univariate statistical tools was applied to unravel the molecular pathogenic impairments that parental obesity may imprint in the offspring.
resultsInterestingly, we found parental obesity to be associated with exacerbated unhealthy metabolic outcomes in the offspring with obesity, as mirrored in higher fasting insulin levels (p = 2.8 × 10
conclusionsTherefore, we hypothesize that insulin resistance could be a major driving force in mediating deleterious programming mechanisms induced by parental obesity in the offspring.
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