ArticleScientific reports2014
Neonatal events, such as androgenization and postnatal overfeeding, modify the response to ghrelin.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- The Gut-Insulin Axis in Polycystic Ovary Syndrome: A Narrative Review of Gut Dysbiosis, Inflammation, and Emerging Therapeutic Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Gut Microbiome and Polycystic Ovary Syndrome: Interplay of Associated Microbial-Metabolite Pathways and Therapeutic Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Interplay of Gut Microbiota in Polycystic Ovarian Syndrome: Role of Gut Microbiota, Mechanistic Pathways and Potential Treatment Strategies.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Communication in non-communicable diseases (NCDs) and role of immunomodulatory nutraceuticals in their management.Frontiers in nutrition · 2022Review
- Exploration of the Relationship Between Gut Microbiota and Polycystic Ovary Syndrome (PCOS): a Review.Geburtshilfe und Frauenheilkunde · 2020Article
- Sequential Exposure to Obesogenic Factors in Females Rats: From Physiological Changes to Lipid Metabolism in Liver and Mesenteric Adipose Tissue.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is currently accepted that ambient, non-genetic factors influence perinatal development and evoke structural and functional changes that may persist throughout life. Overfeeding and androgenization after birth are two of these key factors that could result in "metabolic imprinting" of neuronal circuits early in life and, thereby, increase the body weight homeostatic "set point", stimulate appetite, and result in obesity. Our aim was to determine the influence of these obesogenic factors on the response to ghrelin. We observed the expected orexigenic effect of ghrelin regardless of the nutritional or hormonal manipulations to which the animals were subjected to at early postnatal development and this effect remained intact at later stages of development. In fact, ghrelin responses increased significantly when the animals were subjected to one of the two manipulations, but not when both were combined. An increased response to ghrelin could explain the obese phenotype displayed by individuals with modified perinatal environment.
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