Developmental Programming of Offspring Obesity, Adipogenesis, and Appetite
Open accessAbstract
A newly recognized primary cause of the obesity epidemic is the developmental programming effects of infants born to mothers with obesity or gestational diabetes, intrauterine growth-restricted newborns, and offspring exposed to environmental toxins including bisphenol A. The mechanisms which result in offspring obesity include the programming of the hypothalamic appetite pathway and adipogenic signals regulating lipogenesis. Processes include nutrient sensors, epigenetic modifications, and alterations in stem cell precursors of both appetite/satiety neurons and adipocytes which are modulated to potentiate offspring obesity. Future strategies for the prevention and therapy of obesity must address programming effects of the early life environment.
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Excess nutrient exposure in utero alters fetal metabolic pathways by modifying expression of key metabolic genes and nutrient sensors, increasing susceptibility to metabolic syndrome later in life.
“Excess nutrient exposure in utero alters fetal metabolic pathways by modifying the expression of key metabolic genes and nutrient sensors, increasing susceptibility to metabolic syndrome later in life.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [13]
The Epigenetics and Programming section says the maternal nutritional environment can alter offspring gene expression, and the Adipogenesis and Lipogenesis section reports altered adipogenic signaling and nutrient/energy-sensor responses in offspring of obese, high-fat-fed mothers. The Appetite section links maternal overnutrition to later metabolic syndrome. However, the paper describes changed sensor responses, not specifically changed expression of nutrient sensors. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMaternal overnutrition and obesity expose the fetus to nutrient excess and hyperinsulinemia, promoting excessive fetal growth, altered adipogenesis, and increased risk of metabolic disorders later in life.
“These conditions, often accompanied by relative micronutrient imbalances, expose the fetus to an environment of nutrient excess and hyperinsulinemia, promoting excessive fetal growth, altered adipogenesis, and increased risk of metabolic disorders later in life [12,13].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [13]
The Programmed Obesity > Humans section (page not provided) links maternal obesity with higher birth weight and increased risk of obesity and diabetes later in life. The Adipose Tissue > Adipogenesis and Lipogenesis section (page not provided) reports enhanced adipogenesis in offspring of obese mothers fed a high-fat diet. Our copy does not establish fetal hyperinsulinemia or relative micronutrient imbalances as part of this pathway. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMaternal overnutrition and obesity have emerged as major public health challenges in industrialized societies.
“While undernutrition remains a pressing issue in several developing regions, maternal overnutrition and obesity have emerged as major public health challenges in industrialized societies.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [13]
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- Authors
- ROSS, M. G., & DESAI, M.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- ROSS, MICHAEL G.
- DESAI, MINA
- Venue
- Clinical Obstetrics & Gynecology
- Published
- 2013-09
- Volume
- 56
- Issue
- 3
- Pages
- 529-536
- ISSN
- 0009-9201 (ISSN-L)
- PMC
- PMC4191824
- OpenAlex
- W2066828274
- Cited by
- 120
- References
- 18
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 9 · 2023: 4 · 2022: 10 · 2021: 8 · 2020: 7 · 2019: 16 · 2018: 7 · 2017: 14 · 2016: 12 · 2015: 20 · 2014: 7 · 2013: 1
- FWCI
- 12.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Obstetrics & Gynecology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK081756, P30DK063491)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD054751)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- developmental programming, offspring obesity, adipogenesis, appetite regulation, gestational diabetes mellitus, maternal obesity, fetal growth restriction, bisphenol A, environmental toxins, epigenetic modifications, nutrient sensing, lipogenesis, early life environment, obesity prevention
- MeSH terms
- Bisphenol A Compounds, Animals, Appetite, Benzhydryl Compounds, Estrogens, Non-Steroidal, Female, Fetal Growth Retardation, Humans, Hypothalamus, Obesity, Phenols, Pregnancy, Prenatal Exposure Delayed Effects, Diabetes, Gestational, Maternal Nutritional Physiological Phenomena, Prenatal Nutritional Physiological Phenomena, Epigenesis, Genetic, Fetal Development, Lipogenesis, Adipogenesis
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