Developmental Origins of Obesity: Programmed Adipogenesis
Open accessAbstract
The metabolic syndrome epidemic, including a marked increase in the prevalence of obesity and gestational diabetes mellitus (GDM) among pregnant women, represents a significant public health problem. There is increasing recognition that the risk of adult obesity is clearly influenced by prenatal and infant environmental exposures, particularly nutrition. This tenet is the fundamental basis of developmental programming. Low birth weight, together with infant catch-up growth, is associated with a significant risk of adult obesity. Exposure to maternal obesity, with or without GDM, or having a high birth weight also represents an increased risk for childhood and adult obesity. Animal models have replicated human epidemiologic findings and elucidated potential programming mechanisms that include altered organ development, cellular signaling responses, and epigenetic modifications. Prenatal care has made great strides in optimizing maternal, fetal, and neonatal health, and now has the opportunity to begin interventions which prevent or reduce childhood/adult obesity. Guidelines that integrate optimal pregnancy nutrition and weight gain, management of GDM, and newborn feeding strategies with long-term consequences on adult obesity, remain to be elucidated.
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Female subjects seem to have greater protection against the adverse effects of lipo-toxicity caused by dysfunctional adipose tissue, probably through a differentiated expression of sex-dependent genes involved in adipogenesis.
“Moreover, it has been noted that female subjects seem to have greater protection against the adverse effects of lipo-toxicity caused by dysfunctional adipose tissue, probably through a differentiated expression of sex-dependent genes involved in adipogenesis (Figure 2) [58,82,83].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [58]
The sections on Catch-up Growth and Fat Accrual and Effects of Increased Adipogenesis on DM in offspring discuss adipogenic genes and adverse metabolic effects of altered adipose tissue. They do not address whether females are more protected from lipotoxicity or whether sex-dependent gene expression explains such protection. Searches for female protection, sex differences, and lipotoxicity found no passage establishing that comparison. (LLM, conf=0.73)
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Cites
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- Authors
- Desai, M., Beall, M., & Ross, M. G.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Desai, Mina
- Venue
- Current Diabetes Reports
- Published
- 2012-11-29
- Volume
- 13
- Issue
- 1
- Pages
- 27-33
- ISSN
- 1534-4827 (ISSN-L)
- 1539-0829
- PMC
- PMC3563293
- OpenAlex
- W2124857707
- Cited by
- 171
- References
- 4
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 7 · 2023: 6 · 2022: 4 · 2021: 15 · 2020: 11 · 2019: 14 · 2018: 18 · 2017: 15 · 2016: 10 · 2015: 26 · 2014: 26 · 2013: 10 · 2012: 1
- FWCI
- 3.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Diabetes Reports (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000124)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK081756)
- National Center for Advancing Translational Sciences
- 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
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- developmental programming, obesity, adipogenesis, gestational diabetes mellitus, low birth weight, catch-up growth, maternal obesity, birth weight, prenatal nutrition, epigenetic modifications, organogenesis, signal transduction, metabolic syndrome, prenatal care, infant feeding, gestational weight gain
- MeSH terms
- Animals, Birth Weight, Humans, Nutritional Physiological Phenomena, Obesity, Risk Factors, Growth and Development, Adipogenesis
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