Sirtuins-Mediators of Maternal Obesity-Induced Complications in Offspring?
Abstract
Obesity is a complex metabolic disease, attributed to diverse and interactive genetic and environmental factors. The associated health consequences of obesity are pleiotropic, with individuals being more susceptible to chronic diseases such as type 2 diabetes mellitus, hypertension, and lipotoxicity-related chronic diseases. The contribution of maternal obesity to the offspring's predisposition to both obesity and its complications is increasingly recognized. Understanding the mechanisms underlying these "transmissible" effects is critical to develop therapeutic interventions to reduce the risk for "programmed" obesity. Sirtuins (SIRTs), particularly SIRT1 and SIRT3, are NAD(+)-dependent deacetylases that regulate metabolic balance and stress responses in both central and peripheral tissues, of which dysregulation is a well-established mediator for the development and effects of obesity. Nevertheless, their implication in the transmissible effects of maternal obesity across generations remains largely elusive. In this review, we examine multiple pathways and systems that are likely to mediate such effects, with particular emphasis on the role of SIRTs.-Nguyen, L. T., Chen, H., Pollock, C. A., Saad, S. Sirtuins-mediators of maternal obesity-induced complications in offspring?
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Sirtuins SIRT1 and SIRT3 play key roles in fetal programming by controlling oxidative metabolism, autophagy, and mitochondrial function.
“Furthermore, sirtuins (SIRT1 and SIRT3) play key roles in fetal programming by controlling oxidative metabolism, autophagy, and mitochondrial function.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [54]
Obesity-induced suppression of sirtuin activity contributes to oxidative stress, impaired mitochondrial integrity, and potentially transgenerational metabolic dysfunction.
“Obesity-induced suppression of sirtuin activity contributes to oxidative stress, impaired mitochondrial integrity, and potentially transgenerational metabolic dysfunction [54].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [54]
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Schiera, G., Macajone, G., Volpes, S., Greco, L., Di Liegro, C. M., Serio, G., Caradonna, F., & Naselli, F. (2026) · Cells · doi:10.3390/cells15040366 · Cited by 8 · see citing works
- Authors
- Nguyen, L. T., Chen, H., Pollock, C. A., & Saad, S.
- Affiliations
- The University of Sydney (AU)
- University of Technology Sydney (AU)
- Corresponding author
- Nguyen, Long T.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2015-12-14
- Volume
- 30
- Issue
- 4
- Pages
- 1383-1390
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2216955959
- Cited by
- 19
- References
- 13
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 3
- FWCI
- 0.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The FASEB Journal (publishedVersion)
- PubMed (publishedVersion)
- UTS ePRESS (University of Technology Sydney) (submittedVersion)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- sirtuins, SIRT1, SIRT3, maternal obesity, transgenerational effects, offspring metabolic programming, NAD+-dependent deacetylase, type 2 diabetes, hypertension, lipotoxicity, stress response
- MeSH terms
- Animals, Female, Humans, Models, Biological, Obesity, Pregnancy, Pregnancy Complications, Signal Transduction, Sirtuins, Maternal Nutritional Physiological Phenomena
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