Diet-induced obesity in mice reduces placental efficiency and inhibits placental mTOR signaling
Open accessAbstract
As in humans, obesity during pregnancy in mice results in elevated maternal insulin levels and metabolic programming of offspring. mTOR signaling regulates amino acid transport and may function as a placental nutrient sensor. Because obesity is a condition with increased nutrient availability, we hypothesized that diet-induced obesity activates placental mTOR signaling. To test this hypothesis, female C57BL/6J mice were fed an obesogenic diet or standard chow prior to and throughout pregnancy. Fetuses and placentas were collected at gestational day 18. Using Western blot analysis, placental mTOR activity was determined along with energy, inflammatory, and insulin signaling pathways (upstream modulators of mTOR). At gestational day 18, fetal and placental weights did not differ, however, in obese dams, the fetal/placental weight ratio was lower (P <0.01). In placentas from obese dams, mTOR signaling was inhibited, as determined by decreased Rheb and S6K1 expression, and lower rpS6 phosphorylation (P <0.05). In contrast, energy, inflammatory, and insulin signaling pathways were unaffected. Contrary to our hypothesis, diet-induced obesity in pregnant mice was associated with inhibition of placental mTOR signaling. However, this finding is consistent with the lower fetal/placental weight ratio, indicating reduced placental efficiency.
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Data from over-nutrition models are conflicting: an obesogenic diet causes activation of mTOR in rat placentas, but the opposite was found following over-nutrition in sheep and mice fed an obesogenic diet.
“Thus, whilst an obesogenic diet has been shown to cause activation of mTOR in rat placentas (205), the opposite was found following over-nutrition in sheep (150% of control diet) and mice fed an obesogenic diet (323, 615).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [323]
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- Gaccioli F. Jansson T. Powell T. 2011 Activation of placental mammalian target of rapamycin signaling in obese women. Placenta; 32: A134
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“In contrast, using a different mouse model of diet-induced maternal obesity, Lager and coworkers reported normal placental and fetal weights but a lower fetal/placental ratio, suggesting decreased placental efficiency (Lager et al., 2014).”
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Nutrition and Pregnancy Outcomes
Bellissimo, C. J., Vickers, M. H., & Sloboda, D. M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.64688-3 · Cited by 1 · see citing works
Preconception Chronic Male Alcohol Exposure Induces FAS Like Growth Restriction
Chronister, S. K. (2016) · OakTrust (Texas A&M University Libraries)
Advanced maternal age : identifying mechanisms underlying vulnerability to stillbirth
Lean, S. C. (2016) · Research Explorer (The University of Manchester)
Nutrition and Pregnancy Outcomes
Bellissimo, C. J., Vickers, M. H., & Sloboda, D. M. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21477-6.00199-1
Maternal metformin treatment in obese pregnant dams normalizes neonatal sensory-motor reflexes
Müller-Limberger, E., Frederick, B., Hansen, S., Wohlfarth, M., Janoschek, R., Mahabir, E., Fischer, P., Gründemann, D., Kalis, S., Alcazar, M. A. A., et al. (2026) · Molecular and Cellular Pediatrics · doi:10.1186/s40348-026-00259-8
“Maternal obesity in mouse models was associated with decreased fetal-to-placental weight ratios, suggesting reduced placental efficiency [50].”
- Authors
- Lager, S., Samulesson, A.-M., Taylor, P. D., Poston, L., Powell, T. L., & Jansson, T.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- King's College London (GB)
- Corresponding author
- Lager, Susanne
- Venue
- Physiological Reports
- Publisher
- Wiley
- Published
- 2014-02
- Volume
- 2
- Issue
- 2
- Pages
- e00242
- ISSN
- 2051-817X (ISSN-L)
- PMC
- PMC3966251
- OpenAlex
- W2103602444
- Cited by
- 44
- References
- 31
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 2 · 2022: 1 · 2020: 4 · 2019: 3 · 2018: 7 · 2017: 7 · 2016: 9 · 2015: 7 · 2014: 2
- FWCI
- 7.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Physiological Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Funders
- British Heart Foundation
- Tommy's, the Swedish Research Council
- Swedish Society of Endocrinology
- National Institutes of Health (HD068370)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Keywords
- diet-induced obesity, placenta, mTOR signaling, maternal obesity, pregnancy, placental efficiency, Rheb, S6K1, S6 phosphorylation, insulin signaling, energy metabolism, inflammation, obesogenic diet
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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