A long-term maternal diet transition from high-fat diet to normal fat diet during pre-pregnancy avoids adipose tissue inflammation in next generation
Open accessAbstract
Recent studies have suggested that maternal high-fat (HF) diet caused inflammation changes in adipose tissue; however, it remains unclear if maternal diet intervention before pregnancy rescues such effects in offspring. To address this question, female mice were continued on a normal-fat (NF group), or a HF diet (HF group) or transitioned from a HF diet to a NF diet at 1 (H1N group), 5 (H5N group) or 9 weeks (H9N group) prior to pregnancy. Among the three intervention groups, the H9N offspring displayed less and steady body weight gain, and maintained glucose tolerance, whereas the H1N and H5N offspring showed exacerbate these phenotypes. The H1N and H5N, but not the H9N offspring, displayed adipocyte hypertrophy associated with increased expression of genes involved in fat deposition. The H1N and H5N, but not the H9N adipose tissue, displayed increased macrophage infiltration with enhanced expression of inflammatory cytokine genes. In addition, overactivation of the NF-κB and the JNK signaling were observed in the H1N adipose tissue. Overall, our study showed that a long-term but not a short- or medium-term diet intervention before pregnancy released offspring adipose tissue inflammation induced by maternal HF diet, which adds details in our understanding how the maternal environment either promotes or discourages onset of disease in offspring. Clinically, this study is of great value for providing evidence in the design of clinical trials to evaluate the urgently required intervention strategies to minimize the intergenerational cycle of obesity.
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In mice, the duration of maternal high-fat diet consumption has little effect on the magnitude of changes in offspring adiposity, as long as the diet was consumed within 9 weeks of mating.
“Work in mice suggests that the duration of maternal high fat diet consumption has little effect on the magnitude of changes in offspring adiposity, as long as the diet was consumed within 9 weeks of mating [89].”
From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [89]
The Experimental design section says all high-fat groups received 12 weeks of maternal high-fat diet; what varied was the switch to normal-fat diet 1, 5, or 9 weeks before pregnancy. The Results report that the 1-week group had the highest relative visceral adipose mass, significantly above the 5- and 9-week groups. Thus the paper does not test differing durations of high-fat consumption, and its findings contradict the claim that timing within those nine weeks had little effect on offspring adiposity. Page numbers are unavailable in our copy. (LLM, conf=0.87)
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Experimental — accuracy not yet measuredOffspring from obese/high-fat diet-fed mothers often show increased inflammatory marker expression and a higher infiltration of macrophages and other immune cells in their adipose tissue, which may reflect lipotoxicity and likely contributed to the glucose intolerance seen in such offspring.
“They also often show increased inflammatory marker expression and a higher infiltration of macrophages and other immune cells in their adipose tissue [89, 91, 92], which may reflect lipotoxicity and likely contributed to the glucose intolerance seen in such offspring.”
From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [89]
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Experimental — accuracy not yet measuredOffspring from mothers fed obesogenic diet often demonstrate decreased insulin signaling protein levels in their WAT.
“Indeed, offspring from mothers fed obesogenic diet often also demonstrate decreased insulin signaling protein levels in their WAT [89, 93].”
From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [89]
The Introduction (page unavailable) says offspring of overnourished mothers commonly have impaired insulin sensitivity. The Discussion (page unavailable) links offspring adipocyte hypertrophy with aberrant insulin signaling, but the paper does not report decreased levels of insulin-signaling proteins in offspring white adipose tissue. (LLM, conf=0.82)
Experimental — accuracy not yet measuredOffspring from obese/high-fat diet-fed mothers show increased adiposity and adipocyte hypertrophy postnatally.
“Offspring from obese/high-fat diet-fed mothers show increased adiposity [88–90] and adipocyte hypertrophy postnatally [89, 91].”
From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [89]
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Developmental programming of offspring adipose tissue biology and obesity risk
Rodgers, A., & Sferruzzi-Perri, A. N. (2021) · International Journal of Obesity · doi:10.1038/s41366-021-00790-w · Cited by 57 · see citing works
- Authors
- Summerfield, M., Zhou, Y., Zhou, T., Wu, C., Alpini, G., Zhang, K. K., & Xie, L.
- Affiliations
- Texas A&M University (US)
- Tongji Hospital (CN)
- Central Texas Veterans Health Care System (US)
- Corresponding author
- Xie, Linglin
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2018-12-18
- Volume
- 13
- Issue
- 12
- Pages
- e0209053
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC6298692
- OpenAlex
- W2904397432
- Cited by
- 23
- References
- 5
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 2 · 2022: 5 · 2021: 5 · 2020: 2 · 2019: 2
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (1R01DK112368-01)
- Agricultural Research Service ([Hatch] project [1010406])
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- maternal high-fat diet, nutrition transition, adipose tissue inflammation, offspring obesity, adipocyte hypertrophy, macrophage infiltration, inflammatory cytokines, NF-κB signaling, JNK signaling, glucose tolerance, intergenerational obesity
- MeSH terms
- Diet, Healthy, Adipose Tissue, Animals, Dietary Fats, Female, Gene Expression Regulation, Hypertrophy, Inflammation, Macrophages, Male, Mice, Inbred C57BL, Pregnancy, Prenatal Exposure Delayed Effects, Time Factors, NF-kappa B, Adipocytes, MAP Kinase Signaling System, Maternal Nutritional Physiological Phenomena, Mice, 129 Strain, Diet, High-Fat
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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