The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Maternal high-fat diets cause insulin resistance through inflammatory changes in fetal adipose tissue
Open accessAbstract
Objectives Epidemiological and animal studies have shown that maternal obesity predisposes the offspring to obesity and the metabolic syndrome, possibly via late-onset metabolic programming of the fetus. Little is known, however, about the metabolic effect of maternal obesity on the fetus. This study investigated the effect of a maternal high-fat diet (HFD) on fetal growth and glucose metabolism using a diet-induced obesity mouse model. Study design Female mice (6 weeks old; C57BL/6N) were fed either a normal chow diet (NCD, 10 kcal% fat) or an HFD (60 kcal% fat) for 4 weeks before mating and throughout pregnancy. At 17 days of gestation, gene expression of inflammatory markers and adipokines in fetal subcutaneous adipose tissue was analyzed by quantitative real-time polymerase chain reaction. Results HFD mice were overweight, glucose intolerant and insulin resistant compared with NCD mice of the same gestational age. Although fetal body weight was not significantly different, fetal plasma glucose and insulin levels were higher in the HFD group than the NCD group. Furthermore, examination of fetal subcutaneous adipose tissue in the HFD group revealed hypertrophy with an increase in the levels of cluster of differentiation-68, chemokine receptor-2 and tumor necrosis factor-α mRNA, but a decrease in the level of glucose transporter-4 mRNA. Conclusion Maternal HFD causes inflammatory changes in the adipose tissue of offspring.
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“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 [91]
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“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 [91]
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Metadata
- Authors
- Murabayashi, N., Sugiyama, T., Zhang, L., Kamimoto, Y., Umekawa, T., Ma, N., & Sagawa, N.
- Affiliations
- Tohoku University (JP)
- Mie University (JP)
- Suzuka University of Medical Science (JP)
- Corresponding author
- Sugiyama, T.
- Venue
- European Journal of Obstetrics & Gynecology and Reproductive Biology
- Publisher
- Elsevier BV
- Published
- 2013-07
- Volume
- 169
- Issue
- 1
- Pages
- 39-44
- ISSN
- 0028-2243 (ISSN-L)
- 0301-2115
- OpenAlex
- W2065422716
- Cited by
- 114
- References
- 27
- Citations by year
- 2026: 2 · 2025: 10 · 2024: 5 · 2023: 5 · 2022: 9 · 2021: 8 · 2020: 10 · 2019: 12 · 2018: 5 · 2017: 11 · 2016: 14 · 2015: 9 · 2014: 10 · 2013: 4
- FWCI
- 10.46
- Type
- journal article
- Language
- en
- Open access
- green
- mie-u.repo.nii.ac.jp
- Licence
- Locations
- European Journal of Obstetrics & Gynecology and Reproductive Biology (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- Funders
- Japan Society for the Promotion of Science (25462548, 23791830)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Keywords
- maternal high-fat diet, maternal obesity, fetal adipose tissue, insulin resistance, fetal glucose metabolism, fetal growth, inflammation, adipokines, CD68, CCR2, TNF-α, GLUT4, diet-induced obesity, metabolic programming
- MeSH terms
- CD68 Molecule, Adipose Tissue, Animals, Female, Fetus, Inflammation, Insulin, Insulin Resistance, Mice, Inbred C57BL, Obesity, Pregnancy, Prenatal Exposure Delayed Effects, RNA, Messenger, Tumor Necrosis Factor-alpha, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Fetal Development, Subcutaneous Fat, Glucose Transporter Type 4, Mice, Receptors, CCR2, Diet, High-Fat
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