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Cited by 18Birth, Development, and HealthAdipokines, Inflammation, and Metabolic DiseasesDiet, Metabolism, and Disease

Maternal Protein Restriction Altered Insulin Resistance and Inflammation-Associated Gene Expression in Adipose Tissue of Young Adult Mouse Offspring in Response to a High-Fat Diet

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Kim, Juhae, Choi, Alee, Kwon, Young Hye·2020·Nutrients
DOI 10.3390/nu12041103PMC PMC7230574
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Abstract

Maternal protein restriction is associated with increased risk of insulin resistance and inflammation in adulthood offspring. Here, we investigated whether maternal protein restriction could alter the risk of metabolic syndrome in postweaning high-fat (HF)-diet-challenged offspring, with focus on epididymal adipose tissue gene expression profile. Female ICR mice were fed a control (C) or a low-protein (LP) diet for two weeks before mating and throughout gestation and lactation, and their male offspring were fed an HF diet for 22 weeks (C/HF and LP/HF groups). A subset of offspring of control dams was fed a low-fat control diet (C/C group). In response to postweaning HF diet, serum insulin level and the homeostasis model assessment of insulin resistance (HOMA-IR) were increased in control offspring. Maternal LP diet decreased HOMA-IR and adipose tissue inflammation, and increased serum adiponectin level in the HF-diet-challenged offspring. Accordingly, functional analysis revealed that differentially expressed genes (DEGs) enriched in cytokine production were downregulated in the LP/HF group compared to the C/HF group. We also observed the several annotated gene ontology terms associated with innate immunity and phagocytosis in down-regulated DEGs between LP/HF and C/C groups. In conclusion, maternal protein restriction alleviated insulin resistance and inflammation in young offspring mice fed a HF diet but may impair development of immune system in offspring.

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  • Offspring from low protein fed mothers often display insulin resistance and hyperglycemia in adulthood.

    “However, offspring from low protein fed mothers accumulate greater amounts of fat as they mature [75, 76] and often display insulin resistance and hyperglycemia in adulthood [77, 78].”

    From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [78]

    The Discussion (page not provided) reports hyperglycemia in nine-month-old offspring of low-protein-fed mothers after long-term high-fat, high-sucrose feeding, supporting that part of the claim under a specific dietary condition. But Results §3.2 (page not provided) finds lower insulin-resistance markers in this study’s adult low-protein offspring than in controls fed a high-fat diet; the paper describes findings across studies as inconsistent, so it does not support the general claim that these offspring often display insulin resistance. (LLM, conf=0.86)

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  • Across the species surveyed, changes in offspring adiposity are accompanied by alterations in adipocyte size or number, insulin signaling and metabolic protein levels, including PPARγ, as well as inflammatory markers and leukocytes in the adipose tissue of the offspring born from low protein diet-fed mothers.

    “Across the species surveyed, changes in offspring adiposity are accompanied by alterations in adipocyte size or number, insulin signaling and metabolic protein levels, including PPARγ, as well as inflammatory markers and leukocytes in the adipose tissue of the offspring born from low protein diet-fed mothers [71, 72, 78, 82].”

    From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [78]

    The Results (§3.1; page unavailable) report increased relative adiposity and reduced adipose-tissue macrophage infiltration in offspring of low-protein-fed mice; the Discussion (§4; page unavailable) reports altered adipocyte size and lower inflammation and insulin resistance. This mouse study does not establish the claim across species, and the passages do not report altered PPARγ protein levels or directly measured insulin-signaling proteins. (LLM, conf=0.87)

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Authors
Kim, J., Choi, A., & Kwon, Y. H.
Affiliations
Seoul National University (KR)
Corresponding author
Kwon, Young Hye
ORCID
Venue
Nutrients
Publisher
MDPI AG
Published
2020-04-16
Volume
12
Issue
4
Pages
1103
ISSN
2072-6643 (ISSN-L)
DOI
10.3390/nu12041103
PMC
PMC7230574
OpenAlex
W3016435575
Cited by
18
References
59
Citations by year
2026: 2 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 7 · 2020: 2 · 2019: 1
FWCI
3.36
Type
journal article
Language
en
Open access
Licence
Locations
  • Nutrients (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Ministry of Science, ICT and Future Planning (NRF-2014R1A1A3052400)
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 protein restriction, insulin resistance, adipose tissue inflammation, high-fat diet, metabolic syndrome, offspring, epididymal adipose tissue, adiponectin, cytokine gene expression, innate immunity, phagocytosis, pregnancy and lactation, HOMA-IR
MeSH terms
Adipose Tissue, Animals, Animal Nutritional Physiological Phenomena, Female, Gene Expression Regulation, Immunity, Innate, Inflammation, Insulin Resistance, Male, Maternal-Fetal Exchange, Mice, Inbred ICR, Phagocytosis, Pregnancy, Down-Regulation, Gene Expression, Cytokines, Diet, Protein-Restricted, Diet, High-Fat

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