Evidence map›Paper›PMID 40570821›Full record

ArticleLifestyle genomics2025

Experimental Environment Is a Determinant of Gene Methylation and One-Carbon Metabolism in Obese Adult Mice.

Zeyu Yang, Ruslan Kubant, Eva Kranenburg, Clara E Cho, G Harvey Anderson

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Article in Lifestyle genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Zeyu YangDepartment of Nutritional Sciences, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Ruslan KubantDepartment of Nutritional Sciences, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Eva KranenburgDepartment of Nutritional Sciences, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Clara E ChoDepartment of Human Health and Nutritional Sciences, College of Biological Science, University of Guelph, Guelph, Ontario, Canada.
G Harvey AndersonDepartment of Nutritional Sciences, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiet-induced obesity (DIO) leads to insulin resistance (IR) and alters gene expression through epigenetic mechanisms, including DNA methylation. Here, we aimed to investigate whether experimental environment is an important variable in determining DNA methylation and one-carbon metabolism in DIO mice fed a multi-vitamin-mineral mixture (MVM).

methodsThree experiments with identical design were conducted in three independent animal facilities (i.e., experimental environments or locations). In each location, 12-week-old male C57BL/6J mice were randomly assigned to two dietary groups: high-fat (HF) and HF-MVM for an average of 10 weeks. Global and gene-specific methylation of adipose function related genes in epididymal white adipose tissue (eWAT), and insulin signaling genes in the liver were analyzed using bisulfite pyrosequencing. Hepatic 1-C metabolites were measured and the ratio of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) was used as an indicator of methylation potential.

resultsExperimental location affected global methylation patterns in the eWAT, but not in the liver. At the gene-specific level, experimental location, MVM, and their interaction altered the methylation of genes related to adipose function (Srebf1, Acaca, Fasn, Pparg, and Rbp4) in the eWAT and insulin signaling (Pi3kr1 and Akt1) in the liver (p < 0.05). The SAM/SAH ratio was correlated with gene-specific methylation at some CpG sites of Srebf1, Pi3kr1, Acaca, Fasn, Pparg, Rbp4, and Akt1) genes (p < 0.05).

conclusionThe experimental environment is a significant determinant of the effects of micronutrient supplement on 1-C metabolism and the methylation of genes associated with IR in tissues of DIO adult male mice.

Indexed as

CarbonDNA MethylationObesityAdipose Tissue, WhiteAnimalsDiet, High-FatEpigenesis, GeneticInsulin ResistanceLiverMaleMiceMice, Inbred C57BLMice, ObeseS-AdenosylhomocysteineS-AdenosylmethionineCarbonS-AdenosylhomocysteineS-AdenosylmethionineDiet-induced obesityDNA methylationExperimental environmentMicronutrientsOne-carbon metabolism

Identifiers

PMID40570821
PMCPMC12503451

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.