Evidence map›Paper›PMID 35290440›Full record

ArticleDiabetes2022

Maternal Exercise-Induced SOD3 Reverses the Deleterious Effects of Maternal High-Fat Diet on Offspring Metabolism Through Stabilization of H3K4me3 and Protection Against WDR82 Carbonylation.

Joji Kusuyama, Nathan S Makarewicz, Brent G Albertson, Ana Barbara Alves-Wagner, Royce H Conlin, Noah B Prince, Christiano R R Alves, Krithika Ramachandran, Chisayo Kozuka, Yang Xiudong and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
12.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 36 citations in OpenAlex.

  1. Maternal exercise alters placental proteome in an exercise mode-specific manner.American journal of physiology. Endocrinology and metabolism · 2025
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  16. Developmental origins of adult diseases.Medical review (2021) · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 2 countries.

Joji KusuyamaSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.ORCID 0000-0003-4054-1939
Nathan S MakarewiczSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Brent G AlbertsonSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Ana Barbara Alves-WagnerSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Royce H ConlinSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Noah B PrinceSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Christiano R R AlvesSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Krithika RamachandranSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Chisayo KozukaYCI Laboratory for Metabolic Epigenetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.ORCID 0000-0002-9567-8361
Yang XiudongGraduate School of Biomedical Sciences, University of Texas at Houston, Houston, TX.
Yang XiaGraduate School of Biomedical Sciences, University of Texas at Houston, Houston, TX.
Michael F HirshmanSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Kanazawa, Japan.
Ryoichi NagatomiDivision of Biomedical Engineering for Health and Welfare, Graduate School of Biomedical Engineering, Tohoku University, Sendai, Japan.
Eva S NozikCardiovascular Pulmonary Research Laboratories and Pediatric Critical Care, Department of Pediatrics, University of Colorado Anschutz Medical Center, Aurora, CO.
Laurie J GoodyearSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA.ORCID 0000-0002-6299-2928
Joslin Diabetes Center · USKanazawa Medical University · JPRIKEN Center for Integrative Medical Sciences · JPTohoku University · JPUniversity of Colorado Anschutz Medical Campus · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Exercise Regulation of Glucose Homeostasis Administrative SupplementR01DK101043 · NIDDK · JOSLIN DIABETES CENTER · PI LAURIE J GOODYEAR · 2013 to 2026
$7.3M
SOD3 regulation of redox sensitive signaling in pulmonary vascular diseasesR35HL139726 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI NOZIK, EVA S. · 2018 to 2024
$4.1M
NHLBI NIH HHS R35 HL139726NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK101043
6 · The paper itself

Abstract

Preclinical studies reveal maternal exercise as a promising intervention to reduce the transmission of multigenerational metabolic dysfunction caused by maternal obesity. The benefits of maternal exercise on offspring health may arise from multiple factors and have recently been shown to involve DNA demethylation of critical hepatic genes leading to enhanced glucose metabolism in offspring. Histone modification is another epigenetic regulator, yet the effects of maternal obesity and exercise on histone methylation in offspring are not known. Here, we find that maternal high-fat diet (HFD; 60% kcal from fat) induced dysregulation of offspring liver glucose metabolism in C57BL/6 mice through a mechanism involving increased reactive oxygen species, WD repeat-containing 82 (WDR82) carbonylation, and inactivation of histone H3 lysine 4 (H3K4) methyltransferase leading to decreased H3K4me3 at the promoters of glucose metabolic genes. Remarkably, the entire signal was restored if the HFD-fed dams had exercised during pregnancy. WDR82 overexpression in hepatoblasts mimicked the effects of maternal exercise on H3K4me3 levels. Placental superoxide dismutase 3 (SOD3), but not antioxidant treatment with N-acetylcysteine was necessary for the regulation of H3K4me3, gene expression, and glucose metabolism. Maternal exercise regulates a multicomponent epigenetic system in the fetal liver resulting in the transmission of the benefits of exercise to offspring.

Indexed as

Pregnancy in ObesityPrenatal Exposure Delayed EffectsAnimalsChromosomal Proteins, Non-HistoneDiet, High-FatFemaleGlucoseHistonesHumansMiceMice, Inbred C57BLPlacentaPregnancySuperoxide DismutaseChromosomal Proteins, Non-HistoneGlucosehistone H3 trimethyl Lys4HistonesSOD3 protein, humanSod3 protein, mouseSuperoxide DismutaseWDR82 protein, human

Identifiers

PMID35290440
PMCPMC9163554
OpenAlexW4220963318

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.