ArticleAmerican journal of physiology. Endocrinology and metabolism2026
Nr4a3 deficiency disrupts MEK1-ERK1/2-Drp1 signaling, driving adiposity and glucose intolerance in male mice.
Peter N Ellsworth, Kate E Whalen, Jared D Carter, Jacob A Herring, Kavan H Hess, Kristopher L Wieland, Drake C Watkins, Jeremy Y Saito, Erik D Marchant, Nathan D Marchant and 6 more
Abstract read
In one paragraphArticle in American journal of physiology. Endocrinology and metabolism, 2026. 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 itWhat it found
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
16 authors.
Peter N EllsworthDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0009-0002-0630-5860 Kate E WhalenDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0000-0002-3887-8551 Jared D CarterDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0009-0009-8787-3368 Jacob A HerringDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0000-0002-0084-1091 Kavan H HessDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.
Kristopher L WielandDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.
Drake C WatkinsDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.
Jeremy Y SaitoDepartment of Cell Biology and Physiology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.
Erik D MarchantDepartment of Nutrition, Dietetics, and Food Science, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0000-0002-2222-7594 Nathan D MarchantDepartment of Nutrition, Dietetics, and Food Science, College of Life Sciences, Brigham Young University, Provo, Utah, United States.
Nathan D WalkerDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0009-0008-3420-5721 Garritt L PageDepartment of Statistics, College of Computation, Mathematical, and Physical Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0000-0002-4163-7046 Yang CaoDepartment of Medicine, Physiology, and Biophysics, University of California, Irvine, CA, United States.
Qin YangDepartment of Medicine, Physiology, and Biophysics, University of California, Irvine, CA, United States.
Benjamin T BikmanDepartment of Cell Biology and Physiology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0000-0003-3680-6906 Jeffery S TessemDepartment of Microbiology and Molecular Biology, College of Life Sciences, Brigham Young University, Provo, Utah, United States.ORCID 0000-0003-3081-3187 Funding
Nr4a1 and the expansion of functional beta-cell massR15DK144832 · NIDDK · BRIGHAM YOUNG UNIVERSITY · PI TESSEM, JEFFERY SIVERT · 2025 to 2025
$568kSex dependent function of the orphan nuclear receptor Nr4a1 in the pancreatic beta cell during Type 2 Diabetes disease progressionR15DK124835 · NIDDK · BRIGHAM YOUNG UNIVERSITY · PI TESSEM, JEFFERY SIVERT · 2021 to 2021
$441kHHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R15DK124835HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R15DK144832NIDDK NIH HHS R15 DK124835NIDDK NIH HHS R15 DK144832
6 · The paper itselfAbstract
Obesity is strongly associated with elevated blood glucose levels, glucose intolerance, insulin resistance, and type 2 diabetes. The Nr4a family of orphan nuclear receptors is essential for proliferation, cell survival, mitochondrial function, and fuel utilization in a tissue-dependent manner. Nr4a3 overexpression has been shown to decrease blood glucose levels and improve glucose tolerance. Here, we present the effects of full body Nr4a3 deletion in mice fed a standard chow diet. We demonstrate that male and female
Indexed as
AdiposityDNA-Binding ProteinsDynaminsGlucose IntoleranceMAP Kinase Signaling SystemReceptors, SteroidReceptors, Thyroid HormoneAdipose TissueAnimalsFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaNerve Tissue ProteinsDNA-Binding ProteinsDnm1l protein, mouseDynaminsNerve Tissue ProteinsNr4a3 protein, mouseReceptors, SteroidReceptors, Thyroid Hormoneadipose tissueDrp1glucose tolerancemitochondrial respirationNr4a3
Identifiers
PMID42572167
PMCPMC13528230
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