ArticleMolecular endocrinology (Baltimore, Md.)2010
FoxM1 is up-regulated by obesity and stimulates beta-cell proliferation.
Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 91 citations in OpenAlex.
- Emerging Roles of Post-Translational Modifications in Metabolic Homeostasis and Type 2 Diabetes.International journal of molecular sciences · 2025Review
- FOXM1 Protects Against Myocardial Ischemia-Reperfusion Injury in Rodent and Porcine Models by Suppressing MKRN1-Dependent LKB1 Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- FOXM1 cooperates with ERα to regulate functional β-cell mass.American journal of physiology. Endocrinology and metabolism · 2025Article
- Post translational modification regulation of transcription factors governing pancreatic β-cell identity and functional mass.Frontiers in endocrinology · 2025Review
- Single-housing-induced islet epigenomic changes are related to polymorphisms in diabetic KK mice.Life science alliance · 2024Article
- Article
- Beta-cell compensation and gestational diabetes.The Journal of biological chemistry · 2023Review
- Review
- FOXM1: Functional Roles of FOXM1 in Non-Malignant Diseases.Biomolecules · 2023Review
- Analysis of a genetic region affecting mouse body weight.Physiological genomics · 2023Article
- Disrupting the DREAM complex enables proliferation of adult human pancreatic β cells.The Journal of clinical investigation · 2022Article
- MFAP2 aggravates tumor progression through activating FOXM1/β-catenin-mediated glycolysis in ovarian cancer.The Kaohsiung journal of medical sciences · 2022Article
- Evaluation of the Effects of Harmine on β-cell Function and Proliferation in Standardized Human Islets Using 3D High-Content Confocal Imaging and Automated Analysis.Frontiers in endocrinology · 2022Review
- Identification of direct transcriptional targets of NFATC2 that promote β cell proliferation.The Journal of clinical investigation · 2021Article
- Prostaglandin EP3 receptor signaling is required to prevent insulin hypersecretion and metabolic dysfunction in a non-obese mouse model of insulin resistance.American journal of physiology. Endocrinology and metabolism · 2021Article
- Islet Regeneration: Endogenous and Exogenous Approaches.International journal of molecular sciences · 2021Review
- Exploring the Genetic Conception of Obesity via the Dual Role of FoxO.International journal of molecular sciences · 2021Review
- The Map3k12 (Dlk)/JNK3 signaling pathway is required for pancreatic beta-cell proliferation during postnatal development.Cellular and molecular life sciences : CMLS · 2021Article
- The core clock transcription factor BMAL1 drives circadian β-cell proliferation during compensatory regeneration of the endocrine pancreas.Genes & development · 2020Article
- Preconditioning of Human Decidua Basalis Mesenchymal Stem/Stromal Cells with Glucose Increased Their Engraftment and Anti-diabetic Properties.Tissue engineering and regenerative medicine · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
beta-Cell mass expansion is one mechanism by which obese animals compensate for insulin resistance and prevent diabetes. FoxM1 is a transcription factor that can regulate the expression of multiple cell cycle genes and is necessary for the maintenance of adult beta-cell mass, beta-cell proliferation, and glucose homeostasis. We hypothesized that FoxM1 is up-regulated by nondiabetic obesity and initiates a transcriptional program leading to beta-cell proliferation. We performed gene expression analysis on islets from the nondiabetic C57BL/6 Leptin(ob/ob) mouse, the diabetic BTBR Leptin(ob/ob) mouse, and an F2 Leptin(ob/ob) population derived from these strains. We identified obesity-driven coordinated up-regulation of islet Foxm1 and its target genes in the nondiabetic strain, correlating with beta-cell mass expansion and proliferation. This up-regulation was absent in the diabetic strain. In the F2 Leptin(ob/ob) population, increased expression of Foxm1 and its target genes segregated with higher insulin and lower glucose levels. We next studied the effects of FOXM1b overexpression on isolated mouse and human islets. We found that FoxM1 stimulated mouse and human beta-cell proliferation by activating many cell cycle phases. We asked whether FOXM1 expression is also responsive to obesity in human islets by collecting RNA from human islet donors (body mass index range: 24-51). We found that the expression of FOXM1 and its target genes is positively correlated with body mass index. Our data suggest that beta-cell proliferation occurs in adult obese humans in an attempt to expand beta-cell mass to compensate for insulin resistance, and that the FoxM1 transcriptional program plays a key role in this process.
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Registered trials
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.