ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
LKB1 and AMPK differentially regulate pancreatic β-cell identity.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 82 citations in OpenAlex.
- Mitochondria as Epigenetic Regulators of β-Cell Identity and Plasticity: A Metabolo-Epigenetic Perspective.Cells · 2026Review
- The role of AMPK signaling pathway in the pathogenesis of type 2 diabetes mellitus with its complications and related metabolic disorders.Metabolism open · 2025Review
- Serum NPTX2 and cognitive impairment in geriatric diabetes.Biomolecules & biomedicine · 2025Article
- The metabolic sensor AMPK: Twelve enzymes in one.Molecular metabolism · 2024Review
- Exploring pancreatic beta-cell subgroups and their connectivity.Nature metabolism · 2024Review
- Liver kinase B1 (LKB1) regulates the epigenetic landscape of mouse pancreatic beta cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Liver kinase B-1 modulates the activity of dopamine neurons in the ventral tegmental area and regulates social memory formation.Frontiers in molecular neuroscience · 2024Article
- Integrated transcriptomics contrasts fatty acid metabolism with hypoxia response in β-cell subpopulations associated with glycemic control.BMC genomics · 2023Article
- DNA Methylation NearPediatric diabetes · 2023Article
- Comprehensive and Quantitative Analysis of the Changes in Proteomic and Phosphoproteomic Profiles during Stimulation and Repression of Steroidogenesis in MA-10 Leydig Cells.International journal of molecular sciences · 2022Article
- Milk Exosomal microRNAs: Postnatal Promoters of β Cell Proliferation but Potential Inducers of β Cell De-Differentiation in Adult Life.International journal of molecular sciences · 2022Review
- Article
- Opposing effects on regulated insulin secretion of acute vs chronic stimulation of AMP-activated protein kinase.Diabetologia · 2022Article
- mPGES-2 blockade antagonizes β-cell senescence to ameliorate diabetes by acting on NR4A1.Nature metabolism · 2022Article
- Circulating Tumor Cell-Free DNA Genes as Prognostic Gene Signature for Platinum Resistant Ovarian Cancer Diagnosis.Biomarker insights · 2022Article
- The Transcriptome and Epigenome Reveal Novel Changes in Transcription Regulation During Pancreatic Rat Islet Maturation.Endocrinology · 2021Article
- Single-cell heterogeneity analysis and CRISPR screens in MIN6 cell line reveal transcriptional regulators of insulin.Cell cycle (Georgetown, Tex.) · 2021Article
- Epigenome-Wide Association Study Reveals Methylation Loci Associated With Offspring Gestational Diabetes Mellitus Exposure and Maternal Methylome.Diabetes care · 2021Article
- Sexually dimorphic roles for the type 2 diabetes-associated C2cd4b gene in murine glucose homeostasis.Diabetologia · 2021Article
- The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes.International journal of molecular sciences · 2021Review
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Authors and funding
22 authors at 9 institutions in 5 countries.
Funding
Abstract
Fully differentiated pancreatic β cells are essential for normal glucose homeostasis in mammals. Dedifferentiation of these cells has been suggested to occur in type 2 diabetes, impairing insulin production. Since chronic fuel excess ("glucotoxicity") is implicated in this process, we sought here to identify the potential roles in β-cell identity of the tumor suppressor liver kinase B1 (LKB1/STK11) and the downstream fuel-sensitive kinase, AMP-activated protein kinase (AMPK). Highly β-cell-restricted deletion of each kinase in mice, using an Ins1-controlled Cre, was therefore followed by physiological, morphometric, and massive parallel sequencing analysis. Loss of LKB1 strikingly (2.0-12-fold, E<0.01) increased the expression of subsets of hepatic (Alb, Iyd, Elovl2) and neuronal (Nptx2, Dlgap2, Cartpt, Pdyn) genes, enhancing glutamate signaling. These changes were partially recapitulated by the loss of AMPK, which also up-regulated β-cell "disallowed" genes (Slc16a1, Ldha, Mgst1, Pdgfra) 1.8- to 3.4-fold (E < 0.01). Correspondingly, targeted promoters were enriched for neuronal (Zfp206; P = 1.3 × 10(-33)) and hypoxia-regulated (HIF1; P = 2.5 × 10(-16)) transcription factors. In summary, LKB1 and AMPK, through only partly overlapping mechanisms, maintain β-cell identity by suppressing alternate pathways leading to neuronal, hepatic, and other characteristics. Selective targeting of these enzymes may provide a new approach to maintaining β-cell function in some forms of diabetes.
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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.