ArticleThe Journal of biological chemistry2015
Loss of Liver Kinase B1 (LKB1) in Beta Cells Enhances Glucose-stimulated Insulin Secretion Despite Profound Mitochondrial Defects.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- 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
- Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.Frontiers in molecular biosciences · 2024Review
- Review
- Expression of Pfkfb isoenzymes during in vitro differentiation of mouse embryonic stem cells into insulin-producing cells.Turkish journal of medical sciences · 2023Article
- Of Mice and Men and Plethysmography Systems: Does LKB1 Determine the Set Point of Carotid Body Chemosensitivity and the Hypoxic Ventilatory Response?Advances in experimental medicine and biology · 2023Article
- LKB1 is the gatekeeper of carotid body chemosensing and the hypoxic ventilatory response.Communications biology · 2022Article
- Opposing effects on regulated insulin secretion of acute vs chronic stimulation of AMP-activated protein kinase.Diabetologia · 2022Article
- Islet Biology During COVID-19: Progress and Perspectives.Canadian journal of diabetes · 2022Review
- Article
- Protein Kinases Signaling in Pancreatic Beta-cells Death and Type 2 Diabetes.Advances in experimental medicine and biology · 2021Article
- Regulation of axonal morphogenesis by the mitochondrial protein Efhd1.Life science alliance · 2020Article
- A Nutrient-Sensing Transition at Birth Triggers Glucose-Responsive Insulin Secretion.Cell metabolism · 2020Article
- Nutrient Sensor mTOR and OGT: Orchestrators of Organelle Homeostasis in PancreaticJournal of diabetes research · 2020Review
- Loss of LAMTOR1 in pancreatic β‑cells increases glucose‑stimulated insulin secretion in mice.International journal of molecular medicine · 2020Article
- LKB1 suppresses androgen synthesis in a mouse model of hyperandrogenism via IGF-1 signaling.FEBS open bio · 2019Article
- Transcription factor-7-like 2 (The Journal of biological chemistry · 2018Article
- Mice harboring the humanProceedings of the National Academy of Sciences of the United States of America · 2018Article
- A Novel Phenylchromane Derivative Increases the Rate of Glucose Uptake in L6 Myotubes and Augments Insulin Secretion from Pancreatic Beta-Cells by Activating AMPK.Pharmaceutical research · 2017Article
- Identification of the signals for glucose-induced insulin secretion in INS1 (832/13) β-cells using metformin-induced metabolic deceleration as a model.The Journal of biological chemistry · 2017Article
- Mechanisms of the amplifying pathway of insulin secretion in the β cell.Pharmacology & therapeutics · 2017Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
Abstract
The tumor suppressor liver kinase B1 (LKB1) is an important regulator of pancreatic β cell biology. LKB1-dependent phosphorylation of distinct AMPK (adenosine monophosphate-activated protein kinase) family members determines proper β cell polarity and restricts β cell size, total β cell mass, and glucose-stimulated insulin secretion (GSIS). However, the full spectrum of LKB1 effects and the mechanisms involved in the secretory phenotype remain incompletely understood. We report here that in the absence of LKB1 in β cells, GSIS is dramatically and persistently improved. The enhancement is seen both in vivo and in vitro and cannot be explained by altered cell polarity, increased β cell number, or increased insulin content. Increased secretion does require membrane depolarization and calcium influx but appears to rely mostly on a distal step in the secretion pathway. Surprisingly, enhanced GSIS is seen despite profound defects in mitochondrial structure and function in LKB1-deficient β cells, expected to greatly diminish insulin secretion via the classic triggering pathway. Thus LKB1 is essential for mitochondrial homeostasis in β cells and in parallel is a powerful negative regulator of insulin secretion. This study shows that β cells can be manipulated to enhance GSIS to supra-normal levels even in the face of defective mitochondria and without deterioration over months.
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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.