ArticleThe Journal of biological chemistry2015
Concerted Trafficking Regulation of Kv2.1 and KATP Channels by Leptin in Pancreatic β-Cells.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Ion channels and actin: A tale of two friends.Histology and histopathology · 2025Review
- The impact of sulfonylureas on diverse ion channels: an alternative explanation for the antidiabetic actions.Frontiers in cell and developmental biology · 2025Review
- KCNB1-Leptin receptor complexes couple electric and endocrine function in the melanocortin neurons of the hypothalamus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- The key mediator of diabetic kidney disease: Potassium channel dysfunction.Genes & diseases · 2024Review
- Noncanonical Regulation of cAMP-Dependent Insulin Secretion and Its Implications in Type 2 Diabetes.Comprehensive Physiology · 2023Article
- Genetic Knockout of TRPM2 Increases Neuronal Excitability of Hippocampal Neurons by Inhibiting Kv7 Channel in Epilepsy.Molecular neurobiology · 2022Article
- Interorgan crosstalk in pancreatic islet function and pathology.FEBS letters · 2022Review
- Effect of visfatin on KAging · 2022Article
- Leptin modulates pancreatic β-cell membrane potential through Src kinase-mediated phosphorylation of NMDA receptors.The Journal of biological chemistry · 2020Article
- Cellular and systemic mechanisms for glucose sensing and homeostasis.Pflugers Archiv : European journal of physiology · 2020Review
- The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020Review
- Leptin Induces Hypertension Acting on Transient Receptor Potential Melastatin 7 Channel in the Carotid Body.Circulation research · 2019Article
- AMP-activated protein kinase slows D2 dopamine autoreceptor desensitization in substantia nigra neurons.Neuropharmacology · 2019Article
- What role do fat cells play in pancreatic tissue?Molecular metabolism · 2019Review
- Leptin-induced Trafficking of KInternational journal of molecular sciences · 2019Review
- Insulin Release Mechanism Modulated by Toxins Isolated from Animal Venoms: From Basic Research to Drug Development Prospects.Molecules (Basel, Switzerland) · 2019Review
- Friend and foe: β-cell CaMolecular metabolism · 2019Review
- Kir6.1/K-ATP channel modulates microglia phenotypes: implication in Parkinson's disease.Cell death & disease · 2018Article
- NMDA receptors mediate leptin signaling and regulate potassium channel trafficking in pancreatic β-cells.The Journal of biological chemistry · 2017Article
- Leptin-mediated ion channel regulation: PI3K pathways, physiological role, and therapeutic potential.Channels (Austin, Tex.) · 2016Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
In pancreatic β-cells, voltage-gated potassium 2.1 (Kv2.1) channels are the dominant delayed rectifier potassium channels responsible for action potential repolarization. Here, we report that leptin, a hormone secreted by adipocytes known to inhibit insulin secretion, causes a transient increase in surface expression of Kv2.1 channels in rodent and human β-cells. The effect of leptin on Kv2.1 surface expression is mediated by the AMP-activated protein kinase (AMPK). Activation of AMPK mimics whereas inhibition of AMPK occludes the effect of leptin. Inhibition of Ca(2+)/calmodulin-dependent protein kinase kinase β, a known upstream kinase of AMPK, also blocks the effect of leptin. In addition, the cAMP-dependent protein kinase (PKA) is involved in Kv2.1 channel trafficking regulation. Inhibition of PKA prevents leptin or AMPK activators from increasing Kv2.1 channel density, whereas stimulation of PKA is sufficient to promote Kv2.1 channel surface expression. The increased Kv2.1 surface expression by leptin is dependent on actin depolymerization, and pharmacologically induced actin depolymerization is sufficient to enhance Kv2.1 surface expression. The signaling and cellular mechanisms underlying Kv2.1 channel trafficking regulation by leptin mirror those reported recently for ATP-sensitive potassium (KATP) channels, which are critical for coupling glucose stimulation with membrane depolarization. We show that the leptin-induced increase in surface KATP channels results in more hyperpolarized membrane potentials than control cells at stimulating glucose concentrations, and the increase in Kv2.1 channels leads to a more rapid repolarization of membrane potential in cells firing action potentials. This study supports a model in which leptin exerts concerted trafficking regulation of KATP and Kv2.1 channels to coordinately inhibit insulin secretion.
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