ArticleProceedings of the National Academy of Sciences of the United States of America2013
Leptin promotes K(ATP) channel trafficking by AMPK signaling in pancreatic β-cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 86 citations in OpenAlex.
- Transient receptor potential canonical (TRPC) channels in diabetes and associated complications.Channels (Austin, Tex.) · 2026Review
- Hypoglycemic conditions enhance neonatal β-cell glucose responsiveness via AMPK/mTOR-increased KATP channel density.Endocrinology · 2026Article
- Mechanisms and Functions of Sweet Reception in Oral and Extraoral Organs.International journal of molecular sciences · 2024Review
- The Interplay of Adipokines and Pancreatic Beta Cells in Metabolic Regulation and Diabetes.Biomedicines · 2023Review
- Acupuncture improves immunity and fatigue after chemotherapy in breast cancer patients by inhibiting the Leptin/AMPK signaling pathway.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2023Article
- Rab35 GTPase positively regulates endocytic recycling of cardiac KChannels (Austin, Tex.) · 2022Article
- Leptin receptor signaling sustains metabolic fitness of alveolar macrophages to attenuate pulmonary inflammation.Science advances · 2022Article
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- Glycogen synthesis and beyond, a comprehensive review of GSK3 as a key regulator of metabolic pathways and a therapeutic target for treating metabolic diseases.Medicinal research reviews · 2022Review
- TRP Channels as Molecular Targets to Relieve Endocrine-Related Diseases.Frontiers in molecular biosciences · 2022Review
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Phosphatidylinositol-3 kinase mediates the sweet suppressive effect of leptin in mouse taste cells.Journal of neurochemistry · 2021Article
- Article
- The Glucagon-Like Adipokinetic Hormone inFrontiers in physiology · 2021Review
- 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
- Review
- What role do fat cells play in pancreatic tissue?Molecular metabolism · 2019Review
- Rab8a is involved in membrane trafficking of Kir6.2 in the MIN6 insulinoma cell line.Pflugers Archiv : European journal of physiology · 2019Article
- Leptin-induced Trafficking of KInternational journal of molecular sciences · 2019Review
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Authors and funding
15 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leptin is a pivotal regulator of energy and glucose homeostasis, and defects in leptin signaling result in obesity and diabetes. The ATP-sensitive potassium (K(ATP)) channels couple glucose metabolism to insulin secretion in pancreatic β-cells. In this study, we provide evidence that leptin modulates pancreatic β-cell functions by promoting K(ATP) channel translocation to the plasma membrane via AMP-activated protein kinase (AMPK) signaling. K(ATP) channels were localized mostly to intracellular compartments of pancreatic β-cells in the fed state and translocated to the plasma membrane in the fasted state. This process was defective in leptin-deficient ob/ob mice, but restored by leptin treatment. We discovered that the molecular mechanism of leptin-induced AMPK activation involves canonical transient receptor potential 4 and calcium/calmodulin-dependent protein kinase kinase β. AMPK activation was dependent on both leptin and glucose concentrations, so at optimal concentrations of leptin, AMPK was activated sufficiently to induce K(ATP) channel trafficking and hyperpolarization of pancreatic β-cells in a physiological range of fasting glucose levels. There was a close correlation between phospho-AMPK levels and β-cell membrane potentials, suggesting that AMPK-dependent K(ATP) channel trafficking is a key mechanism for regulating β-cell membrane potentials. Our results present a signaling pathway whereby leptin regulates glucose homeostasis by modulating β-cell excitability.
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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.