Publication:
Contribution of Liver and Pancreatic Islet Crosstalk to β-Cell Function/Dysfunction in the Presence of Fatty Liver.

dc.contributor.authorLópez-Bermudo, Lucía
dc.contributor.authorLuque-Sierra, Amparo
dc.contributor.authorMaya-Miles, Douglas
dc.contributor.authorGallego-Durán, Rocío
dc.contributor.authorAmpuero, Javier
dc.contributor.authorRomero-Gómez, Manuel
dc.contributor.authorBerná, Genoveva
dc.contributor.authorMartín, Franz
dc.date.accessioned2023-05-03T13:40:03Z
dc.date.available2023-05-03T13:40:03Z
dc.date.issued2022-05-16
dc.description.abstractTissue-to-tissue crosstalk regulates organ function, according to growing data. This phenomenon is relevant for pancreatic β-cells and the liver, as both tissues are involved in glucose homeostasis and lipid metabolism. The ability to fine-tune regulation and adaptive responses is enabled through communication between pancreatic β-cells and the liver. However, the crosstalk between both tissues changes when metabolic dysregulation is present. Factors and cargo from extracellular vesicles (EVs) released by liver and pancreatic β-cells that reach the circulation form the words of this interaction. The molecules released by the liver are called hepatokines and are usually secreted in response to the metabolic state. When hepatokines reach the pancreatic islets several mechanisms are initiated for their protection or damage. In the case of the crosstalk between pancreatic β-cells and the liver, only one factor has been found to date. This protein, pancreatic derived factor (PANDER) has been proposed as a novel linker between insulin resistance (IR) and type 2 diabetes mellitus (T2D) and could be considered a biomarker for non-alcoholic fatty liver disease (NAFLD) and T2D. Furthermore, the cargo released by EVs, mainly miRNAs, plays a significant role in this crosstalk. A better knowledge of the crosstalk between liver and pancreatic β-cells is essential to understand both diseases and it could lead to better prevention and new therapeutic options.
dc.identifier.doi10.3389/fendo.2022.892672
dc.identifier.issn1664-2392
dc.identifier.pmcPMC9148952
dc.identifier.pmid35651973
dc.identifier.pubmedURLhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9148952/pdf
dc.identifier.unpaywallURLhttps://www.frontiersin.org/articles/10.3389/fendo.2022.892672/pdf
dc.identifier.urihttp://hdl.handle.net/10668/20566
dc.journal.titleFrontiers in endocrinology
dc.journal.titleabbreviationFront Endocrinol (Lausanne)
dc.language.isoen
dc.organizationHospital Universitario Virgen del Rocío
dc.organizationCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER
dc.organizationInstituto de Biomedicina de Sevilla-IBIS
dc.page.number892672
dc.pubmedtypeSystematic Review
dc.pubmedtypeResearch Support, Non-U.S. Gov't
dc.rightsAttribution 4.0 International
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectcrosstalk
dc.subjectextracellular vesicles (EVs)
dc.subjecthepatokines
dc.subjectliver
dc.subjectnonalcoholic fatty liver disease
dc.subjectpancreatic islets
dc.subjecttype 2 diabetes
dc.subjectβ-cell
dc.subject.meshDiabetes Mellitus, Type 2
dc.subject.meshHumans
dc.subject.meshInsulin-Secreting Cells
dc.subject.meshIslets of Langerhans
dc.subject.meshNon-alcoholic Fatty Liver Disease
dc.titleContribution of Liver and Pancreatic Islet Crosstalk to β-Cell Function/Dysfunction in the Presence of Fatty Liver.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number13
dspace.entity.typePublication

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