Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis

Background and Aims: The molecular mechanisms driving non-alcoholic fatty liver disease (NAFLD) are poorly understood; however, microRNAs might play a key role in these processes. We hypothesize that let-7d- 5p could contribute to the pathophysiol-ogy of NAFLD and serve as a potential diagnostic bio...

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Autores: Infante‐Menéndez, Jorge, López‐Pastor, Andrea R., González‐Illanes, Tamara, González‐López, Paula, Huertas‐Lárez, Raquel, Rey, Esther, González‐Rodríguez, Águeda, García‐Monzón, Carmelo, Patil, Nikita P., Vega De Céniga, Melina, Baker, Aaron B., Gómez Hernández, María De La Almudena, Escribano Illanes, Óscar
Tipo de recurso: artículo
Fecha de publicación:2023
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/92257
Acceso en línea:https://hdl.handle.net/20.500.14352/92257
Access Level:acceso abierto
Palabra clave:577.2
612.015
Biología molecular (Farmacia)
Bioquímica (Farmacia)
2403 Bioquímica
2302.21 Biología Molecular
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spelling Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosisInfante‐Menéndez, JorgeLópez‐Pastor, Andrea R.González‐Illanes, TamaraGonzález‐López, PaulaHuertas‐Lárez, RaquelRey, EstherGonzález‐Rodríguez, ÁguedaGarcía‐Monzón, CarmeloPatil, Nikita P.Vega De Céniga, MelinaBaker, Aaron B.Gómez Hernández, María De La AlmudenaEscribano Illanes, Óscar577.2612.015Biología molecular (Farmacia)Bioquímica (Farmacia)2403 Bioquímica2302.21 Biología MolecularBackground and Aims: The molecular mechanisms driving non-alcoholic fatty liver disease (NAFLD) are poorly understood; however, microRNAs might play a key role in these processes. We hypothesize that let-7d- 5p could contribute to the pathophysiol-ogy of NAFLD and serve as a potential diagnostic biomarker.Methods: We evaluated let-7d- 5p levels and its targets in liver biopsies from a cross- sectional study including patients with NAFLD and healthy donors, and from a mouse model of NAFLD. Moreover, the induction of let-7d- 5p expression by fatty acids was evaluated in vitro. Further, we overexpressed let-7d- 5p in vitro to corroborate the results observed in vivo. Circulating let-7d- 5p and its potential as a NAFLD biomarker was determined in isolated extracellular vesicles from human plasma by RT-qPCR.Results: Our results demonstrate that hepatic let-7d- 5p was significantly up- regulated in patients with steatosis, and this increase correlated with obesity and a decreased expression of AKT serine/threonine kinase (AKT), insulin- like growth factor 1 (IGF1), IGF- I receptor (IGF1R) and insulin receptor (INSR). These alterations were corrobo-rated in a NAFLD mouse model. In vitro, fatty acids increased let-7d- 5p expression, and its overexpression decreased AKT, IGF-IR and IR protein expression. Furthermore, let- 7d- 5p hindered AKT phosphorylation in vitro after insulin stimulation. Finally, cir-culating let-7d- 5p significantly decreased in steatosis patients and receiver operating characteristic (ROC) analyses confirmed its utility as a diagnostic biomarker.WileyUniversidad Complutense de Madrid20232023-04-1420232023-04-14journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/92257reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)InglésengRTI-2018-095098-B100 Not available Not availablePID2021-123076OB-I00 Not available Not availableAENC1 22-29754 Not availablePR75 18-21572 Not availablePI20 00837 Not availablePI19 00123 Not available17IRG33410888 Not available Not availableW81XWH-16-1-0580 Not available Not availableW81XWH-16-1-0582 Not available Not availableR21EB023551-01 Not available Not available1R21EB024147-01A1 Not available Not available1R01HL141761-01 Not available Not availableopen accesshttp://purl.org/coar/access_right/c_abf2Attribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/922572026-06-02T12:44:21Z
dc.title.none.fl_str_mv Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
title Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
spellingShingle Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
Infante‐Menéndez, Jorge
577.2
612.015
Biología molecular (Farmacia)
Bioquímica (Farmacia)
2403 Bioquímica
2302.21 Biología Molecular
title_short Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
title_full Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
title_fullStr Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
title_full_unstemmed Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
title_sort Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis
dc.creator.none.fl_str_mv Infante‐Menéndez, Jorge
López‐Pastor, Andrea R.
González‐Illanes, Tamara
González‐López, Paula
Huertas‐Lárez, Raquel
Rey, Esther
González‐Rodríguez, Águeda
García‐Monzón, Carmelo
Patil, Nikita P.
Vega De Céniga, Melina
Baker, Aaron B.
Gómez Hernández, María De La Almudena
Escribano Illanes, Óscar
author Infante‐Menéndez, Jorge
author_facet Infante‐Menéndez, Jorge
López‐Pastor, Andrea R.
González‐Illanes, Tamara
González‐López, Paula
Huertas‐Lárez, Raquel
Rey, Esther
González‐Rodríguez, Águeda
García‐Monzón, Carmelo
Patil, Nikita P.
Vega De Céniga, Melina
Baker, Aaron B.
Gómez Hernández, María De La Almudena
Escribano Illanes, Óscar
author_role author
author2 López‐Pastor, Andrea R.
González‐Illanes, Tamara
González‐López, Paula
Huertas‐Lárez, Raquel
Rey, Esther
González‐Rodríguez, Águeda
García‐Monzón, Carmelo
Patil, Nikita P.
Vega De Céniga, Melina
Baker, Aaron B.
Gómez Hernández, María De La Almudena
Escribano Illanes, Óscar
author2_role author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv 577.2
612.015
Biología molecular (Farmacia)
Bioquímica (Farmacia)
2403 Bioquímica
2302.21 Biología Molecular
topic 577.2
612.015
Biología molecular (Farmacia)
Bioquímica (Farmacia)
2403 Bioquímica
2302.21 Biología Molecular
description Background and Aims: The molecular mechanisms driving non-alcoholic fatty liver disease (NAFLD) are poorly understood; however, microRNAs might play a key role in these processes. We hypothesize that let-7d- 5p could contribute to the pathophysiol-ogy of NAFLD and serve as a potential diagnostic biomarker.Methods: We evaluated let-7d- 5p levels and its targets in liver biopsies from a cross- sectional study including patients with NAFLD and healthy donors, and from a mouse model of NAFLD. Moreover, the induction of let-7d- 5p expression by fatty acids was evaluated in vitro. Further, we overexpressed let-7d- 5p in vitro to corroborate the results observed in vivo. Circulating let-7d- 5p and its potential as a NAFLD biomarker was determined in isolated extracellular vesicles from human plasma by RT-qPCR.Results: Our results demonstrate that hepatic let-7d- 5p was significantly up- regulated in patients with steatosis, and this increase correlated with obesity and a decreased expression of AKT serine/threonine kinase (AKT), insulin- like growth factor 1 (IGF1), IGF- I receptor (IGF1R) and insulin receptor (INSR). These alterations were corrobo-rated in a NAFLD mouse model. In vitro, fatty acids increased let-7d- 5p expression, and its overexpression decreased AKT, IGF-IR and IR protein expression. Furthermore, let- 7d- 5p hindered AKT phosphorylation in vitro after insulin stimulation. Finally, cir-culating let-7d- 5p significantly decreased in steatosis patients and receiver operating characteristic (ROC) analyses confirmed its utility as a diagnostic biomarker.
publishDate 2023
dc.date.none.fl_str_mv 2023
2023-04-14
2023
2023-04-14
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/92257
url https://hdl.handle.net/20.500.14352/92257
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv RTI-2018-095098-B100 Not available Not available
PID2021-123076OB-I00 Not available Not available
AENC1 22-29754 Not available
PR75 18-21572 Not available
PI20 00837 Not available
PI19 00123 Not available
17IRG33410888 Not available Not available
W81XWH-16-1-0580 Not available Not available
W81XWH-16-1-0582 Not available Not available
R21EB023551-01 Not available Not available
1R21EB024147-01A1 Not available Not available
1R01HL141761-01 Not available Not available
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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