Show simple item record

Authordc.contributor.authorLourido, Fernanda 
Authordc.contributor.authorQuenti, Daniela 
Authordc.contributor.authorSalgado Canales, Daniela 
Authordc.contributor.authorTobar Bachler, Nicolás 
Admission datedc.date.accessioned2021-09-22T15:51:11Z
Available datedc.date.available2021-09-22T15:51:11Z
Publication datedc.date.issued2021
Cita de ítemdc.identifier.citationScientifc Reports (2021) 11:3263es_ES
Identifierdc.identifier.other10.1038/s41598-021-82944-4
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/182051
Abstractdc.description.abstractInsulin resistance is a hallmark of type 2 diabetes resulting from the confluence of several factors, including genetic susceptibility, inflammation, and diet. Under this pathophysiological condition, the dysfunction of the adipose tissue triggered by the excess caloric supply promotes the loss of sensitivity to insulin at the local and peripheral level, a process in which different signaling pathways are involved that are part of the metabolic response to the diet. Besides, the dysregulation of insulin signaling is strongly associated with inflammatory processes in which the JAK/STAT pathway plays a central role. To better understand the role of JAK/STAT signaling in the development of insulin resistance, we used a simple organism, Drosophila melanogaster, as a type 2 diabetes model generated by the consumption of a high-sugar diet. In this model, we studied the effects of inhibiting the expression of the JAK/STAT pathway receptor Domeless, in fat body, on adipose metabolism and glycemic control. Our results show that the Domeless receptor loss in fat body cells reverses both hyperglycemia and the increase in the expression of the insulin resistance marker Nlaz, observed in larvae fed a high sugar diet. This effect is consistent with a significant reduction in Dilp2 mRNA expression and an increase in body weight compared to wild-type flies fed high sugar diets. Additionally, the loss of Domeless reduced the accumulation of triglycerides in the fat body cells of larvae fed HSD and also significantly increased the lifespan of adult flies. Taken together, our results show that the loss of Domeless in the fat body reverses at least in part the dysmetabolism induced by a high sugar diet in a Drosophila type 2 diabetes model.es_ES
Patrocinadordc.description.sponsorshipNational Agency for Research and Development, ANID (Chile) FONDECYT 3160626 PAI77170001es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherNaturees_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceScientifc Reportses_ES
Títulodc.titleDomeless receptor loss in fat body tissue reverts insulin resistance induced by a high-sugar diet in Drosophila melanogasteres_ES
Document typedc.typeArtículo de revistaes_ES
Catalogueruchile.catalogadorcrbes_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


Files in this item

Icon

This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile