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Authordc.contributor.authorMizgier, María Luisa 
Authordc.contributor.authorCasas Atala, Mariana es_CL
Authordc.contributor.authorContreras Ferrat, Ariel Eduardo es_CL
Authordc.contributor.authorLlanos Vidal, Paola es_CL
Authordc.contributor.authorGalgani Fuentes, José es_CL
Admission datedc.date.accessioned2014-12-17T17:33:45Z
Available datedc.date.available2014-12-17T17:33:45Z
Publication datedc.date.issued2014
Cita de ítemdc.identifier.citationObesity reviews 15, July 2014, p. 587–597en_US
Identifierdc.identifier.otherdoi: 10.1111/obr.12166
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/129415
General notedc.descriptionArtículo de publicación ISIen_US
Abstractdc.description.abstractPancreatic beta cells sense glucose flux and release as much insulin as required in order to maintain glycaemia within a narrow range. Insulin secretion is regulated by many factors including glucose, incretins, and sympathetic and parasympathetic tones among other physiological factors. To identify the mechanisms linking obesity-related insulin resistance with impaired insulin secretion represents a central challenge. Recently, it has been argued that a crosstalk between skeletal muscle and the pancreas may regulate insulin secretion. Considering that skeletal muscle is the largest organ in non-obese subjects and a major site of insulin- and exercise-stimulated glucose disposal, it appears plausible that muscle might interact with the pancreas and modulate insulin secretion for appropriate peripheral intracellular glucose utilization. There is growing evidence that muscle can secrete so-called myokines that can have auto/para/endocrine actions. Although it is unclear in which direction they act, interleukin-6 seems to be a possible muscle-derived candidate protein mediating such inter-organ communication. We herein review some of the putative skeletal muscle-derived factors mediating this interaction. In addition, the evidence coming from in vitro, animal and human studies that support such inter-organ crosstalk is thoroughly discussed.en_US
Patrocinadordc.description.sponsorshipThis study received a funding from FONDECYT-Chile, grant number 1130217 (JEG).en_US
Lenguagedc.language.isoenen_US
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Keywordsdc.subjectBeta cellen_US
Títulodc.titlePotential role of skeletal muscle glucose metabolism on the regulation of insulin secretionen_US
Document typedc.typeArtículo de revistaen_US


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