Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/4229
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dc.contributor.authorRafacho, Alex-
dc.contributor.authorOrtsäter, Henrik-
dc.contributor.authorNadal Navajas, Ángel-
dc.contributor.authorQuesada Moll, Iván-
dc.contributor.otherDepartamentos de la UMH::Biología Aplicadaes
dc.date.accessioned2017-11-03T15:38:15Z-
dc.date.available2017-11-03T15:38:15Z-
dc.date.created2014-09-30-
dc.date.issued2017-11-03-
dc.identifier.urihttp://hdl.handle.net/11000/4229-
dc.description.abstractGlucocorticoids (GCs) are broadly prescribed for numerous pathological conditions because of their anti-inflammatory, antiallergic and immunosuppressive effects, among other actions. Nevertheless, GCs can produce undesired diabetogenic side effects through interactions with the regulation of glucose homeostasis. Under conditions of excess and/or long-term treatment, GCs can induce peripheral insulin resistance (IR) by impairing insulin signalling, which results in reduced glucose disposal and augmented endogenous glucose production. In addition, GCs can promote abdominal obesity, elevate plasma fatty acids and triglycerides, and suppress osteocalcin synthesis in bone tissue. In response to GC-induced peripheral IR and in an attempt to maintain normoglycaemia, pancreatic β-cells undergo several morphofunctional adaptations that result in hyperinsulinaemia. Failure of β-cells to compensate for this situation favours glucose homeostasis disruption, which can result in hyperglycaemia, particularly in susceptible individuals. GC treatment does not only alter pancreatic β-cell function but also affect them by their actions that can lead to hyperglucagonaemia, further contributing to glucose homeostasis imbalance and hyperglycaemia. In addition, the release of other islet hormones, such as somatostatin, amylin and ghrelin, is also affected by GC administration. These undesired GC actions merit further consideration for the design of improved GC therapies without diabetogenic effects. In summary, in this review, we consider the implication of GC treatment on peripheral IR, islet function and glucose homeostasis.es
dc.description.sponsorshipThis study was supported by grants from the Spanish foundations Ministry of Science and Innovation (BFU2013-42789; BFU2011-28358)-
dc.description.sponsorshipThis study was supported by grants from the European Foundation for the Study of Diabetes (EFSD / BI Basic Program and the Albert Renold Fellowship)-
dc.description.sponsorshipThis study was supported by grants from the Brazilian National Council for Scientific and Technological Development (CNPq 471397 / 2011-3)-
dc.formatapplication/pdfes
dc.format.extent47es
dc.language.isoenges
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectglucocorticoidses
dc.subjectinsulin resistancees
dc.subjectinsulin sensitivityes
dc.subjectinsulin secretiones
dc.subjectglucagon secretiones
dc.subjectglucose tolerancees
dc.subjectdiabeteses
dc.subject.otherBiologíaes
dc.titleGlucocorticoid treatment and endocrine pancreas function: implications for glucose homeostasis, insulin resistance and diabeteses
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.1530/JOE-14-0373-
dc.relation.publisherversionhttps://doi.org/10.1530/JOE-14-0373-
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