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dc.contributor.authorCinar, Nese
dc.contributor.authorGurlek, Alper
dc.date.accessioned2019-12-10T11:10:23Z
dc.date.available2019-12-10T11:10:23Z
dc.date.issued2013
dc.identifier.issn2049-3614
dc.identifier.urihttps://doi.org/10.1530/EC-13-0061
dc.identifier.urihttp://hdl.handle.net/11655/14850
dc.description.abstractAdipose tissue secretes a variety of active biological substances, called adipocytokines, that act in an autocrine, paracrine, and endocrine manner. They have roles in appetite control, thermogenesis, and thyroid and reproductive functions. All these molecules may lead to local and generalized inflammation, mediating obesity-associated vascular disorders including hypertension, diabetes, atherosclerosis, and insulin resistance. Thyroid dysfunction is associated with changes in body weight, thermogenesis, and energy expenditure. The connections between cardiovascular risk factors such as dyslipidemia, impaired glucose tolerance, insulin resistance, atherosclerosis, and thyroid dysfunction have been reported in several studies. The adipocytokines serve as causative or protective factors in the development of these disorders in the states of thyroid dysfunction. Abnormal levels of adipocytokines (adiponectin (ADP), leptin, resistin, vaspin, and visfatin) in hypo- and hyperthyroidism have been reported with controversial results. This review aims to update the implication of novel adipokines ADP, vaspin, and visfatin in thyroid dysfunction.
dc.language.isoen
dc.publisherBioscientifica Ltd
dc.relation.isversionof10.1530/EC-13-0061
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectEndocrinology & Metabolism
dc.titleAssociation Between Novel Adipocytokines Adiponectin, Vaspin, Visfatin, and Thyroid: An Experimental and Clinical Update
dc.typeinfo:eu-repo/semantics/review
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalEndocrine Connections
dc.contributor.departmentİç Hastalıkları
dc.identifier.volume2
dc.identifier.issue4
dc.identifier.startpageR30
dc.identifier.endpageR38
dc.description.indexWoS


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