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dc.contributor.authorDuntas, L H
dc.contributor.authorOrgiazzi, J
dc.contributor.authorBrabant, Georg E
dc.date.accessioned2012-05-22T18:01:45Z
dc.date.available2012-05-22T18:01:45Z
dc.date.issued2011-02-24
dc.identifier.citationThe Interface between thyroid and diabetes mellitus. 2011, 75(1): 1-9 Clin Endocrinolen_GB
dc.identifier.issn1365-2265
dc.identifier.pmid21521298
dc.identifier.doi10.1111/j.1365-2265.2011.04029.x
dc.identifier.urihttp://hdl.handle.net/10541/225397
dc.description.abstractThyroid disease and type 1 but also type 2 diabetes mellitus are strongly associated and this has important clinical implications for insulin sensitivity and treatment requirements. The pathophysiological basis of this association has only recently been better elucidated. It rests on a complex interaction of common signalling pathways and, in the case of type 1 diabetes and autoimmune thyroid disease, on a linked genetic susceptibility. The pathophysiological mechanisms underlying this linked regulation are increasingly being unravelled. They are exemplified in the regulation of 5' adenosine monophosphate-activated protein kinase (AMPK), a central target not only for the modulation of insulin sensitivity but also for the feedback of thyroid hormones on appetite and energy expenditure. The present review will discuss these concepts and their consequences for the clinical care of patients with diabetes mellitus and thyroid disorders. Moreover, it makes reference to the added effect of metformin in suppressing TSH.
dc.languageENG
dc.language.isoenen
dc.rightsArchived with thanks to Clinical endocrinologyen_GB
dc.titleThe Interface between thyroid and diabetes mellitus.en
dc.typeArticleen
dc.contributor.departmentEndocrine Unit, Evgenidion Hospital, University of Athens Medical School, Athens, Greeceen_GB
dc.identifier.journalClinical Endocrinologyen_GB
html.description.abstractThyroid disease and type 1 but also type 2 diabetes mellitus are strongly associated and this has important clinical implications for insulin sensitivity and treatment requirements. The pathophysiological basis of this association has only recently been better elucidated. It rests on a complex interaction of common signalling pathways and, in the case of type 1 diabetes and autoimmune thyroid disease, on a linked genetic susceptibility. The pathophysiological mechanisms underlying this linked regulation are increasingly being unravelled. They are exemplified in the regulation of 5' adenosine monophosphate-activated protein kinase (AMPK), a central target not only for the modulation of insulin sensitivity but also for the feedback of thyroid hormones on appetite and energy expenditure. The present review will discuss these concepts and their consequences for the clinical care of patients with diabetes mellitus and thyroid disorders. Moreover, it makes reference to the added effect of metformin in suppressing TSH.


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