The role of adipokines in β-cell failure of type 2 diabetes.

2.50
Hdl Handle:
http://hdl.handle.net/2436/611796
Title:
The role of adipokines in β-cell failure of type 2 diabetes.
Authors:
Dunmore, Simon J; Brown, James E P
Abstract:
β-Cell failure coupled with insulin resistance is a key factor in the development of type 2 diabetes. Changes in circulating levels of adipokines, factors released from adipose tissue, form a significant link between excessive adiposity in obesity and both aforementioned factors. In this review, we consider the published evidence for the role of individual adipokines on the function, proliferation, death and failure of β-cells, focusing on those reported to have the most significant effects (leptin, adiponectin, tumour necrosis factor α, resistin, visfatin, dipeptidyl peptidase IV and apelin). It is apparent that some adipokines have beneficial effects whereas others have detrimental properties; the overall contribution to β-cell failure of changed concentrations of adipokines in the blood of obese pre-diabetic subjects will be highly dependent on the balance between these effects and the interactions between the adipokines, which act on the β-cell via a number of intersecting intracellular signalling pathways. We emphasise the importance, and comparative dearth, of studies into the combined effects of adipokines on β-cells.
Citation:
The role of adipokines in β-cell failure of type 2 diabetes. 2013, 216 (1):T37-45 J. Endocrinol.
Publisher:
Bioscientifica
Journal:
The Journal of endocrinology, 216 (1) T37-T45
Issue Date:
Sep-2012
URI:
http://hdl.handle.net/2436/611796
DOI:
10.1530/JOE-12-0278
PubMed ID:
22991412
Type:
Article
Language:
en
ISSN:
1479-6805
Appears in Collections:
FSE

Full metadata record

DC FieldValue Language
dc.contributor.authorDunmore, Simon Jen
dc.contributor.authorBrown, James E Pen
dc.date.accessioned2016-06-06T10:56:31Zen
dc.date.available2016-06-06T10:56:31Zen
dc.date.issued2012-09en
dc.identifier.citationThe role of adipokines in β-cell failure of type 2 diabetes. 2013, 216 (1):T37-45 J. Endocrinol.en
dc.identifier.issn1479-6805en
dc.identifier.pmid22991412en
dc.identifier.doi10.1530/JOE-12-0278en
dc.identifier.urihttp://hdl.handle.net/2436/611796en
dc.description.abstractβ-Cell failure coupled with insulin resistance is a key factor in the development of type 2 diabetes. Changes in circulating levels of adipokines, factors released from adipose tissue, form a significant link between excessive adiposity in obesity and both aforementioned factors. In this review, we consider the published evidence for the role of individual adipokines on the function, proliferation, death and failure of β-cells, focusing on those reported to have the most significant effects (leptin, adiponectin, tumour necrosis factor α, resistin, visfatin, dipeptidyl peptidase IV and apelin). It is apparent that some adipokines have beneficial effects whereas others have detrimental properties; the overall contribution to β-cell failure of changed concentrations of adipokines in the blood of obese pre-diabetic subjects will be highly dependent on the balance between these effects and the interactions between the adipokines, which act on the β-cell via a number of intersecting intracellular signalling pathways. We emphasise the importance, and comparative dearth, of studies into the combined effects of adipokines on β-cells.en
dc.language.isoenen
dc.publisherBioscientificaen
dc.rightsArchived with thanks to The Journal of endocrinologyen
dc.subjectBeta-cellen
dc.subjecttype 2 diabetesen
dc.subjectadipokinesen
dc.subject.meshAdipokinesen
dc.subject.meshAdipose Tissueen
dc.subject.meshAnimalsen
dc.subject.meshCytokinesen
dc.subject.meshDiabetes Mellitus, Type 2en
dc.subject.meshDipeptidyl Peptidase 4en
dc.subject.meshHumansen
dc.subject.meshInsulin-Secreting Cellsen
dc.subject.meshIntercellular Signaling Peptides and Proteinsen
dc.subject.meshObesityen
dc.subject.meshPancreasen
dc.titleThe role of adipokines in β-cell failure of type 2 diabetes.en
dc.typeArticleen
dc.identifier.journalThe Journal of endocrinology, 216 (1) T37-T45en

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