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
BioscientificaJournal
The Journal of endocrinology, 216 (1) T37-T45PubMed ID
22991412Type
Journal articleLanguage
enISSN
1479-6805ae974a485f413a2113503eed53cd6c53
10.1530/JOE-12-0278
Scopus Count
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