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Role of K ATP channels in β‐cell resistance to oxidative stress
Author(s) -
Drews G.,
Düfer M.
Publication year - 2012
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2012.01644.x
Subject(s) - oxidative stress , secretion , insulin resistance , insulin , type 2 diabetes mellitus , oxidative phosphorylation , microbiology and biotechnology , endocrinology , chemistry , diabetes mellitus , medicine , biology , biochemistry
The importance of K ATP channels in stimulus‐secretion coupling of β‐cells is well established, although they are not indispensable for the maintenance of glycaemic control. This review article depicts a new role for K ATP channels by showing that genetic or pharmacological ablation of these channels protects β‐cells against oxidative stress. Increased production of oxidants is a crucial factor in the pathogenesis of type 2 diabetes mellitus ( T2DM ). T2DM develops when β‐cells can no longer compensate for the high demand of insulin resulting from excess fuel intake. Instead β‐cells start to secrete less insulin and β‐cell mass is diminished by apoptosis. Both, reduction of insulin secretion and β‐cell mass induced by oxidative stress, are prevented by deletion or inhibition of K ATP channels. These findings may open up new insights into the early treatment of T2DM .