title: Role of K(ATP)  channels in β-cell resistance to oxidative stress.
abstract: 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.
authors.affiliation: Department of Pharmacology, Institute of Pharmacy, University of Tübingen, Tübingen, Germany. gisela.drews@uni-tuebingen.de
authors.forename: G
authors.initials: G
authors.lastname: Drews
authors.forename: M
authors.initials: M
authors.lastname: Düfer
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005907:Gliclazide / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D054086:KATP Channels / Q000037:antagonists & inhibitors*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D015854:Up-Regulation
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D054086:KATP Channels; D005907:Gliclazide