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Differential expression of mitoK ATP subunits in cardiac mitochondrial subpopulations and the influence of Type I diabetes
Author(s) -
Fancher Ibra Seaphus,
Baseler Walter A,
Croston Tara L,
Thapa Dharendra,
Shepherd Danielle,
Nichols Cody,
Lewis Sara,
Jagannathan Rajaganapathi,
Asano Shinichi,
Dick Gregory M,
Hollander John M
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1057.6
Subject(s) - diabetes mellitus , mitochondrion , endocrinology , medicine , sulfonylurea receptor , type 2 diabetes mellitus , kir6.2 , protein subunit , diabetic cardiomyopathy , western blot , glibenclamide , biology , microbiology and biotechnology , heart failure , biochemistry , cardiomyopathy , gene
Mitochondrial dysfunction is an underlying risk for heart failure in Type I diabetes mellitus. MitoK ATP channels are likely composed of an inwardly rectifying K + channel subunit (Kir6.1) and a sulphonylurea receptor (SUR1). MitoK ATP regulate mitochondrial volume and membrane potential: two functions disturbed by diabetes mellitus. In the heart, two mitochondrial populations exist: subsarcolemmal (SSM) and interfibrillar (IFM) which differ in their subcellular locations. It is not known whether: a) Kir6.1 or SUR1 expression is similar in IFM and SSM or whether b) diabetes mellitus alters the expression of Kir6.1 or SUR1 subunits in either SSM or IFM. Male FVB mice were made diabetic via multiple low‐dose injections of streptozoticin and examined after 5 weeks. Western blot analyses on cardiac mitochondrial subpopulations revealed Kir6.1 expression in non‐diabetic IFM was greater relative to SSM (p < 0.05), but SUR1 expression was equivalent. Kir6.1 protein was reduced (p < 0.05) in the IFM of diabetic mice. In contrast, diabetes mellitus had no effect on Kir6.1 protein expression in SSM or SUR1 expression in either IFM or SSM. These data show that expression Kir6.1 may be higher in IFM than SSM and that diabetes mellitus reduces Kir6.1 expression in IFM. This suggests that mitoK ATP components may be differentially impacted by diabetes mellitus and that these effects may be specific to a subset of mitochondria.