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The type 2 diabetic patient and cardiac mitochondrial dysfunction: a new perspective (688.10)
Author(s) -
Shepherd Danielle,
Croston Tara,
Holden Anthony,
Tveter Kevin,
Thapa Dharendra,
Nichols Cody,
Olfert I. Mark,
Hollander John
Publication year - 2014
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.28.1_supplement.688.10
Subject(s) - medicine , diabetes mellitus , cardiology , type 2 diabetes , type 2 diabetes mellitus , diabetic cardiomyopathy , body mass index , endothelial dysfunction , coronary artery disease , cardiac dysfunction , endocrinology , heart failure , cardiomyopathy
Cardiac complications are the leading cause of mortality among diabetic patients, with the mitochondrion being implicated in the etiology. We have previously observed enhanced dysfunction to cardiac subsarcolemmal mitochondria (SSM) in db/db mice as a result of type 2 diabetes mellitus. The goal of this study was to determine whether hyperglycemia or hemoglobin A1c (HbA1c) level correlates with the extent of SSM dysfunction observed in type 2 diabetic patients. Using linear spline models to assess correlative risks we determined that diabetic patients display dysfunctional SSM state 3 respiration rate and ETC complex I activity irrespective of the absolute blood glucose or HbA1c level. In addition, we found that SSM dysfunction observed in type 2 diabetic patients with comorbidities, such as coronary artery disease (CAD) and hypertension is not due to either CAD or hypertension independently. Further, a scatter plot analysis of patients’ body mass index (BMI) indicated that BMI is not an effective predictor of mitochondrial dysfunction. These findings suggest that independent of comorbidities cardiac SSM dysfunction is present in the type 2 diabetic patient heart. Interestingly, the degree of mitochondrial dysfunction in diabetic patients remains consistent despite the extent of elevated blood glucose or HbA1c level. (Support: AHA 13PRE16850066; NIH DP2DK083095; NSF DGE1144676; NIH T32HL090610)