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Mitochondrial dynamics in the type 2 diabetic heart (1159.6)
Author(s) -
Gonzalez Eileen,
Brito Alfonso,
Peltekian Lila,
Lopez Vanessa,
Delgado Daniel,
Yamazaki Katrina
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.1159.6
Subject(s) - in vivo , type 2 diabetes , diabetic cardiomyopathy , cardioprotection , streptozotocin , pharmacology , medicine , mitochondrial fission , myocyte , chemistry , diabetes mellitus , apoptosis , endocrinology , ischemia , biology , biochemistry , heart failure , cardiomyopathy , microbiology and biotechnology
Type 2 Diabetes (T2D) mitochondrial effects include imbalanced dynamic events of fusion, fission, and autophagy. The flavanol epicatechin has been previously observed to provide cardioprotection in the setting of ischemia‐reperfusion by reducing inflammation and ROS production. Our objectives are to observe the protective effects of epicatechin in the T2D setting via in vitro and in vivo models. In vitro, C2C12 myoblasts were cultured in glucolipotoxicity treatment (GLT) for 3 days in high glucose (~33 mM) and high fatty acids (0.6 mM) media, ± epicatechin. Our in vivo rat model included controls, sham ± epicatechin (1 mg/kg/day), and diabetes ± epicatechin (1 mg/kg/day). T2D was induced in vivo by high‐energy diet (HED) of 20% lard and 10% glucose. Low dose streptozotocin (30 mg/kg) injection was given at four weeks to decrease insulin secretion, after which epicatechin treatment began with maintained HED. In vitro results thus far show GLT average cell counts of 7.54E+04, which show significant increase in cell death compared to control (3.56E+05). Cells maintained in GLT setting with 100 nM epicatechin yielded an average cell count of 1.78E+0, thus demonstrating a reduction in cell death. Western analysis show enhanced mitochondrial proteins with epicatechin treatment compared to diabetic controls. We predict further data analysis will show a positive correlation between epicatechin and the restoration of normal mitochondrial dynamics in the T2D setting. As the incidence of T2D rises, further investigation into possible therapies and treatments is warranted. Grant Funding Source : Supported by CSU‐LSAMP fund from the National Science Foundation under Grant No. HRD‐0802628

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