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STRUCTURAL REMODELLING IN THE LEFT VENTRICLE OF STREPTOZOTOCIN ‐INDUCED TYPE 1 DIABETIC RAT
Author(s) -
Singh Jaipaul,
Bidasee Keshore,
Moore Caronda,
Iqbal Tehreem,
D'souza Alicia
Publication year - 2013
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.27.1_supplement.1189.6
Subject(s) - ventricle , medicine , streptozotocin , endocrinology , fibrosis , muscle hypertrophy , myocyte , atrophy , diabetes mellitus , diabetic cardiomyopathy , myocardial fibrosis , heart failure , cardiology , cardiomyopathy
Heart failure in diabetes mellitus is a major cause of premature morbidity and mortality but the underlying mechanisms are elusive and treatment remains empirical. This study investigated the role of chronic hyperglycemia (HG) in the development of hypertrophy and fibrosis in the left ventricle (LV) of streptozotocin (STZ)‐induced type 1 diabetic (T1DM) rats compared to age‐matched Wistar controls. T1DM rats and their hearts weighed significantly ( p <0.05) less than age‐matched controls along with a reduction in the heart weight/body weight ratio. Plasma glucose levels were 5–6 folds higher in T1DM animals. Visual analysis of the stained LV sections revealed general disorganization of myocardial architecture characterized by thinner fibers, disarray of myofibers and scarcity of myofibrils in the T1DM group compared to control. The width and diameter of myocytes from the T1DM group were significantly less compared to age‐matched controls. In addition, the LV of T1DM rats were infiltrated with increased ECM deposition in both interstitial and perivascular regions and area of interstitial fibrosis was significantly greater in T1DM hearts compared to controls. LV of T1DM rats exhibited signs of end stage apoptosis, manifesting as condensation of nuclei and cell shrinkage. The results show that chronic HG can produce marked alterations in myocardial architecture characterized by fibrosis proliferation, apoptotic cell death and atrophy of myocytes. Supported in part by University of Central Lancanshire and NIH HL085061.