Premium
Myocardial Effects of Ethanol Consumption in the Rat With Streptozotocin‐Induced Diabetes
Author(s) -
Giles Thomas D.,
Given Michael B.,
Greenberg Stan S.,
Zhao Xinfang,
Kerut Edmund Kenneth,
McElwain Elizabeth,
Allen Gayle
Publication year - 2002
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2002.tb02648.x
Subject(s) - diabetes mellitus , protein kinase c , streptozotocin , medicine , ethanol , endocrinology , cardiac function curve , population , chemistry , kinase , biochemistry , heart failure , environmental health
Background Rats with streptozotocin (STZ)‐induced diabetes exhibit alterations in cardiac function, ventricular remodeling, and changes in cell signaling, which includes protein kinase C (PKC) isoforms. Moderate consumption of ethanol has a beneficial effect on cardiovascular outcomes in the general population, an effect that has recently been found to extend to patients with diabetes mellitus. We studied the effect of low‐dose ethanol consumption on cardiac function, geometry, and PKC isoforms in the rat with STZ‐induced diabetes. Methods Four groups of rats were studied over 8 to 10 weeks: control, STZ‐induced diabetes, 12% (v/v) ethanol consumption, and STZ‐induced diabetes plus 4% (v/v) ethanol consumption. Invasive hemodynamic measurements were performed; myocardial tissue was obtained for analysis for total PKC and cytosolic and membrane protein content of PKC‐α, PKC‐δ, and PKC‐ε, and two‐dimensional and M‐mode echocardiograms were obtained. Results Compared with rats with diabetes alone, consumption of 4% ethanol prevented the decrease in left ventricular dP/dt seen with diabetes alone, as well as the increase in left ventricular internal dimension. Up‐regulation of PKC‐α, ‐δ, and ‐ε occurring in the diabetic animals was also prevented by ethanol consumption, whereas ethanol alone had no effect on PKC isoform pattern. Conclusions These data suggest that STZ‐induced cardiac remodeling and dysfunction are associated with increases in PKC activity, particularly PKC‐α, ‐δ, and ‐ε, and that consumption of ethanol can prevent these changes.