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Alcohol Clin Exp Res. 2002 Aug;26(8):1128-33.

Myocardial effects of ethanol consumption in the rat with streptozotocin-induced diabetes.

Author information

1
Section of Cardiology, Department of medicine, Louisiana State University Health Sciences Center, 1542 Tulane Avenue, New Orleans, LA 70112, USA. tgiles@lsumc.edu

Abstract

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-alpha, PKC-delta, and PKC-epsilon, 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-alpha, -delta, and -epsilon 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-alpha, -delta, and -epsilon, and that consumption of ethanol can prevent these changes.

[Indexed for MEDLINE]

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