Exercise improves diabetic heart performance by reducing the levels of diacylglycerol
Loganathan, Rajprasad Novikova, Lesya Boulatnikov, Igor Smirnova, Irina V.
Loganathan, Rajprasad
Novikova, Lesya
Boulatnikov, Igor
Smirnova, Irina V.
Other Names
Location
Time Period
Advisors
Original Date
Digitization Date
Issue Date
2010-11-23
Type
Genre
Keywords
Type 1 diabetes,Protein kinase C,Physical activity,Cardiac rehabilitation,Hemodynamics
Subjects (LCSH)
Citation
Loganathan, R., Novikova, L., Boulatnikov, I., & Smirnova, I. V. (2010). Fujita, E., Hirotsu, M., & Rogers, M. E. (2024). Exercise improves diabetic heart performance by reducing the levels of diacylglycerol. Circulation, 122(suppl_21). https://www.ahajournals.org/doi/10.1161/circ.122.suppl_21.A20528
Abstract
Cardiac dysfunction occurs in a substantial proportion of the population with type 1 diabetes through a process of hyperglycemia-induced increase in diacylglycerol (DAG) levels and subsequent activation of protein kinase C βII (PKC-βII). Exercise training attenuates poor cardiovascular performance in type 1 diabetes. In this study, we hypothesized that exercise training modulates cardiac PKC-βII signaling, to elicit its benefits on the diabetic heart. BioBreeding Diabetes Resistant rats, a model of autoimmune type 1 diabetes, were randomly assigned to 4 groups (n=8/group): 1) non-diabetic (control), 2) diabetic, 3) exercised non-diabetic, and 4) exercised diabetic. Exercise training began at diabetes onset. At the end of 8 weeks of diabetes, steady state left ventricular hemodynamic assessment revealed compromised cardiac function in diabetes. Specifically, a 48% decrease in the stroke volume, an 18% decrease in the ejection fraction, and a 51% decrease in the left ventricular output were observed in diabetic group compared to control. Exercise training alleviated these changes. While both +dP/dt and -dP/dt decreased with diabetes (30% and 46%, respectively), compared to control, exercise was able to improve the +dP/dt. Left ventricular collagen fractional area was increased 1.4 fold in diabetic group compared to control, and was returned to the control levels in the exercised diabetic group. The above physiological and anatomical evaluations showed that exercise training was able to prevent the deterioration of left ventricular function and structure in diabetes. To determine a possible mechanism, PKC-βII protein levels and in vitro activity were analyzed and no changes were found with diabetes. Further, molecules involved in PKC-βII signaling were studied. Levels of DAG, a PKC-βII activator, increased with diabetes and exercise training prohibited that increase, returning DAG to control levels. No changes were observed in the levels of sphingosine, a PKC-βII inhibitor, with diabetes or exercise. These results suggest that exercise-induced benefits on cardiac performance in diabetes may be mediated by prevention of an increase in DAG levels.
Table of Contents
Description
Circulation, Volume 122, Number suppl_21, Abstract 20528
Published in print: 23 November 2010 Published online: 23 March 2018
Published in print: 23 November 2010 Published online: 23 March 2018
Publisher
American Heart Association
Journal
Circulation