Increased myocardial lipid deposition is a feature of the cardiomyopathy associated with obesity and diabetes mellitus. The long-term objective of this proposal is to understand the contribution of intracellular lipid deposition (steatosis) to the development of cardiac hypertrophy and cardiomyopathy. We hypothesize that excessive intracellular lipid deposition leads to lipotoxicity of the cardiac myocyte, which, in turn, results in compensatory hypertrophy and, in many instances, cell damage and cell death. Accordingly, the specific aims are to: 1. Examine the effects of triglyceride accumulation (steatosis) on hypertrophy and apoptosis in neonatal rat ventricular myocytes. 2. Examine the effect of triglyceride accumulation on cardiac structure and function using a murine model of cardiac-restricted over expression of diacylglycerol acyltransferase.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32HL074643-01A1
Application #
6790181
Study Section
Special Emphasis Panel (ZRG1-F10 (20))
Program Officer
Commarato, Michael
Project Start
2004-08-16
Project End
2005-06-23
Budget Start
2004-08-16
Budget End
2005-06-23
Support Year
1
Fiscal Year
2004
Total Cost
$48,985
Indirect Cost
Name
University of California San Francisco
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143
Glenn, Denis J; Wang, Feng; Nishimoto, Minobu et al. (2011) A murine model of isolated cardiac steatosis leads to cardiomyopathy. Hypertension 57:216-22