Abstract
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Objectives The significance and mechanism of the adipose tissue - heart crosstalk for adaptive processes of cardiac energy morphology/ function and metabolism during chronic physical exercise was assessed in a mouse model.
Methods Mice deficient for adipose triglyceride lipase (ATGL) in adipose tissue (atATGL-KO) and littermate wild-type animals were stressed with chronic treadmill running or kept sedentary. Assessments were done using PET (applying both [18F]-2-fluorodesoxyglucose, FDG and [18F]-fluoro-4-thia-palmitate, FTP) along with biochemistry, echocardiography, MRI and indirect calorimetry.
Results Exercise-induced lipolytic activity in adipose tissue was significantly lower in atATGL-KO mice accompanied by the absence of changes in plasma lipids. The lack of an exercise-induced plasma fatty acid increase in atATGL-KO mice was directly associated with a prominent attenuation of myocardial fatty acid uptake as assessed by PET using the freefatty acid (FFA) analogue FTP. In compensation, the glucose analogue FDG was more avidly taken up. atATGL-KO mice exhibited a significantly reduced cardiac hypertrophic response to exercise as assessed by echocardiography. Distinct free fatty acids were identified as prohypertrophic factors involved in beneficial cardiac growth.
Conclusions This data suggests that the adipose tissue - heart communication involving adipose lipolysis, FFA mobilisation and cardiac energy substrate utilization is an important process for the morphological adaptation of the exercising heart.