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Journal of Lipid Research, Vol. 50, 2314-2323, November 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Patient-Oriented and Epidemiological Research

Myocardial lipid accumulation in patients with pressure-overloaded heart and metabolic syndrome^[S]

Raffaele Marfella^1,2,*, Clara Di Filippo^1,, Michele Portoghese, Michelangela Barbieri^*, Franca Ferraraccio^**, Mario Siniscalchi^*, Federico Cacciapuoti^*, Francesco Rossi, Michele D'Amico and Giuseppe Paolisso^*

^* Department of Geriatrics and Metabolic Diseases, Second University of Naples, Italy
Department of Experimental Medicine, Second University of Naples, Italy
^** Department of Preventive Medicine, Second University of Naples, Italy
Cardiovascular Surgery Unit, Sassari Hospital, Sassari, Italy

² To whom correspondence should be addressed. e-mail: raffaele.marfella{at}unina2.it

We evaluated the role of sterol-regulatory element binding protein (SREBP)-1c/peroxisome proliferator activated receptor- (PPAR) pathway on heart lipotoxicity in patients with metabolic syndrome (MS) and aortic stenosis (AS). Echocardiographic parameters of heart function and structural alterations of LV specimens were studied in patients with (n = 56) and without (n = 61) MS undergoing aortic valve replacement. Tissues were stained with hematoxylin-eosin (H and E) and oil red O for evidence of intramyocyte lipid accumulation. The specimens were also analyzed with PCR, Western blot, and immunohistochemical analysis for SREBP-1c and PPAR. Ejection fraction (EF) was lower in MS compared with patients without MS (P < 0.001); no difference was found in aortic orifice surface among the groups. H and E and oil red O staining of specimens from MS patients revealed several myocytes with intracellular accumulation of lipid, whereas these alterations were not detected in biopsies from patients without MS. Patients without MS have low levels and weak immunostaining of SREBP-1c and PPAR in heart specimens. In contrast, strong immunostaining and higher levels of SREBP-1c and PPAR were seen in biopsies from the MS patients. Moreover, we evidenced a significative correlation between both SREBP-1c and PPAR and EF and intramyocyte lipid accumulation (P < 0.001). SREBP-1c may contribute to heart dysfunction by promoting lipid accumulation within myocytes in MS patients with AS; SREBP-1c may do it by increasing the levels of PPAR protein.

Supplementary key words aortic stenosis • heart function • surgery

Abbreviations: apM1, adipose most-abundant gene transcript 1; AS, aortic stenosis; BMI, body mass index; EF, ejection fraction; H and E, hematoxylin-eosin; HF, heart failure; HOMA, homeostasis model assessment; HPRT, hypoxanthine-phosporybosil transferase; LV, left ventricular; MDA, malondialdehyde; MPI, myocardial performance index; MS, metabolic syndrome; PPAR, peroxisome proliferator activated receptor; SERCA, sarco-endoplasmic reticulum ATPase; SREBP, sterol-regulatory element binding protein; WC, waist circumference

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