title: Increased mediastinal fat and impaired left ventricular energy metabolism in young men with newly found fatty liver.
abstract: Fatty liver is characterized by metabolic abnormalities at the liver, but also at skeletal muscle and adipose tissue sites. It is hypothesized that the heart may be suffering metabolic alterations, and this study was undertaken to ascertain whether individuals with fatty liver have left ventricular (LV) alterations of energy metabolism, structure, and function and abnormal amounts of epicardial fat as a specific marker of visceral fat accumulation. To this end we studied young, nondiabetic men matched for anthropometric features with (n = 21) or without (n = 21) fatty liver by means of (1) cardiac magnetic resonance imaging (MRI); (2) cardiac (31)P-MR spectroscopy (MRS); and (3) hepatic (1)H-MRS to assess quantitatively the intrahepatic fat (IHF) content. Insulin sensitivity was determined by the updated HOMA-2 computer model. Individuals with fatty liver showed reduced insulin sensitivity, increased serum free fatty acid (FFA), and E-selectin, abnormal adipokine concentrations, and higher blood pressure. LV morphology and systolic and diastolic functions were not different; however, in the scanned intrathoracic region, the intrapericardial (7.8 +/- 3.1 versus 5.9 +/- 2.5 cm(2); P < 0.05) and extrapericardial (11.7 +/- 6.1 versus 7.8 +/- 3.2 cm(2); P < 0.03) fat was increased in men with fatty liver compared with those without fatty liver. The phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio, a recognized in vivo marker of myocardial energy metabolism, was reduced in men with fatty liver in comparison with normals (1.85 +/- 0.35 versus 2.11 +/- 0.31; P < 0.016). In conclusion, in newly found individuals with fatty liver, fat was accumulated in the epicardial area and despite normal LV morphological features and systolic and diastolic functions, they had abnormal LV energy metabolism.
authors.affiliation: Department of Internal Medicine, Section of Nutrition/Metabolism, San Raphael Scientific Institute, Milan, Italy. perseghin.gianluca@hsr.it
authors.forename: Gianluca
authors.initials: G
authors.lastname: Perseghin
authors.forename: Guido
authors.initials: G
authors.lastname: Lattuada
authors.forename: Francesco
authors.initials: F
authors.lastname: De Cobelli
authors.forename: Antonio
authors.initials: A
authors.lastname: Esposito
authors.forename: Elena
authors.initials: E
authors.lastname: Belloni
authors.forename: Georgia
authors.initials: G
authors.lastname: Ntali
authors.forename: Francesca
authors.initials: F
authors.lastname: Ragogna
authors.forename: Tamara
authors.initials: T
authors.lastname: Canu
authors.forename: Paola
authors.initials: P
authors.lastname: Scifo
authors.forename: Alessandro
authors.initials: A
authors.lastname: Del Maschio
authors.forename: Livio
authors.initials: L
authors.lastname: Luzi
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D000886:Anthropometry; D016022:Case-Control Studies; D004734:Energy Metabolism / Q000502:physiology; D005234:Fatty Liver / Q000378:metabolism / Q000473:pathology*; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism / Q000502:physiology; D008297:Male; D008482:Mediastinum / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010725:Phosphocreatine / Q000378:metabolism; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D007328:Insulin; D010725:Phosphocreatine; D000255:Adenosine Triphosphate