title: No evidence of ectopic lipid accumulation in the pathophysiology of the acromegalic cardiomyopathy.
abstract: BACKGROUND
  PATIENTS with acromegaly frequently display disturbances of glucose and lipid metabolism, which might contribute to their increased cardiovascular risk. Because insulin resistance and increased lipolysis have been linked to ectopic lipid deposition, altered lipid accumulation in the liver and the myocardium might contribute to metabolic and cardiac complications in these patients.
  
  
  OBJECTIVE
  The aim of this study was to investigate myocardial (MYCL) and hepatic lipid content (HCL), insulin sensitivity, and cardiac function in active acromegaly and after control of GH excess through transsphenoidal surgery.
  
  
  METHODS
  Ten patients with newly diagnosed acromegaly (ACRO_active) were compared with 12 healthy controls (CON), matched for age, body mass index, and gender. In seven patients GH excess was controlled, and they were compared with their active state.
  
  
  METHODS
  MYCL and HCL were assessed by (1)H-magnetic resonance spectroscopy, pericardial fat and cardiac function by (1)H-magnetic resonance imaging, and insulin sensitivity and secretion by an oral glucose tolerance test.
  
  
  RESULTS
  Although MYCL tended to be lower, HCL was significantly lower in ACRO_active compared with CON (HCL: 1.2% ± 1.2% vs 4.3% ± 3.5% of (1)H-magnetic resonance spectroscopy signal, P < .02). Parameters of systolic function and hypertrophy were significantly increased in ACRO_active compared with CON, as were insulin secretion and resistance. After the control of GH excess, HCL and MYCL remained unchanged, but pericardial fat was increased in the patients in whom GH excess was controlled (from 11.6 ± 5.5 to 14.7 ± 6.2 cm(2), P = .02).
  
  
  CONCLUSIONS
  Acromegaly represents a unique condition characterized by low myocardial and hepatic lipid content despite decreased insulin sensitivity, hyperinsulinemia, and hyperglycemia. Hence, ectopic lipid accumulation does not appear to contribute to cardiac morbidity, and increased lipid oxidation might counteract ectopic lipid accumulation in GH excess.
authors.affiliation: Department of Internal Medicine III, Division of Endocrinology and Metabolism (Y.W., P.W., M.Krš., A.G., W.R., A.K.-W., M.Kre., A.L.), Department of Biomedical Imaging and Image Guided therapy, Centre of Excellence High-field MR (M.Krš., I.J.K., S.T.), and Department of Neurosurgery (S.W., E.K.), Medical University of Vienna, A-1090 Vienna, Austria; and Institute of Biomedical Engineering (A.T., G.P.), National Research Council, Metabolic Unit, I-35127 Padova, Italy.
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Winhofer
authors.forename: Peter
authors.initials: P
authors.lastname: Wolf
authors.forename: Martin
authors.initials: M
authors.lastname: Krššák
authors.forename: Stefan
authors.initials: S
authors.lastname: Wolfsberger
authors.forename: Andrea
authors.initials: A
authors.lastname: Tura
authors.forename: Giovanni
authors.initials: G
authors.lastname: Pacini
authors.forename: Alois
authors.initials: A
authors.lastname: Gessl
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Raber
authors.forename: Ivica Just
authors.initials: IJ
authors.lastname: Kukurova
authors.forename: Alexandra
authors.initials: A
authors.lastname: Kautzky-Willer
authors.forename: Engelbert
authors.initials: E
authors.lastname: Knosp
authors.forename: Siegfried
authors.initials: S
authors.lastname: Trattnig
authors.forename: Michael
authors.initials: M
authors.lastname: Krebs
authors.forename: Anton
authors.initials: A
authors.lastname: Luger
mesh_terms: D000172:Acromegaly / Q000150:complications / Q000378:metabolism* / Q000601:surgery; D000328:Adult; D009202:Cardiomyopathies / Q000150:complications / Q000378:metabolism*; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D050356:Lipid Metabolism / Q000502:physiology*; D008055:Lipids / Q000032:analysis*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D012307:Risk Factors
chemical_list: D008055:Lipids