title: Increased catabolic activity in adipose tissue of patients with chronic heart failure.
abstract: OBJECTIVE
  Patients with chronic heart failure (CHF) have an increased catabolic state that affects both muscle and adipose tissue (AT), and may ultimately result in cardiac cachexia. Increased plasma levels of ANP might contribute to increased lipid mobilization and oxidation in CHF. We tested the hypothesis that increased plasma ANP levels are associated with an increased catabolic (lipolytic) state of white AT in patients with CHF.
  
  
  RESULTS
  After an overnight fast, AT metabolism was studied by microdialysis in patients with CHF and healthy controls of a similar age and body composition (both n = 8). AT glycolytic and lipolytic activities were assessed at rest (fasting) and after an oral glucose load (oGL). Fasting and post-prandial profiles of serum glucose, insulin, and free fatty acids and of dialysate glucose did not differ significantly between patients and controls. In contrast, fasting dialysate lactate and glycerol levels were two-fold higher in patients vs. controls (lactate, 0.51 ± 0.10 and 0.26 ± 0.06 mmol/L, P < 0.01; glycerol, 116 ± 18 and 50 ± 8 µmol/L, P < 0.001), indicating increased AT glycolytic and lipolytic rates in patients. After an oGL, dialysate lactate increased ∼2- and 2.5-fold, whereas dialysate glycerol decreased by ∼60% and 50% in patients vs. controls, but metabolite levels were always significantly higher in patients vs. controls (all P < 0.05). Plasma ANP levels were increased in patients and significantly correlated with adipose tissue dialysate glycerol.
  
  
  CONCLUSIONS
  In patients wiuth CHF, there is a direct correlation between plasma ANP levels and increased AT catabolic (lipolytic) state. This might contribute to AT wasting and the development of cardiac cachexia in patients with CHF.
authors.affiliation: Charité University Medicine, Campus Virchow-Klinikum, Department of Cardiology, Applied Cachexia Research, Berlin, Germany.
authors.forename: Tibor
authors.initials: T
authors.lastname: Szabó
authors.forename: Elisa
authors.initials: E
authors.lastname: Postrach
authors.forename: Anja
authors.initials: A
authors.lastname: Mähler
authors.forename: Thomas
authors.initials: T
authors.lastname: Kung
authors.forename: Guelistan
authors.initials: G
authors.lastname: Turhan
authors.forename: Stephan
authors.initials: S
authors.lastname: von Haehling
authors.forename: Stefan D
authors.initials: SD
authors.lastname: Anker
authors.forename: Michael
authors.initials: M
authors.lastname: Boschmann
authors.forename: Wolfram
authors.initials: W
authors.lastname: Doehner
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000368:Aged; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D002100:Cachexia / Q000209:etiology / Q000378:metabolism; D016022:Case-Control Studies; D002908:Chronic Disease; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D005990:Glycerol / Q000378:metabolism; D006019:Glycolysis / Q000502:physiology*; D006333:Heart Failure / Q000150:complications / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D008066:Lipolysis / Q000502:physiology*; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D010084:Oxidation-Reduction
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D019344:Lactic Acid; D009320:Atrial Natriuretic Factor; D005990:Glycerol
keywords: Cachexia; Glycolysis; Heart failure; Insulin resistance; Lipolysis; Metabolism; Microdialysis; Muscle; Natiuretic peptide