title: Abnormalities of whole body protein turnover, muscle metabolism and levels of metabolic hormones in patients with chronic heart failure.
abstract: OBJECTIVE
  It is well known that chronic heart failure (CHF) is associated with insulin resistance and cachexia, but little is known about the underlying substrate metabolism. The present study was undertaken to identify disturbances of basal glucose, lipid and protein metabolism.
  
  
  METHODS
  We studied eight nondiabetic patients with CHF (ejection fraction 30 +/- 4%) and eight healthy controls. Protein metabolism (whole body and regional muscle fluxes) and total glucose turnover were isotopically assayed. Substrate oxidation were obtained by indirect calorimetry. The metabolic response to exercise was studied by bicycle ergometry exercise.
  
  
  RESULTS
  Our data confirm that CHF patients have a decreased lean body mass. CHF patients are characterised by (i) decreased glucose oxidation [glucose oxidation (mg kg(-1) min(-1)): 1.25 +/- 0.09 (patients) vs. 1.55 +/- 0.09 (controls), P < 0.01] and muscle glucose uptake [a - v diff(glucose) (micromol L(-1)): -10 +/- 25 (patients) vs. 70 +/- 22 (controls), P < 0.01], (ii) elevated levels of free fatty acids (FFA) [FFA (mmol L(-1)): 0.72 +/- 0.05 (patients) vs. 0.48 +/- 0.03 (controls), P < 0.01] and 3-hydroxybutyrate and signs of elevated fat oxidation and muscle fat utilization [a - v diff(FFA) (mmol L(-1)): 0.12 +/- 0.02 (patients) vs. 0.05 +/- 0.01 (controls), P < 0.05] and (iii) elevated protein turnover and protein breakdown [phenylalanine flux (micromol kg(-1) h(-1)): 36.4 +/- 1.5 (patients) vs. 29.6 +/- 1.3 (controls), P < 0.01]. Patients had high circulating levels of noradrenaline, glucagon, and adiponectin, and low levels of ghrelin. We failed to observe any differences in metabolic responses between controls and patients during short-term exercise.
  
  
  CONCLUSIONS
  In the basal fasting state patients with CHF are characterized by several metabolic abnormalities which may contribute to CHF pathophysiology and may provide a basis for targeted intervention.
authors.affiliation: Medical Department M (Endocrinology and Diabetes), Aarhus Universitets-Hospital, Aarhus, Denmark. helenenorrelund@dadlnet.dk
authors.forename: H
authors.initials: H
authors.lastname: Nørrelund
authors.forename: H
authors.initials: H
authors.lastname: Wiggers
authors.forename: M
authors.initials: M
authors.lastname: Halbirk
authors.forename: J
authors.initials: J
authors.lastname: Frystyk
authors.forename: A
authors.initials: A
authors.lastname: Flyvbjerg
authors.forename: H E
authors.initials: HE
authors.lastname: Bøtker
authors.forename: O
authors.initials: O
authors.lastname: Schmitz
authors.forename: J O L
authors.initials: JO
authors.lastname: Jørgensen
authors.forename: J S
authors.initials: JS
authors.lastname: Christiansen
authors.forename: N
authors.initials: N
authors.lastname: Møller
mesh_terms: D000368:Aged; D000596:Amino Acids / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002153:Calorimetry, Indirect; D015444:Exercise; D005080:Exercise Test / Q000379:methods; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005542:Forearm / Q000098:blood supply; D006333:Heart Failure / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D006728:Hormones / Q000097:blood*; D006801:Humans; D050356:Lipid Metabolism; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000378:metabolism*; D010084:Oxidation-Reduction; D011506:Proteins / Q000378:metabolism*; D012039:Regional Blood Flow
chemical_list: D000596:Amino Acids; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D006728:Hormones; D011506:Proteins