title: Dynamics in insulin resistance and plasma levels of adipokines in patients with acute decompensated and chronic stable heart failure.
abstract: BACKGROUND
  Patients with heart failure (HF) develop metabolic derangements including increased adipokine levels, insulin resistance, inflammation and progressive catabolism. It is not known whether metabolic dysfunction and adipocyte activation worsen in the setting of acute clinical decompensation, or conversely, improve with clinical recovery.
  
  
  RESULTS
  We assessed insulin resistance using homeostasis model assessment of insulin resistance (HOMA-IR), and measured plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP), adiponectin, visfatin, resistin, leptin, and tumor necrosis factor (TNF) α in 44 patients with acute decompensated HF (ADHF) due to left ventricular (LV) systolic dysfunction and again early (<1 wk) and late (> 6 mo) after clinical recovery, in 26 patients with chronic stable HF, and in 21 patients without HF. NT-proBNP was not increased in control subjects, mildly elevated in patients with stable HF, markedly elevated in patients with ADHF, and decreased progressively early and late after treatment. Compared to control subjects, plasma adiponectin, visfatin, leptin, resistin, and TNF-α were elevated in patients with chronic stable HF and increased further in patients with ADHF. Likewise, HOMA-IR was increased in chronic stable HF and increased further during ADHF. Adiponectin, visfatin, and HOMA-IR remained elevated at the time of discharge from the hospital, but returned to chronic stable HF levels. Adipokine levels were not related to body mass index in HF patients. HOMA-IR correlated positively with adipokines and TNF-α in HF patients.
  
  
  CONCLUSIONS
  ADHF is associated with worsening of insulin resistance and elevations of adipokines and TNF-α, indicative of adipocyte activation. These metabolic abnormalities are reversible, but they temporally lag behind the clinical resolution of decompensated HF.
authors: Division of Cardiology, New York-Presbyterian Hospital/Columbia University Medical Center, New York, New York 10032, USA. pcs2121@columbia.edu
authors: P Christian
authors: PC
authors: Schulze
authors: Andreia
authors: A
authors: Biolo
authors: Deepa
authors: D
authors: Gopal
authors: Khurram
authors: K
authors: Shahzad
authors: Joshua
authors: J
authors: Balog
authors: Mark
authors: M
authors: Fish
authors: Deborah
authors: D
authors: Siwik
authors: Wilson S
authors: WS
authors: Colucci
mesh_terms: D054392:Adipokines / Q000097:blood*; D052242:Adiponectin / Q000097:blood; D000704:Analysis of Variance; D015992:Body Mass Index; D002908:Chronic Disease; D018450:Disease Progression; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D052243:Resistin / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D054392:Adipokines; D052242:Adiponectin; D010446:Peptide Fragments; D052243:Resistin; D014409:Tumor Necrosis Factor-alpha; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain