title: Hyperleptinaemia in chronic heart failure. Relationships with insulin.
abstract: BACKGROUND
  Leptin, a product of the ob gene, is known to increase energy expenditure. Given that chronic heart failure is a hypercatabolic state, we sought to determine whether congestive heart failure involves elevations in plasma leptin levels. Since leptin secretion is up-regulated by insulin, we also explored whether in congestive heart failure, a hyperinsulinaemic state, plasma leptin levels relate to plasma insulin levels.
  
  
  METHODS
  Male patients with weight-stable congestive heart failure (n = 25, aged 55.5 +/- 2.0, mean +/- SEM, body mass index = 27.4 +/- 0.8, radionuclide left ventricular ejection fraction = 29.3 +/- 3.0%) and 18 controls, matched for age, sex and body fat (dual energy X-ray absorptiometry), underwent measurement of fasting plasma leptin (radioimmunoassay) and insulin levels.
  
  
  RESULTS
  Compared to controls, patients with congestive heart failure had higher plasma leptin [8.12 (-1.12, +1.31) vs 4.48 (-0.61, +0.70) ng.ml-1, mean +/- asymmetrical SEM, P = 0.003], 41.5% higher plasma leptin per percent body fat mass (P < 0.001), and higher fasting insulin levels [67.8 (-11.1, +13.3) vs 32.9 (-5.7, +6.9) pmol.l-1, P = 0.010]. In the congestive heart failure group, plasma leptin correlated with total body fat (r = 0.66) and fasting insulin (r = 0.68) (both P < 0.001). In multivariate regression analyses of the congestive heart failure group, fasting insulin (standardized coefficient = 0.41, P = 0.011) emerged as a predictor of plasma leptin levels, independent of total body fat (standardized coefficient = 0.73, P = 0.002, R2 = 0.66, P < 0.001).
  
  
  CONCLUSIONS
  Plasma leptin levels are raised in patients with congestive heart failure. The observation of a positive relationship between plasma leptin and insulin concentrations suggests that the insulin-leptin axis may be related to the increased energy expenditure observed in patients with congestive heart failure.
authors.affiliation: Department of Cardiac Medicine, Imperial College, National Heart and Lung Institute, London, U.K.
authors.forename: F
authors.initials: F
authors.lastname: Leyva
authors.forename: S D
authors.initials: SD
authors.lastname: Anker
authors.forename: K
authors.initials: K
authors.lastname: Egerer
authors.forename: J C
authors.initials: JC
authors.lastname: Stevenson
authors.forename: W J
authors.initials: WJ
authors.lastname: Kox
authors.forename: A J
authors.initials: AJ
authors.lastname: Coats
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002311:Cardiomyopathy, Dilated / Q000150:complications; D002908:Chronic Disease; D003327:Coronary Disease / Q000150:complications; D006333:Heart Failure / Q000097:blood* / Q000209:etiology; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000150:complications; D007328:Insulin / Q000097:blood*; D020738:Leptin; D008297:Male; D008875:Middle Aged; D011506:Proteins / Q000378:metabolism*; D011863:Radioimmunoassay
chemical_list: D015415:Biomarkers; D007328:Insulin; D020738:Leptin; D011506:Proteins