PMID- 19337797
OWN - NLM
STAT- MEDLINE
DCOM- 20090625
LR  - 20221207
IS  - 1615-2573 (Electronic)
IS  - 0910-8327 (Linking)
VI  - 24
IP  - 2
DP  - 2009 Mar
TI  - Association between variants in the genes for leptin, leptin receptor, and 
      proopiomelanocortin with chronic heart failure in the Czech population.
PG  - 131-7
LID - 10.1007/s00380-008-1090-5 [doi]
AB  - Patients with chronic heart failure (CHF) express enhanced catabolic metabolism 
      finally resulting in overall weight loss, whereas adipokines might play a crucial 
      role in signaling among tissues. The aim of this study was to investigate the 
      possible associations of defined variability in leptin (dbSNP ID rs7799039), 
      proopiomelanocortin (dbSNP ID rs3754860 and dbSNP ID rs1009388), and leptin 
      receptor gene (dbSNP rs1137101) with CHF and evaluate their potential as the CHF 
      susceptibility genes. The case-control study comprised a total of 372 patients of 
      Caucasian origin with chronic heart failure (New York Heart Association [NYHA] 
      functional classes II-IV, ejection fraction (EF) <40%) and 407 healthy controls. 
      They were genotyped for the leptin (LEP) -2548 G/A, leptin receptor (LEPR) 
      Gln223Arg, and proopiomelanocortin (POMC) RsaI (5'-untranslated region) and 
      C1032G variants (intron 1) using PCR-based methodology. No case-control 
      differences in genotype as well as allele frequencies were observed between CHF 
      patients and controls. We constructed POMC RsaI/C1032G haplotypes, having found 
      no significant association with body mass index (BMI), left ventricle ejection 
      fraction (LVEF), left ventricle hypertrophy (LVH) and diabetes mellitus (DM). 
      Multivariate regression analyses revealed an approximately 2-fold risk for NYHA 
      class IV associated with the LEPR Gln223Arg (P = 0.0000001, odds ratio [OR] = 
      2.10, 95% confidence interval [CI] = 1.56-2.84); it also displayed an independent 
      prediction role for LVEF in heart failure cases of all etiologies (P = 0.002, OR 
      = 4.05, 95% CI = 1.36-10.06). In subanalyses according to CHF etiology the LEPR 
      Gln223Arg showed an independent prediction role for NYHA IV in IHD patients (P = 
      0.0001, OR = 2.50, 95% CI = 1.69-3.82) and both for NYHA IV(P = 0.007, OR = 2.04, 
      95% CI = 1.20-3.84) and LVEF (P = 0.004, OR = 11.87, 95% CI = 2.08-55.6) in DCMP 
      patients. The role of the polymorphic variants in the genes encoding for 
      adipokines as potential CHF susceptibility genes is unclear. Based on our 
      findings, the LEPR Gln223Arg polymorphism could be considered a disease 
      susceptibility modulating factor both in ischemic heart disease or dilated 
      cardiomyopathy patients.
FAU - Bienertova-Vasku, Julie Anna
AU  - Bienertova-Vasku JA
AD  - Institute of Pathological Physiology, Faculty of Medicine, Masaryk University, 
      Brno, Czech Republic. jbienert@med.muni.cz
FAU - Spinarova, Lenka
AU  - Spinarova L
FAU - Bienert, Petr
AU  - Bienert P
FAU - Vasku, Anna
AU  - Vasku A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090401
PL  - Japan
TA  - Heart Vessels
JT  - Heart and vessels
JID - 8511258
RN  - 0 (LEPR protein, human)
RN  - 0 (Leptin)
RN  - 0 (Receptors, Leptin)
RN  - 66796-54-1 (Pro-Opiomelanocortin)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Case-Control Studies
MH  - Chronic Disease
MH  - Czech Republic
MH  - Female
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease
MH  - Heart Failure/ethnology/*genetics/physiopathology
MH  - Humans
MH  - Leptin/*genetics
MH  - Male
MH  - Middle Aged
MH  - Odds Ratio
MH  - Phenotype
MH  - *Polymorphism, Single Nucleotide
MH  - Pro-Opiomelanocortin/*genetics
MH  - Receptors, Leptin/*genetics
MH  - Risk Assessment
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Stroke Volume/genetics
MH  - Ventricular Function, Left/genetics
MH  - White People/*genetics
MH  - Young Adult
EDAT- 2009/04/02 09:00
MHDA- 2009/06/26 09:00
CRDT- 2009/04/02 09:00
PHST- 2008/03/27 00:00 [received]
PHST- 2008/07/03 00:00 [accepted]
PHST- 2009/04/02 09:00 [entrez]
PHST- 2009/04/02 09:00 [pubmed]
PHST- 2009/06/26 09:00 [medline]
AID - 10.1007/s00380-008-1090-5 [doi]
PST - ppublish
SO  - Heart Vessels. 2009 Mar;24(2):131-7. doi: 10.1007/s00380-008-1090-5. Epub 2009 
      Apr 1.