PMID- 24206404
OWN - NLM
STAT- MEDLINE
DCOM- 20141031
LR  - 20211214
IS  - 1735-3947 (Electronic)
IS  - 1029-2977 (Linking)
VI  - 16
IP  - 11
DP  - 2013 Nov
TI  - Association of the 223A/G LEPR polymorphism with serum leptin levels in Iranian 
      subjects with type 2 diabetes.
PG  - 636-41
AB  - BACKGROUND: Leptin, an adipocyte-derived hormone, has a pivotal role in the 
      regulation of body weight through acting on its specific leptin receptor (LEPR). 
      The 223A/G polymorphism of the LEPR gene is one of the most common polymorphism 
      in all populations.  In this study, we aimed to investigate the impact of the 
      223A/G polymorphism of the LEPR gene on serum levels of leptin in type 2 diabetes 
      mellitus (T2DM) in a sample of Iranian population. MATERIALS AND METHODS: One 
      hundred and forty-four T2DM patients were screened and compared to 147 healthy 
      controls.  The 223A/G LEPR polymorphism was genotyped using polymerase chain 
      reaction (PCR) followed by restriction fragment length polymorphism (RFLP). The 
      serum levels of leptin were measured. RESULTS: The mean serum levels of leptin in 
      T2DM patients were significantly higher than that of healthy control subjects; 
      22.90 ng/ml (95 % confidence interval [CI] = 20.79 - 25.23) vs.  8.70 ng/ml (95 % 
      CI = 7.87 - 9.63). The genotypes (AA, AG, and GG) distributions of the 223A/G 
      polymorphism were 55.5 %, 41 %, and 3.5 % in T2DM and 54.4 %, 42.2 %, and 3.4 % 
      in healthy controls. The results showed no significant differences in the 223A/G 
      LEPR genotype and allele frequencies between T2DM and control subjects (chi2 = 
      0.043, P = 0.979 and chi2 = 0.003, P = 0.957), respectively. In addition, the serum 
      leptin levels were markedly higher in subjects with GG genotype than those with 
      AG or GG genotype only in T2DM CONCLUSION: The 223A/G LEPR gene polymorphism is 
      associated with markedly increased serum leptin levels in T2DM. However, no 
      differences were determined in genotype and allele frequencies between T2DM 
      patients and control subjects.
FAU - Mohammadzadeh, Ghorban
AU  - Mohammadzadeh G
AD  - Hyperlipidemia Research Center, Department of Clinical Biochemistry, Faculty of 
      Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 
      mohammadzadeh@ajums.ac.i.
FAU - Nikzamir, Abdolrahim
AU  - Nikzamir A
FAU - Mohammadi, Javad
AU  - Mohammadi J
FAU - Pourdashti, Sara
AU  - Pourdashti S
FAU - Shabazian, Hajeh
AU  - Shabazian H
FAU - Latifi, Seyed-Mahmoud
AU  - Latifi SM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Iran
TA  - Arch Iran Med
JT  - Archives of Iranian medicine
JID - 100889644
RN  - 0 (LEPR protein, human)
RN  - 0 (Leptin)
RN  - 0 (Receptors, Leptin)
SB  - IM
MH  - Case-Control Studies
MH  - Diabetes Mellitus, Type 2/*blood/*genetics
MH  - Female
MH  - Gene Frequency
MH  - Humans
MH  - Iran
MH  - Leptin/*blood
MH  - Male
MH  - Middle Aged
MH  - Polymorphism, Restriction Fragment Length
MH  - Receptors, Leptin/*genetics
EDAT- 2013/11/12 06:00
MHDA- 2014/11/02 06:00
CRDT- 2013/11/12 06:00
PHST- 2013/11/12 06:00 [entrez]
PHST- 2013/11/12 06:00 [pubmed]
PHST- 2014/11/02 06:00 [medline]
AID - 005 [pii]
PST - ppublish
SO  - Arch Iran Med. 2013 Nov;16(11):636-41.