EFFECT OF THE Pro12Ala POLYMORPHISM OF THE PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR γ2 GENE ON LIPID PROFILE AND ADIPOKINES LEVELS IN OBESE SUBJECTS
Becer E1,2,*, Çırakoğlu A3
*Corresponding Author: Eda Becer, Ph.D., M.Sc., Department of Biochemistry, Faculty of Pharmacy, Near East University, Nicosia, Mersin 10, Turkey. Tel: +90-392-680-2000, Ext: 128. Fax:+90-392-680-2038. E-mail: edabecer@yahoo.com
page: 71

INTRODUCTION

The proxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear hormone receptor superfamily and plays an important role in energy storage, adipocyte differentiation, insulin sensitization and fatty acid metabolism [1]. The PPARγ1, PPARγ2 and PPARγ3 are generated by separate promoters and 5’ exons. Separate promoters and 5’ exons generate three mRNA isoforms: PPARγ1, PPARγ2 and PPARγ3. The PPARγ1 and PPARγ3 mRNAs encode the same protein products, whereas PPARγ2 protein contains an additional NH2-terminal region composed of 30 amino acids. The PPARγ1 gene is expressed in nearly all cells, while PPARγ2 expression is limited mainly to adipose tissue [2]. Both PPARγ1 and PPARγ2 isoforms are an important adipogenic regulator and essential for the control of insulin sensitivity. However, PPARγ2 regulates response to nutrient intake and obesity. These characteristic properties make it a key molecule to be involved in the expression of adipokines such as leptin, adiponectin, resistin and chemerin, which may act as modulators of energy metabolism and insulin action [3]. Moreover, PPARγ2 mediates the expression of specific fat tissue cell genes that also participates in lipogenic pathways and adipocyte hypertrophy [4]. The PPARγ2 gene is located on chromosome 3p25 [5]. Several single nucleotide polymorphisms (SNPs) of the PPARγ2 gene have been identified and one of these poly-morphisms is Pro12Ala (rs1801282). The Pro12Ala polymorphism results from a cytosine to guanine substitution at nucleotide 34 of exon B and leads to a proline to alanine at position 12 of the PPARγ2 protein [6]. The alanine allele was shown to have reduced affinity for response element and lower capacity for activating target genes [7]. In recent years, several studies have focused on the association between the Pro12Ala polymorphism and complex traits such as obesity, type 2 diabetes mellitus (T2DM) and insulin sensitivity, have been reported [8,9]. Many studies have indicate that the alanine allele decreased risk of T2DM and increased insulin sensitivity [10,11]. However, studies on an association between the Pro12Ala polymorphism and obesity-related metabolic diseases have yielded inconsistent results [8,12,13]. The mechanisms underlying the association of obesity and insulin sensitivity mainly involve altering the production of hormones and molecules related to adipose tissue and energy metabolism, such as leptin, adiponectin, resistin and chemerin. Therefore, the impact of the Pro12Ala polymorphism of the PPARγ2 gene on regulating adipokines expression will provide a better appreciation of the pathogenic mechanisms underlying obesity and associated comorbidities. However, the available data are still limited and conflicting. Thus, the aim of this study was to investigate the associations between the PPARγ2 gene Pro12Ala polymorphism, body mass index (BMI), lipid parameters, homeostasis model assessment of insulin resistance (HOMA-IR), serum leptin, adiponectin, resistin and chemerin levels in obese subjects versus non obese subjects.



Number 27
VOL. 27 (2), 2024
Number 27
VOL. 27 (1), 2024
Number 26
Number 26 VOL. 26(2), 2023 All in one
Number 26
VOL. 26(2), 2023
Number 26
VOL. 26, 2023 Supplement
Number 26
VOL. 26(1), 2023
Number 25
VOL. 25(2), 2022
Number 25
VOL. 25 (1), 2022
Number 24
VOL. 24(2), 2021
Number 24
VOL. 24(1), 2021
Number 23
VOL. 23(2), 2020
Number 22
VOL. 22(2), 2019
Number 22
VOL. 22(1), 2019
Number 22
VOL. 22, 2019 Supplement
Number 21
VOL. 21(2), 2018
Number 21
VOL. 21 (1), 2018
Number 21
VOL. 21, 2018 Supplement
Number 20
VOL. 20 (2), 2017
Number 20
VOL. 20 (1), 2017
Number 19
VOL. 19 (2), 2016
Number 19
VOL. 19 (1), 2016
Number 18
VOL. 18 (2), 2015
Number 18
VOL. 18 (1), 2015
Number 17
VOL. 17 (2), 2014
Number 17
VOL. 17 (1), 2014
Number 16
VOL. 16 (2), 2013
Number 16
VOL. 16 (1), 2013
Number 15
VOL. 15 (2), 2012
Number 15
VOL. 15, 2012 Supplement
Number 15
Vol. 15 (1), 2012
Number 14
14 - Vol. 14 (2), 2011
Number 14
The 9th Balkan Congress of Medical Genetics
Number 14
14 - Vol. 14 (1), 2011
Number 13
Vol. 13 (2), 2010
Number 13
Vol.13 (1), 2010
Number 12
Vol.12 (2), 2009
Number 12
Vol.12 (1), 2009
Number 11
Vol.11 (2),2008
Number 11
Vol.11 (1),2008
Number 10
Vol.10 (2), 2007
Number 10
10 (1),2007
Number 9
1&2, 2006
Number 9
3&4, 2006
Number 8
1&2, 2005
Number 8
3&4, 2004
Number 7
1&2, 2004
Number 6
3&4, 2003
Number 6
1&2, 2003
Number 5
3&4, 2002
Number 5
1&2, 2002
Number 4
Vol.3 (4), 2000
Number 4
Vol.2 (4), 1999
Number 4
Vol.1 (4), 1998
Number 4
3&4, 2001
Number 4
1&2, 2001
Number 3
Vol.3 (3), 2000
Number 3
Vol.2 (3), 1999
Number 3
Vol.1 (3), 1998
Number 2
Vol.3(2), 2000
Number 2
Vol.1 (2), 1998
Number 2
Vol.2 (2), 1999
Number 1
Vol.3 (1), 2000
Number 1
Vol.2 (1), 1999
Number 1
Vol.1 (1), 1998

 

 


 About the journal ::: Editorial ::: Subscription ::: Information for authors ::: Contact
 Copyright © Balkan Journal of Medical Genetics 2006