DUAL EFFECT OF THE GHRL GENE VARIANT IN THE MOLECULAR PATHOGENESIS OF OBESITY
Becer E1,2, Ergoren MC2,3,*
*Corresponding Author: Associate Professor Mahmut C. Ergoren, Ph.D., Department of Medical Biology, Faculty of Medicine, Near East University, Near East Boulevard, 99138 Nicosia, Cyprus. Tel.: +90-392-675-1000, Ext: 3035. Fax: +90-392-223-6461. Mobile: +90-0548-865-8889. E-mail: mahmutcerkez.ergoren@ neu.edu.tr
page: 27

RESULTS

Demographic Statistics and Biochemical Parameters. The demographic characteristics and biochemical parameters of the studied individuals are shown in Table 2. This case-control study comprised 211 Turkish- Cypriots (106 obese and 95 non obese). One hundred and six obese adult patients with an age of 41.56 ± 9.87 and BMI of 41.58 ± 4.93 kg/m2 were a generated case group. The control group included 95 non obese subjects with the mean age of 39.03 ± 9.45 years and BMI mean was 22.61 ± 1.82 kg/m2. There was no statistical difference of gender between the two groups. The statistically significant difference between biochemical parameters including fasting glucose, TC, LDL-C, HDL-C, TG and HOMA-IR was observed between obese and non obese (p <0.001 in all parameters) as well as physical parameters of BMI, waist circumferences, hip circumferences showed significant difference (p <0.001 in all parameters) except age (p = 0.066) Table 2). Genotype Distribution and Allele Frequencies of the GHRL Gene Variants (Arg51Gln and Leu72Met) in the Studied Population. The allele frequencies and genotype distributions of the GHRL rs34911341 (C>T) (Arg51 Gln) and rs696217 (G>T) (Leu72Met) gene variants are shown in Table 3. Distribution of the GHRL rs34911341 (C>T) genotypes were 98.12% for CC, 0.94% for CT and 0.94% for TT in the obese group. The frequencies of CC, CT and TT genotypes were 95, 0.0 and 0.0%, respectively, in non obese subjects. There was significant deviation of genotypic distribution from HWE in obese subjects (χ2 = 46.43, p <0.05). The deficit of the CT genotype frequencies in obese subjects probably accounts for the deviation from HWE. No significant difference in genotype frequencies of the rs34911341 polymorphism was detected between obese and non obese subjects (p = 0.40). On the other hand, the rs696217 (G>T) genotype frequencies were calculated and are shown in Table 3. In obese subjects, the genotype frequencies were 34.91% for GG, 53.77% for GT and 11.32% for TT. The frequencies of GG, GT and TT genotypes were 60, 35.79 and 4.12%, respectively, in non obese subjects. There were no significant deviation of genotypic distribution from HWE in both obese (χ2 = 2.04, p = 0.15) and non obese subjects (χ2 = 0.14, p = 0.7). A significant difference in genotype frequencies of the rs696217 polymorphism was detected between obese and non obese subjects (p = 0.0012). However, the results were in agreement with the global minor allele frequency (MAF) observations by Ensembl Genome Browser [29]. The MAF of GHRL rs696217 T allele was determined as ~38.0% in obese patients and ~22.0% in non obese individuals. The case-control genetic association analysis indicated a statistically significant difference in the allele frequencies of the GHRL rs696217 (G>T) variant between obese and non obese subjects [p = 0.0005; odds ratio (OR) = 0.459; 95% confidence interval (95% CI) = 0.295-0.713] (Table 3). Associations Between the GHRL Leu72Met Gene Polymorphisms and Clinical Parameters. The genotype distributions of all studied subjects were tested according to anthropometric and metabolic characteristics. The GHRL rs696217 T allele that substituted Leu→Met at position 72 was found to be significant when associated with waist circumference and hip circumference levels in the population (p = 0.005, p = 0.002, respectively) (Table 4). No other statistically significant parameter was observed in other clinical characteristics except for HDL-C (p = 0.018). Strikingly, subjects with the rs696217 GT genotype (heterozygous) had significantly lower HDL-C (p = 0.015) than GG (wild type) subjects (Table 4).



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