ASSOCIATIONS BETWEEN VASPIN RS2236242 GENE
POLYMORPHISM, WALKING TIME AND THE RISK
OF METABOLIC SYNDROME
Suliga E1, Kozieł D2, Cieśla E3, Rębak D2, Wawszczak M2,*,
Adamus-Białek W2, Naszydłowska E4, Piechowska A2, Głuszek S2
*Corresponding Author: Monika Wawszczak, MSc, Department of Surgery and Surgical Nursery with Genetics
and Research Laboratory, Institute of Medical Sciences, Jan Kochanowski University, al. IX Wieków
Kielc 19a, 25-516, Kielce, Poland. Tel: +48-413696978. E-mail: mwawszczak@ujk.edu.pl
page: 41
|
|
DISCUSSION
In our study, the possible association between the
vaspin rs2236242 gene polymorphism and the risk of
developing MetS in a group of Polish men and women
was investigated. To the best of our knowledge, this is
the first time such an association has been studied in the
Polish population. Both in the unadjusted and adjusted
models, there have been no statistically significant association
between the vaspin rs2236242 polymorphism and the
risk of the occurrence of individual components of MetS.
However, in the model adjusted for known confounders
(smoking, BMI, walking), it was noted that carrying the TA
genotype was related to a greater risk of MetS, compared
to the TT genotype.
Results of other studies are ambiguous in this respect.
Hashemi et al. [7] in a study conducted on Iranian population
observed that the A allele of the vaspin rs2236242
polymorphism plays a protective role against MetS. The
risk of MetS was decreased significantly by being a carrier
of the AA and TA genotypes compared to the TT
genotype. The associations remained almost unchanged
after adjusted for gender and age [7]. Mehanna et al. [8]
in a study of Egyptian women, also found that the rare
A allele of the vaspin rs2236242 polymorphism and the
TA and AA genotypes appeared with higher frequencies
among the control group individuals than in MetS subjects.
A similar tendency, related to the protective function of
the AA genotype against MetS, was shown in the results
of our study, in the unadjusted model. The tendency to
a slightly more frequent occurrence of TA genotype in
MetS-subjects, compared to control-subjects (51.86 vs.
45.45%), as well as a higher risk of MetS in TA genotype
carriers. However, these results did not reach a level of
statistical significance. Different results were achieved on
Egyptian women by Alnory et al. [6] who did not observe
any significant associations between the A allele of the
vaspin rs2236242 polymorphism and risk of MetS when
compared to the T allele. The AA and AT genotypes also
showed no association with MetS when compared to the
TT genotype. Moreover, the authors did not find any associations
between genotypes of the vaspin rs2236242
polymorphism and different serum vaspin levels [6].
In the Iranian population, the analysis of the associations
between the vaspin rs2236242 gene polymorphism
and health conditions such as obesity, PCOS and T2DM,
showed ambiguous results. Kohan et al. [11] observed
a decreased risk of PCOS in the A allele carriers when
compared to the T carriers. However, this relationship
was not statistically significant after adjusting genotypes
for BMI [12]. Abdel Ghany et al. [12] concluded that
the minor (A) allele of the vaspin rs2236242 gene polymorphism
occurred less frequently in obese women compared
to control group. It played a protective role against
obesity in dominant, codominant, additive, and recessive
inheritance models. However, after adjusting genotypes
for T2DM there were no significant associations between
polymorphism of this gene and obesity. According to the
authors, the vaspin rs2236242 gene polymorphism shows
protective effects in obesity, but this association results
mainly from its effect on insulin sensitivity [12]. The analysis of the German population conducted by Kempf
et al. [13] revealed that the AA genotype carriers had an
increased risk of T2DM, compared with the TT genotype
carriers, but contrary to all other studies they analyze the
vaspin rs2236242 polymorphism in the reverse strand of
the vaspin gene. The results of the meta-analysis of three
populations only enforce the theory that A allele plays a
protective role against MetS occurrence and TT genotype
increase the risk of syndrome progression.
It has been shown that lifestyle factors, such as physical
activity, can modify associations between variants of
several genes and the risk of developing obesity, T2DM
and cardiovascular disease in various populations [14-16].
Metabolic syndrome is also treated as a result of interactions
between genetic factors and unhealthy lifestyle. It is
thought that despite the significant role of genetic factors,
a lack of regular PA and obesity are the main causes of the
increase of occurrence of metabolic disorders, especially
in developed countries [17,18]. According to our current
knowledge, none of the previously published studies on the
relationship between the vaspin rs2236242 polymorphism
and the risk of MetS included PA or walking. Thus, our
study provides the first vaspin rs2236242 gene polymorphism
× PA/walking time interaction data on MetS and
its components. Studies of the influence of other genes
and PA on adiposity and metabolic characteristics provide
diverse results. Brito et al. [19] evaluated the effect of
‘genes-physical activity’ interaction on impaired glucose
regulation risk for 17 loci related to T2DM and showed
that three polymorphisms were statistically significant:
CDKN2A/B rs10811661, HNF1B rs4430796 and PPARG
rs1801282. Similar to our analysis, the inclusion or exclusion
of BMI as a covariate in the SNP × physical activity
interaction models made no essential difference to the
interaction results. Thus the authors concluded that the
genetic predisposition to hyperglycemia is partially dependent
on a person’s lifestyle [19]. Kilpeläinen [14] found
that the effect of increasing of BMI by rs9939609 gene
FTO polymorphism was weakened by 27.0% in physically
active individuals compared to non active ones. However,
Graff et al. [20] did not find any evidence of the interaction
with PA for loci other than FTO.
The analysis of interactions revealed that in our study
population, longer walking (>60 min./day) lowered the
risk of MetS and elevated blood pressure in the TA and
TA+ AA genotype carriers and the risk of increased TG
concentration in the AA genotype carriers, results were
statistically significant. Walking is the most frequent form
of physical activity. Results of several studies show that
despite its low intensity, it is associated with lower risks
of cardiovascular disease, T2DM and all cause mortality
in men and women [21,22]. In a prospective study of
Japanese workers aged 30-69, walking less than 60 min./
day comprised one of the crucial lifestyle elements increasing
the risk of MetS, during 1 year of observation [23].
A decrease of MetS occurrence related to longer walking
time, was also observed in several cross-sectional studies
[24] and meta-analysis of cohort studies [25].
The strength of the conducted study is the inclusion
of confounding factors in statistical analysis, which may
have a modifying effect on the risk of MetS occurrence
and its components. The limitations are considered to be
the small number of participants and the fact that PA was
assessed with the use of questionnaires, which are prone
to bias and errors.
Conclusions. In the unadjusted model, no associations
between the vaspin rs2236242 polymorphism and
the risk of MetS and its components have been observed.
Only the tendency to a decreased risk of MetS and its
components in the AA genotype carriers has been noted,
but the result was statistically insignificant. The results of
the conducted study suggest that any unfavorable effect of
the TA genotype of the vaspin rs2236242 polymorphism
can be essentially reduced, or even reversed, in a case
of individuals walking longer than 60 min. The analysis
of interaction between the vaspin rs2236242 gene polymorphism
and walking has revealed that walking time
longer than 60 min./day considerably reduces the risk of
MetS, elevated blood pressure and TG concentration. It
is necessary to conduct further studies on a bigger group
of participants, which will allow us to determine whether
these results will be useful in MetS prophylaxis.
Declaration of Interest. The authors report no conflicts
of interest. The authors alone are responsible for the
content and writing of this article.
Funding. This study was conducted with the support
of the Maria Skłodowska-Curie Institute of Oncology
in Warsaw and the Polish-Norwegian Foundation
Research Fund. The research data were collected within
the scope of PONS research: “Establishing infrastructure
for studies concerning health state of the population of
Poland” (PNRF-228-AI-1/07) (data collection). This study
was supported by a grant from The Ministry of Science
and Higher Education from the funds received within
financing statutory activity for Faculty of Medicine and
Health Sciences, Jan Kochanowski University, research
project No. 615507 (data analysis and preparation of the
manuscript). This study was supported under the program
of the Minister of Science and Higher Education under
the name Regional Initiative of Excellence in 2019-2022
project number: 024/RID/2018/19, financing amount:
11.999.000,00 PLN.
|
|
|
|
 |
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 |
|
|
|
