Analysis of -11391G>A and +45T>G polymorphisms of ADIPOQ gene in women with excessive weight gain during pregnancy
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(3) po ł o ż n i c t wo. Analysis of -11391G>A and +45T>G polymorphisms of ADIPOQ gene in women with excessive weight gain during pregnancy Analiza polimorfizmów -11391G>A oraz +45T>G genu ADIPOQ u kobiet z nadmiernym przyrostem masy ciała w ciąży
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(10) )* + 1,4,5 1. Division of Perinatology and Women’s Diseases, Poznan University of Medical Sciences, Poznan, Poland Division of Gynecology and Obstetrics, Podhale Multidisciplinary Hospital, Nowy Targ, Poland 3 Laboratory of Experimental Pharmacogenetics, Department of Clinical Pharmacy and Biopharmacy, University of Medical Sciences, Poznan, Poland 4 Department of Pharmacology and Phytochemistry, Institute of Natural Fibers and Medicinal Plants, Poznan, Poland 5 Laboratory of Molecular Biology in Division of Perinatology and Women’s Diseases, Poznan University of Medical Sciences, Poznan, Poland 6 Department of General Pharmacology and Pharmacoeconomics, Pomeranian Medical University, Szczecin, Poland 7 Department of Stem Cells and Regenerative Medicine, Institute of Natural Fibres and Medicinal Plants, Poznan, Poland 8 Department of Gynecology and Obstetrics with Gynecological Oncology Subdivision, Regional Hospital in Zielona Góra, Poland 2. Abstract Objectives: The aim of our study was to evaluate the frequency of genotypes and alleles of the -11391G>A and +45T>G polymorphisms of the ADIPOQ gene in Polish women with excessive weight gain during pregnancy. A possible correlation between these polymorphisms and selected clinical and anthropometric parameters has been analyzed. Material and methods: A total of 153 pregnant Caucasian women of Polish origin with normal pre-pregnancy body mass were analyzed: 78 women with excessive weight gain (study group) and 75 women with normal weight gain during pregnancy (control group). The analysis of the polymorphisms was performed by PCR/RFLP. Results: The influence of the -11391G>A polymorphism on body mass and BMI values at the end of pregnancy (p<0.05) was observed. We also detected a correlation of the +45T>G polymorphism with body mass at the end of pregnancy and pre-pregnancy WHR values (p<0.05). Conclusions: The observed effect of the -11391G>A polymorphism on the parameters assessed at the end of pregnancy (BMI and body mass), suggests a protective role of the -11391A genetic variant in excessive weight gain. It is claimed that the mutated +45G allele of the +45T>G ADIPOQ polymorphism shows a possible connection with higher pre-pregnancy WHR values and body mass at the end of pregnancy. Our findings suggest a possible contribution of the -11391G>A and +45T>G polymorphisms of the ADIPOQ gene to the pathomechanism of excessive weight gain in pregnant women from the Polish population. This observation should be confirmed in a larger sample size study.. Key words: excessive weight gain / genetic polymorphism / adiponectin / ADIPOQ /. Corresponding author: Magdalena Barlik Department of Perinatology and Women’s Diseases, University of Medical Sciences, Poznan, Poland ul. Polna 33, 60-535 Poznań, Poland tel. 0048 61 8419 613 e-mail: magda.barlik@op.pl. 352. © Polskie Towarzystwo Ginekologiczne. Otrzymano: 13.05.2014 Zaakceptowano do druku: 17.08.2014. Nr 5/2015.
(11) Ginekol Pol. 2015, 86, 352-356. P R A C E. O R Y G I N A L N E po ł o ż n i c t wo. Hubert Wolski, et al. Analysis of -11391G>A and +45T>G polymorphisms of ADIPOQ gene in women with excessive weight gain during pregnancy.. Streszczenie Cel pracy: Celem pracy była ocean częstości występowania genotypów i alleli polimorfizmu -11391G>A oraz +45T>G genu ADIPOQ u kobiet z nadmiernym przyrostem masy ciała w ciąży w populacji polskiej. Zbadano również korelację obydwu polimorfizmów z wybranymi parametrami klinicznymi i antropometrycznymi. Materiały i metody: Badaniem objęto 153 kobiety ciężarne rasy kaukaskiej z prawidłową masą ciała: 78 kobiet z nadmiernym oraz 75 kobiet z prawidłowym przyrostem masy ciała w ciąży stanowiących grupę kontrolną. Analizę badanych polimorfizmów przeprowadzono z wykorzystaniem metody PCR/RFLP. Wyniki: Odnotowano wpływ polimorfizmu -11391G>A na masę ciała i wartość BMI pod koniec ciąży (p<0.05). Obserwowano również korelację polimorfizmu +45T>G z masą ciała pod koniec ciąży i wartość WHR przed ciążą (p<0.05). Wnioski: Obserwowany wpływ polimorfizmu -11391G>A na parametry badane po koniec ciąży: wskaźnik BMI oraz masę ciała, sugeruje protekcyjną rolę wariantu -11391A na nadmierny przyrost masy ciała. Potwierdzono, że zmutowany allel +45G polimorfizmu +45T>G wykazuje możliwy związek z większą wartością WHR przed ciążą oraz masą ciała pod koniec ciąży. Uzyskane wyniki sugerują możliwy udział polimorfizmów -11391G>A oraz +45T>G genu ADIPOQ z w patomechanizmie nadmiernego przyrostu masy ciała u ciężarnych kobiet z populacji polskiej. Obserwacja ta powinna być potwierdzona w większej liczebnie grupie pacjentek.. Słowa kluczowe:
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(522) pregnancy. pregnancy. Observed value . Expected value . Observed value . Expected value . -11391GG. 65 (83.33). 84.04. 65 (86.67). 87.1. -11391GA. 13 (16.67). 15.27. 10 (13.33). 12.5. -11391AA. 0 (0,00). 0.69. 0 (0.00). 0.4. 78 (100). 100. 75 (100). 100. Genotypes. Total Alleles -11391G. 143 (91.67). 140 (93.33). -11391A. 13 (8.33). 10 (6.67). 156 (100). 150 (100). Total. Table II. The frequency of genotypes and alleles of +45T>G ADIPOQ polymorphism.
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(524) . Genotypes +45TT. 72 (92.31). 92.41. 69 (92.00). 92.16. +45TG. 5 (6.41). 7.44. 6 (8.00). 7.68. +45GG. 1 (1.28). 0.15. 0 (0.00). 0.16. Total. 78 (100). 100. 75 (100). 100. Alleles +45T. 149 (96.13). 144 (96.00). +45G. 6 (3.87). 6 (4.00). Total. 155 (100). 150 (100). /*
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(710) 7. References 1. Kushner RF, Blatner DJ. Risk assessment of the overweight and obese patient. J Am Diet Assoc. 2005, 105, 53-62. 2. Kozakowski J, Kapuścińska R, Zgliczyński W. Associations of vitamin D concentration with metabolic and hormonal indices in women with polycystic ovary syndrome presenting abdominal and gynoidal type of obesity. Ginekol Pol. 2014, 85, 765-770. 3. Lee H, Lee IS, Choue R. Obesity, inflammation and diet. Pediatr Gastroenterol Hepatol Nutr. 2013, 16, 143-152. doi: 10.5223/pghn.2013.16.3.143. 4. Nigro E, Scudiero O, Monaco ML, [et al.]. New insight into adiponectin role in obesity and obesity-related diseases. Biomed Res Int. 2014;2014:658913. doi: 10.1155/2014/658913. 5. Menzaghi C, Trischitta V, Doria A. Genetic influences of adiponectin on insulin resistance, type 2 diabetes, and cardiovascular disease. Diabetes. 2007, 56, 1198-209. 6. Kadowaki T, Yamauchi T. Adiponectin and adiponectin receptors. Endocr Rev. 2005, 26, 439451. 7. Qi Y, Takahashi N, Hileman SM, [et al.]. Adiponectin acts in the brain to decrease body weight. Nat Med. 2004, 10, 524-529. 8. Fantuzzi G. Adiponectin in inflammatory and immune-mediated diseases. Cytokine. 2013, 64, 1-10. doi: 10.1016/j.cyto.2013.06.317. 9. Scotece M, Conde J, López V, [et al.]. Adiponectin and leptin: new targets in inflammation. Basic Clin Pharmacol Toxicol. 2014, 114, 97-102. doi: 10.1111/bcpt.12109. 10. Lee YY, Lee NS, Cho YM, [et al.]. Genetic association study of adiponectin polymorphisms with risk of Type 2 diabetes mellitus in Korean population. Diabet Med. 2005, 22, 569-575. 11. Withers SB, Bussey CE, Saxton SN, [et al.]. Mechanisms of adiponectin-associated perivascular function in vascular disease. Arterioscler Thromb Vasc Biol. 2014, 34, 1637-1642. doi: 10.1161/ATVBAHA.114.303031. 12. Ntaios G, Gatselis NK, Makaritsis K, Dalekos GN. Adipokines as mediators of endothelial function and atherosclerosis. Atherosclerosis. 2013, 227, 216-221. 13. Gómez R, Conde J, Scotece M, [et al.]. What’s new in our understanding of the role of adipokines in rheumatic diseases? Nat Rev Rheumatol. 2011, 7, 528-536. 14. Itoh N. FGF21 as a Hepatokine, Adipokine, and Myokine in Metabolism and Diseases. Front Endocrinol (Lausanne). 2014, 5, 107. doi: 10.3389/fendo.2014.00107. eCollection 2014. 15. Sabouri S, Ghayour-Mobarhan M, Moohebati M, [et al.]. Association between 45T/G Polymorphism of Adiponectin Gene and Coronary Artery Disease in an Iranian Population. Scientific World Journal. 2011, 11, 93-101. 16. Lim S, Quon MJ, Koh KK. Modulation of adiponectin as a potential therapeutic strategy. Atherosclerosis. 2014, 233, 721-728. doi: 10.1016/j.atherosclerosis.2014.01.051. 17. Shibata R, Ohashi K, Murohara T, Ouchi N. The potential of adipokines as therapeutic agents for cardiovascular disease. Cytokine Growth Factor Rev. 2014, 25, 483-487. doi: 10.1016/j. cytogfr.2014.07.005. 18. de Faria AP, Modolo R, Fontana V, Morenott A. Adipokines: novel players in resistant hypertension. J Clin Hypertens (Greenwich). 2014, 16, 754-759. doi: 10.1111/jch.12399. 19. Tabatabaei-Malazy Z, Hasani-Ranjbar S, Amdi MM, [et al.]. Gender-specific differences in the association of adiponectin gene polymorphisms with body mass index. Rev Diabet Stud. 2010, 7, 241-246. 20. Warodomwichit D, Shen J, Arnett DK, [et al.]. ADIPOQ polymorphisms, monounsaturated fatty acids, and obesity risk: the GOLDN study. Obesity (Silver Spring). 2009, 17, 510-517.. Oświadczenie autorów: 1. Hubert Wolski – autor koncepcji i założeń pracy, analiza i interpretacja wyników, przygotowanie manuskryptu i piśmiennictwa, zebranie materiału – autor zgłaszający i odpowiedzialny za manuskrypt,. 2. Witold Kraśnik – zebranie materiału, analiza statystyczna wyników, przygotowanie manuskryptu. 3. Anna Bogacz – współautor tekstu pracy i protokołu, korekta i aktualizacja literatury. 4. Joanna Bartkowiak-Wieczorek – analiza i interpretacja wyników, przygotowanie, korekta i akceptacja ostatecznego kształtu manuskryptu. 5. Krzysztof Drews – analiza i interpretacja wyników, przygotowanie, korekta i akceptacja ostatecznego kształtu manuskryptu. 6. Agnieszka Greber – wykonanie badań laboratoryjnych, opracowanie wyników badań, przechowywanie dokumentacji. 7. Bogusław Czerny – analiza i interpretacja wyników, przygotowanie, korekta i akceptacja ostatecznego kształtu manuskryptu. 8. Krzysztof Piątek – zebranie materiału, analiza statystyczna wyników, przygotowanie manuskryptu. 9. Agnieszka Seremak-Mrozikiewicz – analiza i interpretacja wyników, ostateczna weryfikacja oraz akceptacja manuskryptu.. 21. Morandi A, Maffeis C, Lobbens S, [et al.]. Early detrimental metabolic outcomes of rs17300539-A allele of ADIPOQ gene despite higher adiponectinemia. Obesity (Silver Spring). 2010, 18, 14691473. 22. Lee S, Kwak HB. Role of adiponectin in metabolic and cardiovascular disease. J Exerc Rehabil. 2014, 10, 54-59. doi: 10.12965/jer.140100. 23. Yang WS, Ling Tsou PL, Lee WJ, [et al.]. Allele-specific differential expression of a common adiponectin gene polymorphism related to obesity. Mol Med. 2003, 81, 428-434. 24. Wu J, Liu Z, Meng K, Zhang L. Association of adiponectin gene (ADIPOQ) rs2241766 polymorphism with obesity in adults: a meta-analysis. PLoS One. 2014, 9(4):e95270. doi: 10.1371/journal.pone.0095270. 25. Yan WL, Chen SF, Huang JF, [et al.]. Common SNPs of APM1 gene are not associated with hypertension or obesity in Chinese population. Biomed Environ Sci. 2006, 19, 179-184. 26. Fisman EZ, Tenenbaum A. Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease? Cardiovasc Diabetol. 2014, 13, 103. doi: 10.1186/1475-284013-103. 27. O’Neill SM, Hinkle C, Chen SJ, [et al.]. Targeting adipose tissue via systemic gene therapy. Gene Ther. 2014, 21, 653-661. doi: 10.1038/gt.2014.38. 28. Khan S, Shukla S, Sinha S, Neeran SM. Role of adipokines and cytokines in obesity-associated breast cancer: therapeutic targets. Cytokine Growth Factor Rev. 2013, 24, 503-513. doi: 10.1016/j.cytogfr.2013.10.001.. Źródło finansowania: Badania statutowe Kliniki Perinatologii i Chorób Kobiecych, Uniwersytet Medyczny im. Karola Marcinkowskiego w Poznaniu; No. 502-01-0221834403344. Konflikt interesów: Autorzy nie zgłaszają konfliktu interesów oraz nie otrzymali żadnego wynagrodzenia związanego z powstawaniem pracy.. 356. © Polskie Towarzystwo Ginekologiczne. Nr 5/2015.
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