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Association of the T45G polymorphism in exon 2 of the adiponectin gene with polycystic ovary syndrome: role of Delta4-androstenedione.
Hum Reprod. 2004 Aug; 19(8):1728-33.HR

Abstract

BACKGROUND

Insulin resistance is a prominent feature of polycystic ovary syndrome (PCOS), independent of obesity. It is possible that insulin resistance in PCOS is genetically determined. Adiponectin is a protein that modulates insulin action and is regarded as a possible link between adiposity and insulin resistance. The objective of this study was to examine the role of the adiponectin gene T45G polymorphism, located in exon 2, in PCOS, since this polymorphism has been shown to be associated with obesity and insulin resistance.

SUBJECTS AND METHODS

Two hundred and thirty-two women were studied, and were classified as follows: 132 women with PCOS [62 with body mass index (BMI) > 25 kg/m2 and 70 with BMI < 25 kg/m2] and 100 ovulating women without hyperandrogenemia (controls: 19 with BMI > 25 kg/m2 and 81 with BMI < 25 kg/m2). From all subjects a whole-blood sample was taken and was used for isolation of peripheral blood leukocytes. The adiponectin T45G polymorphism, located in exon 2, was genotyped by amplification of genomic DNA. In all subjects, serum gonadotropin, androgen, 17-OH-progesterone, fasting glucose, insulin and adiponectin levels were measured between the third and sixth day of the menstrual cycle.

RESULTS

A statistically significant difference was observed in the frequency of GG and TG genotypes between women with PCOS (40/132; 30.3%) and controls (19/100; 19.0%). In a subgroup of PCOS women with high Delta4-androstenedione levels (Delta4A > 3.11 ng/ml), a statistically significant difference between the frequencies of the genotypes was also noticed compared with the control group, in contrast to the subgroup with relatively low Delta4-androstenedione levels (Delta4A < 3.11 ng/ml). No significant associations were found between this adiponectin polymorphism and BMI, testosterone level, adiponectin levels and glucose-to-insulin ratio.

CONCLUSIONS

Our study suggests that adiponectin polymorphisms are not causatively involved in the metabolic disturbances of PCOS, but that an interaction between adiponectin and steroid synthesis or action might exist.

Authors+Show Affiliations

Division of Endocrinology and Human Reproduction, Second Department of Obstetrics and Gynecology, Aristotle University of Thessaloniki, Thessaloniki, Greece. argic@med.auth.grNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15178661

Citation

Panidis, Dimitrios, et al. "Association of the T45G Polymorphism in Exon 2 of the Adiponectin Gene With Polycystic Ovary Syndrome: Role of Delta4-androstenedione." Human Reproduction (Oxford, England), vol. 19, no. 8, 2004, pp. 1728-33.
Panidis D, Kourtis A, Kukuvitis A, et al. Association of the T45G polymorphism in exon 2 of the adiponectin gene with polycystic ovary syndrome: role of Delta4-androstenedione. Hum Reprod. 2004;19(8):1728-33.
Panidis, D., Kourtis, A., Kukuvitis, A., Farmakiotis, D., Xita, N., Georgiou, I., & Tsatsoulis, A. (2004). Association of the T45G polymorphism in exon 2 of the adiponectin gene with polycystic ovary syndrome: role of Delta4-androstenedione. Human Reproduction (Oxford, England), 19(8), 1728-33.
Panidis D, et al. Association of the T45G Polymorphism in Exon 2 of the Adiponectin Gene With Polycystic Ovary Syndrome: Role of Delta4-androstenedione. Hum Reprod. 2004;19(8):1728-33. PubMed PMID: 15178661.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Association of the T45G polymorphism in exon 2 of the adiponectin gene with polycystic ovary syndrome: role of Delta4-androstenedione. AU - Panidis,Dimitrios, AU - Kourtis,Anargyros, AU - Kukuvitis,Asterios, AU - Farmakiotis,Dimitrios, AU - Xita,Nectaria, AU - Georgiou,Ioannis, AU - Tsatsoulis,Agathocles, Y1 - 2004/06/03/ PY - 2004/6/5/pubmed PY - 2005/1/28/medline PY - 2004/6/5/entrez SP - 1728 EP - 33 JF - Human reproduction (Oxford, England) JO - Hum Reprod VL - 19 IS - 8 N2 - BACKGROUND: Insulin resistance is a prominent feature of polycystic ovary syndrome (PCOS), independent of obesity. It is possible that insulin resistance in PCOS is genetically determined. Adiponectin is a protein that modulates insulin action and is regarded as a possible link between adiposity and insulin resistance. The objective of this study was to examine the role of the adiponectin gene T45G polymorphism, located in exon 2, in PCOS, since this polymorphism has been shown to be associated with obesity and insulin resistance. SUBJECTS AND METHODS: Two hundred and thirty-two women were studied, and were classified as follows: 132 women with PCOS [62 with body mass index (BMI) > 25 kg/m2 and 70 with BMI < 25 kg/m2] and 100 ovulating women without hyperandrogenemia (controls: 19 with BMI > 25 kg/m2 and 81 with BMI < 25 kg/m2). From all subjects a whole-blood sample was taken and was used for isolation of peripheral blood leukocytes. The adiponectin T45G polymorphism, located in exon 2, was genotyped by amplification of genomic DNA. In all subjects, serum gonadotropin, androgen, 17-OH-progesterone, fasting glucose, insulin and adiponectin levels were measured between the third and sixth day of the menstrual cycle. RESULTS: A statistically significant difference was observed in the frequency of GG and TG genotypes between women with PCOS (40/132; 30.3%) and controls (19/100; 19.0%). In a subgroup of PCOS women with high Delta4-androstenedione levels (Delta4A > 3.11 ng/ml), a statistically significant difference between the frequencies of the genotypes was also noticed compared with the control group, in contrast to the subgroup with relatively low Delta4-androstenedione levels (Delta4A < 3.11 ng/ml). No significant associations were found between this adiponectin polymorphism and BMI, testosterone level, adiponectin levels and glucose-to-insulin ratio. CONCLUSIONS: Our study suggests that adiponectin polymorphisms are not causatively involved in the metabolic disturbances of PCOS, but that an interaction between adiponectin and steroid synthesis or action might exist. SN - 0268-1161 UR - https://www.unboundmedicine.com/medline/citation/15178661/Association_of_the_T45G_polymorphism_in_exon_2_of_the_adiponectin_gene_with_polycystic_ovary_syndrome:_role_of_Delta4_androstenedione_ L2 - https://academic.oup.com/humrep/article-lookup/doi/10.1093/humrep/deh336 DB - PRIME DP - Unbound Medicine ER -