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ORIGINAL ARTICLE
Year : 2016  |  Volume : 143  |  Issue : 6  |  Page : 739-747

A cross-sectional study to assess any possible linkage of C/T polymorphism in CYP17A1 gene with insulin resistance in non-obese women with polycystic ovarian syndrome


1 Department of Biochemistry, Burdwan Medical College & Hospital, Burdwan; Department of Biochemistry, North Bengal Medical College, Siliguri 734 012, India
2 Department of Biochemistry, Burdwan Medical College & Hospital, Burdwan; Department of Biochemistry, Calcutta National Medical College, Kolkata 700 014, India
3 Department of Gynecology & Obstetrics, Burdwan Medical College & Hospital, Burdwan; Department of Gynaecology & Obstetrics, R.G. Kar Medical College, Kolkata 700 004, India
4 Department of Radiology & Radiodiagnosis, Burdwan Medical College & Hospital, Burdwan, India
5 Department of Biotechnology, Burdwan University, Burdwan; Department of Biotechnology, Haldia Institute of Technology, Haldia 721 657, West Bengal, India
6 Department of Biochemistry, Burdwan Medical College & Hospital, Burdwan; Department of Biochemistry, R.G. Kar Medical College, Kolkata 700 004, India
7 Department of Forensic Medicine & Toxicology, North Bengal Medical College & Hospital, Susrutanagar; North Bengal Medical College, Siliguri 734 012, India
8 Department of Biochemistry, Burdwan Medical College & Hospital, Burdwan, India

Correspondence Address:
Ushasi Banerjee
Assistant Professor, Department of Biochemistry, Calcutta National Medical College, Kolkata 700 014, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-5916.191990

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Background & objectives: Insulin resistance (IR) is a major confounding factor in polycystic ovarian syndrome (PCOS) irrespective of obesity. Its exact mechanism remains elusive till now. C/T polymorphism in the -34 promoter region of the CYP17 gene is inconsistently attributed to elucidate the mechanism of IR and its link to hyperandrogenemia in obese PCOS patients. In the present study we aimed to evaluate any association of this polymorphism with IR in non-obese women with PCOS. Methods: Polymorphism study was performed by restriction fragment length polymorphism (RFLP) analysis of the Msp A1 digest of the PCR product of the target gene in 75 PCOS cases against 73 age and BMI matched control women. Serum testosterone, BMI and HOMA-IR (homeostatic model of assessment-insulin resistance) were analyzed by standard techniques. A realistic cut-off value for the HOMA-IR was obtained through receiver operating characteristic (ROC) curve for exploring any possible link between IR and T/C polymorphism in the case group. Results: Significant increases in serum testosterone and HOMA-IR values were observed among the case group (P<0.001) without any significant elevation in BMI and FBG compared to controls. Cut-off value for IR in the PCOS patients was 1.40 against a maximum sensitivity of 0.83 and a minimum false positivity of 0.13. The analysis revealed an inconclusive link between the C/T polymorphic distribution and insulin resistant case subjects. Interpretation & conclusions: The results showed that CYP17A1 gene was not conclusively linked to either IR or its associated increased androgen secretion in non-obese women with PCOS. We propose that an increased sensitivity of insulin on the ovarian cells may be the predominant reason for the clinical effects and symptoms of androgen excess observed in non-obese PCOS patients in our region.


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