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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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Psoriasis is a chronic inflammatory disease associated with an increased insulin resistance, obesity and cardiovascular risk. The present study was aimed to assess insulin resistance and pattern of body fat deposition in psoriasis. Body mass index (BMI) and waist circumference (WC) were measured in 40 psoriatic patients and 46 age- and sex-matched control subjects. Fasting blood glucose (FBG) and serum insulin level were measured by standard photometric method and ELISA respectively. HOMA-IR (homeostatic model of insulin resistance) was calculated by appropriate software. The results indicated that case and control groups were comparable in terms of age and sex (p = 0.934) with an increased prevalence of psoriasis among male subjects (60 %). FBG and mean WC between the two groups were statistically not significant (p value = 0.271 and 0.21 respectively). BMI was significantly higher in case group compared to the control group (p = 0.049). Serum insulin level and insulin resistance in the psoriatic patients were significantly higher (p value <0.001). Multiple regression analysis revealed that insulin resistance (measured by HOMA) was dependent on BMI and WC at a significance level of p < 0.001 and 0.043 respectively. Therefore, the psoriatic patients in this region have significantly high amount of fasting serum insulin level along with an increased IR though their FBG level remains normal. Furthermore, these abnormalities are significantly dependent on total body fat as well as abdominal fat deposits. We suggest that psoriatic patients need to be evaluated for metabolic syndrome and managed accordingly.