Plasma visfatin concentrations in polycystic ovary syndrome: relationships with indices of insulin resistance and hyperandrogenism

Visfatin, a protein secreted by adipose tissue, is suggested play a role in pathogenesis of insulin resistance. In polycystic ovary syndrome [PCOS], insulin resistance might be involved in the development of endocrine and metabolic abnormalities. The aim of the study was to measure plasma visfatin levels in PCOS women and to assess the relationship between plasma visfatin concentration and indices of insulin resistance and markers of hyperandrogenism in PCOS patients. A total of 50 women were studied. Twenty five women had PCOS, and the remaining 25 were healthy women with regular menstrual cycles who served as control subjects. Blood samples were collected between the 3 rd and the 5 th days of a menstrual cycle in the control group and 3-5 days after a spontaneous menses, or independent of cycle phase in the presence of amenorrhea in the PCOS group for estimation of insulin, glucose, lipid parameters, sex-hormone and visfatin levels. Plasma visfatin concentrations were significantly higher in the PCOS group [72.94 +/- 33.3ng/ml] than in the control group [54.69 +/- 3l.5ng/ml] [p= 0.039]. The PCOS group had higher insulin resistance [HOMA-lR] [3.12 +/- 0.98] in comparison to the control group [2.27 +/- 0. 68] [p=0.017]. In the PCOS group, plasma visfatin levels were found to be positively correlated with BMI and waist circumference, HOMA-lR as well as with free androgen index, and negatively correlated with LH, total testosterone and sex hormone-binding globulin[SHBG] levels. In the whole study group, plasma vislatin levels was positively correlated with BMI and waist circumference, FSH and SHBG levels as well as with free androgen index, and negatively correlated with LH, total testosterone values. Visfatin levels are increased in women with PCOS compared to healthy controls. Visfatin is associated with insulin resistance in PCOS patients. Positive correlation found between visfatin and free androgen index in PCOS patients

Searching for optimal serum marker for early prediction of gestational diabetes

To examine which serum marker [sex hormone binding globulin [SHBG], C-reactive protein [CRP], insulin. glucose] is accurate in early predicting the occurrence of GDM. One hundred and fifty six pregnant mothers high risk to develop gestational diabetes mellitus [GDM] were included in the study. When GDM was excluded at hooking setting [using OGTT], mothers are candidate for assaying fasting and non fasting sex hormone binding globulin [SHBO], fasting and non fasting quantitative C-reactive protein [CRP] and fasting insulin levels [from the same blood samples withdrawn during performing the OGTT], OGTT was repeated at 28 weeks and 36 weeks of gestation to diagnose GDM. According to the results of follow up OGTT, participant were divided into cases who developed GDM and those who did not develop GDM to assess the accuracy of each of the studied markers in predicting the occurrence of 0DM in high risk mothers. Sex hormone binding globulin levels [fasting and non fasting] were significantly lower among women who subsequently developed GDM compared with the control group [[276.9 +/- 78.7nmol/L vs 322.4 +/- 71.6nmol/L, P=0.001], [261.5 +/- 66.7 nmol/L vs 299 +/- 59.7 nmol/L, P0.00l] respectively]. No difference was detected in C-reactive protein levels [fasting and non lasting] [P=0.33, 0.349], fasting insulin [P0.082], lasting glucose levels [P=0.119], between the study group who subsequently developed GDM and the control group. SHBG can he used as an early marker to identify the group at highest risk for subsequent GDM allowing earlier intervention and possible benefits to the mothers and their offspring

Serum resistin as a predictor of ovarian response to clomiphene therapy in PCOS infertile patients

To measure serum resistin levels on day 3-6 of the menstrual cycle of infertile women with Polycystic ovary syndrome [PCOS] undergoing induction of ovulation using clomiphene citrate [CC] to ascertain whether these levels could allow us to predict the ovarian response to CC in those patients. 40 women with the diagnosis of infertility due to polycystic ovary syndrome [PCOS], were included in the study. Participants were included after fulfilling the Rotterdam criteria, 2004. All included participants were investigated by measuring body mass index [BMI], serum follicle stimulating hormone [FSH], serum luteinizing hormone [LH], serum fasting glucose, serum fasting insulin, fasting glucose-to-insulin ratio and serum resistin levels. Participants were treated with clomiphene citrate protocol to induce ovulation. Clomiphene was started as 100mg/day [2 tablets of 50mg] at day 2 for 5 consecutive days for 3 cycles. Ovulation was assessed by midluteal serum progesterone measurement combined with transvaginal sonographic monitoring of follicle growth until the appearance of a preo-vulatory follicle [mean diameter, >/= 18mm] and subsequent follicle rupture. According to the final ovarian response [which is the primary outcome], the study participants were divided into proper response group [ovulation has occurred at least once under treatment during the treatment period] and poor response group [ovulation has never occurred during the 3 study cycles]. Serum resistin was compared between the 2 outcome groups to test its relation to ovarian response. No significant correlation was found between the 2 outcome groups [proper and poor responders] regarding body mass index [BMI], 28.76 +/- 4.86, 29.13 +/- 5.09 respectively, p=0.817. Similarly no statistically significant difference was found between the 2 outcome groups regarding serum LH, FSH, total testosterone levels [p=0.437, 0.327, 0.672 respectively]. Serum fasting glucose, fasting insulin, fasting glucose-to-insulin ratio were not statistically significant when compared between the outcome groups [p=0.456, 0.108, 0.191 respectively]. Serum resistin levels in women who succeeded to ovulate and those who failed to ovulate under clomiphene therapy were not statistically significant when compared between both groups [22.16 +/- 21.6, 24.37 +/- 22.9, respectively, p=0.757]. However, serum resistin levels were positively correlated to serum total testosterone, fasting serum glucose and insulin levels [p=0.008, 0.024, 0.011 respectively]. Serum resistin is likely not a predictor for ovarian response in infertile women with PCOS undergoing induction of ovulation using CC

endothelial nitric oxide synthase gene intron 4 polymorphism in Egyptian patients with end-stage renal disease

Nitric oxide [NO] synthesized by endothelial cell NO synthase [ecNOS] is a potent regulator of intrarenal haemodynamics. A polymorphism in intron 4 of the ecNOS gene is a candidate gene in renal diseases. The aim of this work is to study the gene polymorphism of ecNOS intron 4 in patients with end-stage renal failure and compared it with that of healthy subjects. The study was performed on 40 patients with end stage renal disease [ESRD] patients on regular hemodialysis, and was classified into 2 groups: Group I ESRD patients with diabetic nephropathy [10 patients] and group II includes 30 patients with ESRD due to different etiologies [all causes except diabetic nephropathy], and group III 15 apparently healthy subjects as control group. ecNOS genotypes were determined using polymerase chain reaction. The results showed that two alleles of ecNOS intron 4, labeled a and b could be detected. The frequencies of aa, ba, bb genotypes were 5% [2/40], 12.5% [5/40] 82.5% [33/40] in all the patients, 3.3% [1/30], 13.3% [4/30], 83.3% [25/30] in-group II patients, and 10% [1/10], 10% [1/10] 80% [8/10] in group I patients respectively, and in the control group all were bb100% [15/15]. There is significant difference in the frequencies of ecNOS genotypes between all ESRD patients and the control group [OR 1.423; 95% CI 1.253-1.615, p<0.01]. Compared with controls; the group I patients had much higher frequency of the ecNOS 4a allele than in-group II patients [OR 2.765, 1.556, 95% CI 1.891-4.042, 1.423-1.615, p<0.001, p<0.01] respectively. There was a significantly higher frequency of the ecNOS 4a allele among ESRD patients both diabetic and non-diabetic than in control subjects. This suggests that the ecNOS gene polymorphism in intron 4 appears to be prognostic of renal failure and the ecNOS gene polymorphism in intron 4 is a useful parameter for studying the relationship between NO and the progression of renal failure. This suggests that the ecNOS gene polymorphism might be associated with an increased risk of chronic renal failure