No abstract

The aim of this study is to evaluate whether ultrasonographic visceral fat thickness measurement in the early gestational period is useful for predicting the development of gestational diabetes mellitus (GDM) and metabolic syndrome (MS). The visceral fat thickness and subcutaneous fat thickness were measured via ultrasound at the first prenatal visit. The correlation between visceral and subcutaneous fat thickness and MS parameters, such as dyslipidemia, hypertension, and insulin resistance, was assessed. We also compared the use of visceral fat thickness measurement with body mass index (BMI) and waist circumference (WC) measurements for predicting the development of GDM. The subcutaneous fat thickness was found to be similar in the normal glucose metabolism and GDM groups at the first visit, whereas the visceral fat thickness was found to be considerably higher in the GDM groups (p = 0.04). The visceral fat thickness in the early stage of the gestation was correlated with hyperglycemia, dyslipidemia, high diastolic blood pressure, and insulin resistance. In contrast to subcutaneous fat thickness, BMI, and WC, only the visceral fat thickness was correlated with insulin resistance. The subcutaneous and visceral fat thicknesses at the first visit were significantly higher in the MS group (p = 0.02). There was a good correlation between visceral and subcutaneous fat thicknesses (r = 0.492, p < 0.001); however, there were poor correlations between visceral fat thickness and BMI and WC (r = 0.338, p = 0.01; r = 0.312, p = 0.02). The visceral fat thickness seemed to be a more sensitive predictor of GDM than WC and BMI. The optimal cutoff points for predicting GDM were visceral fat thickness 19.5 mm [area under curve (AUC) = 0.66, p = 0.043], WC 103.5 cm (AUC = 0.64, p = 0.079), and BMI 34.5 (AUC = 0.64, p = 0.069). Ultrasonographic visceral fat thickness measurement in the early period of gestation may be an easy, safe, and cost-effective scan test for predicting the development of metabolic diseases and GDM.

With the exception of ESR, demographic, clinical, laboratory, and imaging findings and prognoses of our patients were comparable to the previous reports.

In our study, because those participants were young and non- obese patients with PCOS, malondialdehyde, nitric oxide and disulfide levels and Carotid Artery Intima-Media Thickness measurements as a pre-indicator of cardiovascular disease were not found to be different from those of the controls.

No abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women. Experimental research and clinical observations suggest that PCOS may originate in the very early stages of development, possibly even during intrauterine life. This suggests that PCOS is either genetically-transmitted or is due to epigenetic alterations that develop in the intrauterine microenvironment. Although familial cases support the role of genetic factors, no specific genetic pattern has been defined in PCOS. Several candidate genes have been implicated in its pathogenesis, but none can specifically be implicated in PCOS development. Hypotheses based on the impact of the intrauterine environment on PCOS development can be grouped into two categories. The first is the "thrifty" phenotype hypothesis, which states that intrauterine nutritional restriction in fetuses causes decreased insulin secretion and, as a compensatory mechanism, insulin resistance. Additionally, an impaired nutritional environment can affect the methylation of some specific genes, which can also trigger PCOS. The second hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues, causing the PCOS phenotype to develop in adult life. This review aimed to examine the role of fetal programming in development of PCOS.

Gene polymorphism of IL-6 -174 G>C is a risk factor for PCOS in Turkish patients. IL-6 gene polymorphisms are not related to NO, MDA, and SH levels in PCOS. Our negative results in risks factors of CV disorders can probably be explained by the fact that metabolic parameters and endothelial systems of patients may not yet be affected in this short period of time.

We aimed to evaluate the relationship between 174 promoter region of the interleukin-6 (IL-6) C/G gene polymorphism and high sensitive C-reactive protein (hs-CRP), fibrinogen and carotis intima-media thickness (CIMT), body mass index, homeostatic model assessment (HOMA) insulin resistance index, serum lipid parameters, in polycystic ovary syndrome (PCOS) patients carrying a potential risk for developing cardiovascular disease (CVD). We studied 88 PCOS patients and 119 healthy controls. PCOS was defined by the Rotterdam PCOS consensus criteria. The genotype IL-6 distribution did differ between the control group (CC 10.1%, GC 63.0%, GG 29.6%) and the PCOS patients (CC 5.7%, GC 29.5%, GG 64.8%) (P < 0.001). The frequency of the polymorphic G allele was also no similar for the group with PCOS as for the control group with 79.5% and 58.4% respectively (P < 0.001). Both in PCOS patients and in control group, no statistically significant difference was determined between C/C, G/C and G/G, and blood cholesterol levels, triglyceride levels, high-density lipoprotein levels, low density lipoprotein levels, fasting blood sugar levels, insulin levels, HOMA values, CIMT measurements either on the right or left side, hs-CRP, f-testosterone, fibrinogen and 17 alpha-hydroxy-progesterone levels (P > 0.05). Gene polymorphism of IL-6 -174 G>C is a risk factor for PCOS in Turkish patients, but we found no relationship between the cardiovascular risk factors and IL-6 -174 G>C gene polymorphism in women with PCOS and healthy subjects. Our negative results in risk factors of CVD can probably be explained by the fact that metabolic parameters and endothelial systems of patients may not yet be affected in this short time of period.