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.
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.
Vaginal bleeding in postmenopausal women is indicative of a wide array of gynecological pathologies, including endometrial carcinoma. However, uterine fibroids, pelvic masses, or even endometrial cancer may develop without co-morbid vaginal bleeding. Therefore we advocate that postmenopausal women should undergo yearly screening and consultation, without waiting for an episode of vaginal bleeding.
PurposeTo evaluate the efficacy of myo-inositol (MI) pretreatment in OHSS.MethodsIn this experimental OHSS rat model, 42 immature Wistar albino female rats were divided into 6 groups: (1) the control group, (2) the ovarian stimulation group, (3) the OHSS group, (4) the OHSS + Metformin group, (5) OHSS + MI group, (6) OHSS + Metformin + MI group. OHSS was established after treatment with metformin and myo-inositol for 14 days, in the meanwhile the treatment of metformin and myo-inositol was also continued. All animals were killed 48 h after hCG administration and were compared in terms of vascular permeability, ovarian weight and diameter, ovarian VEGF, COX-2 and PEDF expression (immunohistochemistry), serum PEDF and estradiol (E2) levels.ResultsVascular permeability, VEGF and COX-2 expressions were reduced in animals treated with MI and/or metformin. While PEDF expression was increased in the groups taking metformin, there was no difference in PEDF expression in the group taking MI and OHSS group. There was no significant difference in serum PEDF levels between groups. Blood E2 levels were decreased in groups treated with MI or metformin compared to the OHSS group.ConclusionsOur data demonstrate that myo-inositol is effective in preventing OHSS, similar to metformin. Although the two drugs are thought to act through distinct mechanisms, there is no apparent benefit to co-treatment with both drugs in an animal model of OHSS. Administration of myo-inositol prior to IVF treatment may favor the control of ovulation induction. Further studies are necessary to elucidate the mechanism of action and further support our findings.
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