Early detection of risk factors for enhanced primary prevention and novel therapies for treating the chronic consequences of cardiovascular disease are of the utmost importance for reducing morbidity. Recently, fibroblast growth factors (FGFs) have been intensively studied as potential new molecules in the prevention and treatment of cardiovascular disease mainly attributable to metabolic effects and angiogenic actions. Members of the endocrine FGF family have been shown to increase metabolic rate, decrease adiposity, and restore glucose homeostasis, suggesting a multiple metabolic role. Serum levels of FGFs have been associated with established cardiovascular risk factors as well as with the severity and extent of coronary artery disease and could be useful for prediction of cardiovascular death. Furthermore, preclinical investigations and clinical trials have tested FGF administration for therapeutic angiogenesis in ischemic vascular disease, demonstrating a potential role in improving angina and limb function. FGF21 has lately emerged as a potent metabolic regulator with multiple effects that ultimately improve the lipoprotein profile. Early studies show that FGF21 is associated with the presence of atherosclerosis and may play a protective role against plaque formation by improving endothelial function. The present review highlights recent investigations suggesting that FGFs, in particular FGF21, may be useful as markers of cardiovascular risk and may also serve as protective/therapeutic agents in cardiovascular disease.

ObjectivePolycystic ovary syndrome (PCOS) is a common endocrine disorder of premenopausal women, characterized by hyperandrogenism, polycystic ovaries, and chronic anovulation along with insulin resistance and abdominal obesity as frequent metabolic traits. Although, PCOS manifests clinically during adolescence, emerging data suggest that the natural history of PCOS may originate in intrauterine life. Evidence AcquisitionEvidence from experimental, clinical, and genetic research supporting the hypothesis for the fetal origins of PCOS has been analyzed. Evidence SynthesisFemale primates, exposed in utero to androgen excess, exhibit the phenotypic features of PCOS during adult life. Clinical observations also support a potential fetal origin of PCOS. Women with fetal androgen excess disorders, including congenital 21-hydroxylase deficiency and congenital adrenal virilizing tumors, develop features characteristic of PCOS during adulthood despite the normalization of androgen excess after birth. The potential mechanisms of fetal androgen excess leading to a PCOS phenotype in humans are not clearly understood. However, maternal and/or fetal hyperandrogenism can provide a plausible mechanism for fetal programming of PCOS, and this, in part, may be genetically determined. Thus, genetic association studies have indicated that common polymorphic variants of genes determining androgen activity or genes that influence the availability of androgens to target tissues are associated with PCOS and increased androgen levels. These genomic variants may provide the genetic link to prenatal androgenization in human PCOS. ConclusionPrenatal androgenization of the female fetus induced by genetic and environmental factors, or the interaction of both, may program differentiating target tissues toward the development of PCOS phenotype in adult life. ABSTRACT ObjectiveTo perform a review and meta-analysis of the studies evaluating the status of serum inflammatory markers in women with polycystic ovary syndrome (PCOS). DesignSystematic review and meta-analysis of articles published in English before January 2010 and identified using the PubMed search engine. SettingAcademic hospital. Patient(s)Women with PCOS and appropriate controls. Intervention(s)Measurement of serum concentrations of inflammatory markers by high-sensitivity techniques. Main Outcome Measure(s)Meta-analyses of the mean difference in serum C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) concentrations among patients with PCOS and appropriate controls, applying random-effects models to limit interstudy variability and using appropriate estimates of evidence dissemination bias. Result(s)Meta-analysis of the 31 articles meeting inclusion criteria showed that circulating CRP was 96% higher in women with PCOS compared to controls (95% confidence interval, 71%-122%; z = 7.32) without evidence of dissemination bias (Egger's regression intercept, 0.45; 95% confidence interval, -2.30 to 3.21). These findings persisted after excluding five studie...

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Adiponectin represents one of the most abundant and well-studied adipokines that has been implicated as a major protective factor against the adverse metabolic and cardiovascular consequences of obesity. The main insulin-sensitizing action of adiponectin results from decrease in hepatic gluconeogenesis and increase in muscle glucose transport and, secondly from enhancement of energy consumption and fatty acid oxidation in peripheral tissues with the aim of increasing ATP production. Besides these effects, the potential role of adiponectin on insulin secretion, as well as on energy expenditure, through central action, has also been investigated. Accumulating evidence from clinical, experimental animal and genetic studies support a close association between hypoadiponectinemia and insulin resistance/ type 2 diabetes. The question that arises is whether hypoadiponectinemia is the result of insulin resistance/type 2 diabetes or the cause of this disorder. Based on the observation that various drug classes exert beneficial effects on insulin resistance partly by increasing plasma adiponectin levels, it could hypothesized that substances that enhance or mimic adiponectin to activate its receptors and/or postreceptor signaling pathway may be a promising therapeutic strategy in the prevention and treatment of diabetes. However, many questions need to be addressed before adiponectin can be used as a potent therapeutic target.

This report highlights the fact that in case of simultaneous presentation of polyendocrinopathies and renal disease early in childhood, KSS should be considered.