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Ovarian hyperstimulation syndrome (OHSS) is a complication of pregnancy caused by an excessive response to follicle-stimulating hormone (FSH). OHSS can arise spontaneously or after exogenous FSH administration duringin vitrofertilization procedures. Novel genetic predictors of OHSS, including mutations and polymorphisms of the FSH receptor, are described in this Viewpoint.
Prader–Willi syndrome (PWS) is associated with uncontrolled appetite and morbid obesity. Management of PWS is particularly challenging and requires the involvement of both the family and health-care providers, as well as the affected individual. In this Viewpoint the efficacy of the strategies currently used to control obesity in PWS is discussed.
Oxyntomodulin and peptide tyrosine–tyrosine are gut hormones that act as satiety signals and decrease food intake; oxyntomodulin may also increase energy expenditure. Studies in humans show these effects in normal-weight and overweight volunteers; these peptides and their derivatives are, therefore, potential therapies for conditions such as obesity.
Most tissues express glucocorticoid receptors but tissue-specific modulation of this receptor affects homeostasis, immune responses and cell differentiation mediated by glucocorticoids. This Review describes the mechanisms involved—including nucleocytoplasmic shuttling, degradation and gene polymorphisms—and details the effects on the metabolic syndrome.
Many of the genes involved in development of adrenocortical tumors have been identified, and their effects on well-known signaling pathways (for example those involving cyclic AMP or β-catenin and Wnt) have been investigated. These advances have important implications for understanding disease development, identifying molecular markers and designing new therapeutic strategies for adrenocortical tumors.