Exercise and Polycystic Ovary Syndrome.

Polycystic ovary syndrome (PCOS) is a complex endocrinopathy affecting both the metabolism and reproductive system of women of reproductive age. Prevalence ranges from 6.1-19.9% depending on the criteria used to give a diagnosis. PCOS accounts for approximately 80% of women with anovulatory infer-tility, and causes disruption at various stages of the reproductive axis. Evidence suggests lifestyle modification should be the first line of therapy for women with PCOS. Several studies have examined the impact of exercise interventions on reproductive function, with results indicating improvements in menstrual and/or ovulation frequency following exercise. Enhanced insulin sensitivity underpins the mechanisms of how exercise restores reproductive function. Women with PCOS typically have a cluster of metabolic abnormalities that are risk factors for CVD. There is irrefutable evidence that exercise mitigates CVD risk factors in women with PCOS. The mechanism by which exercise improves many CVD risk factors is again associated with improved insulin sensitivity and decreased hyperinsulinemia. In addition to cardiometabolic and reproductive complications, PCOS has been associated with an increased prevalence of mental health disorders. Exercise improves psychological well-being in women with PCOS, dependent on certain physiological factors. An optimal dose-response relationship to exercise in PCOS may not be feasible because of the highly individualised characteristics of the disorder. Guidelines for PCOS suggest at least 150 min of physical activity per week. Evidence confirms that this should form the basis of any clinician or healthcare professional prescription

Congenic mapping identifies a novel Idd9 subregion regulating type 1 diabetes in NOD mice

Type 1 diabetes (T1D) results from complex interactions between genetic and environmental factors. The nonobese diabetic (NOD) mouse develops spontaneous T1D and has been used extensively to study the genetic control of this disease. T1D is suppressed in NOD mice congenic for the C57BL/10 (B10)-derived Idd9 resistance region on chromosome 4. Previous studies conducted by other investigators have identified four subregions (Idd9.1, Idd9.2, Idd9.3, and Idd9.4) where B10-drived genes suppress T1D development in NOD mice. We independently generated and characterized six congenic strains containing B10-derived intervals that partially overlap with the Idd9.1 and Idd9.4 regions. T1D incidence studies have revealed a new B10-derived resistance region proximal to Idd9.1. Our results also indicated that a B10-derived gene(s) within the Idd9.4 region suppressed the diabetogenic activity of CD4 T cells and promoted CD103 expression on regulatory T cells indicative of an activated phenotype. In addition, we suggest the presence of a B10-derived susceptibility gene(s) in the Idd9.1/Idd9.4 region. These results provide additional information to improve our understanding of the complex genetic control by the Idd9 region