Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism and hyperinsulinaemia. Despite being one of the most common endocrine disorders in women of reproductive age, understanding of the disorder and effective treatments is still lacking. In a rat model of PCOS, researchers have now determined that exercise activates the phosphoinositide 3-kinase (PI3K)–protein kinase B (PKB, also known as AKT) pathway by reducing the expression of 5α-reductase type 1 (5αR1; an enzyme that regulates androgen levels).

Chuyan Wu and co-workers generated the rat model by injecting 21-day old Wistar female rats with testosterone propionate for 28 days, while feeding them a high-fat diet. The rats were then divided into seven groups: sedentary; sedentary and 5αR1 inhibitor (5αR1I); sedentary and 5αR2I; exercise; exercise and 5αR1I; exercise and 5αR2I; and control (no PCOS). The exercised rats swam for 120 min per day, 6 days a week for 2 weeks. At the end of the treatment period, blood and skeletal muscle samples were taken and Western blots were used to determine expression levels of 5αR and phosphorylation levels of PI3K and AKT.

The researchers found that the ‘sedentary’, ‘sedentary and 5αR1I’, ‘sedentary and 5αR2I’ and ‘exercise and 5αR1I’ groups had increased levels of 5αR1 compared with the control group. The expression of 5αR1 was reduced in the ‘sedentary and 5αR1I’, ‘exercise’, ‘exercise and 5αR1I’ and ‘exercise and 5αR2I’ groups compared with the sedentary group. In addition, the ‘sedentary’ and ‘exercise and 5αR1I’ groups had reduced phosphorylation of PI3K and AKT, whereas the ‘exercise and 5αR2I’ group had increased phosphorylation levels. The researchers therefore suggest that exercise activates the signalling pathways involved in glucose metabolism in the skeletal muscle of rats with PCOS by reducing the expression of 5αR1.