The effect of γ-linolenic acid on Polycystic Ovary Syndrome associated Focal Segmental Glomerulosclerosis via TGF-β pathway.

BACKGROUND

In recent years, female infertility from Polycystic Ovary Syndrome (PCOS) has gained scientific interest. PCOS alters the metabolic and endocrine functioning in females. The elevation in androgens can damage the androgen receptors present on the kidney giving rise to renal disorders like Focal Segmental Glomerulosclerosis (FSGS). Transforming Growth Factor Beta (TGF-β) in the ovary is activated by activin for Follicle Stimulating Hormone (FSH) secretion and in the kidney by thrombospondin 1 (TSP1) for cell growth and apoptosis. Studies show that gamma-linolenic acid (GLA) effectively treats breast cancer, eczema, inflammatory conditions and PCOS.

AIM

The study aimed to find out the possibility of FSGS development in PCOS and to understand the effect of GLA on FSGS via the TGF-β pathway.

METHOD

To carry out the study, the dehydroepiandrosterone (DHEA) induced PCOS model was used. Three groups namely vehicle control, DHEA, and DHEA+GLA, were used with six animals in each. TGF-β1, TGF-β2, and TSP1 genes were studied using real-time PCR.

RESULTS

The study showed an increase in the level of renal fibrosis biomarker, TSP1, in the DHEA group, which was further decreased by an anti-inflammatory agent, GLA. The TGF-β1 and TGF-β2 genes associated with the TGF-β pathway were seen to be increased in DHEA-induced PCOS rats which showed a possible relation between the two conditions.

CONCLUSION

The study shows a possible development of renal fibrosis in the DHEA-induced PCOS model. The GLA might act as a ligand to regulate TGF-β signaling in glomerulosclerosis in a DHEA-induced PCOS model.