Consumption of soya isoflavones improved polycystic ovary syndrome-associated metabolic disorders in a rat model

Abstract

Polycystic ovary syndrome is associated with increased risks for certain metabolic disorders such as insulin resistance, non-alcoholic fatty liver disease and suppressed ovarian follicular development. This study aimed to examine whether soya isoflavones (ISF) mitigate these polycystic ovary syndrome-associated metabolic disorders in a rat model. Weanling Sprague-Dawley female rats were randomly divided into six groups and were treated with either 0 or 83 µg/d dihydrotestosterone (DHT) to induce polycystic ovary syndrome and fed diets containing 0, 0·5, or 1 g ISF/kg diet for 8 weeks. DHT treatment increased food intake, body weight gain (P < 0·001), percentage of primordial follicles (60 % v. 50·9 %, P < 0·05) and accumulation of lipid droplets in the livers. It also elevated serum total cholesterol, free cholesterol, TAG, NEFA and leptin and hepatic total cholesterol and NEFA. Additionally, DHT treatment reduced the percentage of primary follicles (13·8 % v. 30·2 %, P < 0·05), ovary weight and length (P < 0·001), as well as insulin sensitivity (P < 0·01) compared with the Control. ISF intake at 1 g/kg reduced body weight gain, serum total cholesterol, free cholesterol, NEFA, leptin and hepatic TAG and DHT-induced insulin resistance (P < 0·01). ISF intake at both levels decreased DHT-induced lipid droplet accumulation in the livers and changes in the percentages of primordial and primary follicles. Dietary soya ISF alleviated DHT-induced body weight gain, insulin resistance and hepatic lipid droplet accumulation, as well as suppressed ovarian follicular development. This suggests that the consumption of soya foods or ISF supplements may be beneficial for individuals with polycystic ovary syndrome, mitigating the associated metabolic disorders such as diabetes and non-alcoholic fatty liver disease.

Keywords: Insulin resistance; Non-alcoholic fatty liver disease; Polycystic ovary syndrome; Rat; Soya isoflavones.

Fig. 1.

Body weight gain (a), food intake (b), ovary weight (c) and length (d) of the rats treated with 0 µg/d (Control, open bars) or 83 µg/d (DHT, solid bars) of dihydrotestosterone and fed diets containing 0, 0·5, or 1 g/kg diet of soya isoflavones for 8 weeks. Values are mean (sem), n 8. Means with different letters within Control or DHT groups differ, P < 0·05.

Fig. 2.

Plasma glucose levels (a) and insulin sensitivity (b) of the rats treated with 0 µg/d (Control, open bars) or 83 µg/d (DHT, solid bars) of dihydrotestosterone and fed diets containing either 0, 0·5, or 1 g/kg diet of soya isoflavones for 8 weeks. Values are mean (sem), n 8. Means with different letters within Control or DHT groups differ, P < 0·05.

Fig. 3.

Histomorphology of the liver after stained with haematoxylin and eosin (a) or oil red O staining (b) in the rats treated with 0 µg/d (Control) or 83 µg/d dihydrotestosterone (DHT) and fed diets containing either 0, 0·5 or 1 g/kg diet of soya isoflavones (ISF) for 8 weeks. The total areas of lipid droplets in the liver sections were measured (c). The images shown are representatives of ten replicates of each treatment group. Values are mean (sem), n 3. Means with different letters within Control or DHT groups differ, P < 0·05.

Fig. 4.

Ovary histomorphology with haematoxylin and eosin staining in the rats treated with 0 µg/d (Control, open bars) or 83 µg/d (DHT, solid bars) of dihydrotestosterone and fed diets containing either 0, 0·5, or 1 g/kg diet of soya isoflavones for 8 weeks. The images shown are representatives of ten replicates of each treatment group. n 3. ISF, isoflavones.

Fig. 5.

Percentages of the rats with regular oestrous cycle measured in the last 2 weeks prior to the end of the 8 weeks’ treatment with 0 µg/d (Control, open bars) or 83 µg/d (DHT, solid bars) of dihydrotestosterone and fed diets containing either 0, 0·5 or 1 g/kg diet of soya isoflavones. n 8.