Serum preptin levels were significantly higher in women with PCOS compared with controls. This peptide might be an independent predictor of PCOS in the future.

Among new peptides responsible for the pathogenesis of metabolic disorders and carbohydrate metabolism, adipokines are of great importance. Adipokines are substances of hormonal character, secreted by adipose tissue. Apart from the well-known adipokines, adropin and preptin are relatively newly discovered, hence their function is not fully understood. They are peptides not secreted by adipose tissue but their role in the metabolic regulations seems to be significant. Preptin is a 34-amino acid peptide, a derivative of proinsulin growth factor II (pro-IGF-II), secreted by pancreatic β cells, considered to be a physiological enhancer of insulin secretion. Additionally, preptin has a stimulating effect on osteoblasts, inducing their proliferation, differentiation and survival. Adropin is a 76-amino acid peptide, encoded by the energy homeostasis associated gene (Enho), mainly in liver and brain, and its expression is dependent on a diet. Adropin is believed to play an important role in metabolic homeostasis, fatty acids metabolism control, insulin resistance prevention, dyslipidemia, and impaired glucose tolerance. The results of studies conducted so far show that the diseases resulting from metabolic syndrome, such as obesity, type 2 diabetes mellitus, polycystic ovary syndrome, non-alcoholic fatty liver disease, or cardiovascular disease are accompanied by significant changes in the concentration of these peptides. It is also important to note that preptin has an anabolic effect on bone tissue, which might be preventive in osteoporosis.

Introduction: Women with polycystic ovary syndrome (PCOS) frequently develop metabolic complications. Among the newly found factors responsible for metabolic disorders, adropin seems to be of a great significance. Material and methods: In total 134 women aged 17-45 years were enrolled. The PCOS group consisted of 73 women, diagnosed on the basis of Executive Committee of the European Society of Human Reproduction and Embryology -American Society for Reproductive Medicine (ESHRE-ASRM) criteria. All PCOS women presented phenotype A of PCOS. The control group consisted of 61 women with regular menstrual cycles, matched for nutritional status. All women underwent anamnesis, physical examination, anthropometric measurements, abdominal and transvaginal ultrasound, and dual-energy X-ray absorptiometry (DXA). Serum adropin levels were determined by ELISA. Biochemical [fasting glucose and insulin, oral glucose tolerance test, lipid and sex hormone-binding globulin (SHBG)] and hormonal (testosterone, androstenedione, luteinizing hormone, follicle-stimulating hormone and oestradiol) measurements were performed. Insulin resistance indices [(Homeostasis Model Assessment for Insulin Resistance (HOMA-IR), Quantitative Insulin Sensitivity Check Index (QUICKI), Matsuda] and free androgen index (FAI) were calculated according to the standard formula. Results: Serum adropin levels were lower in the PCOS group (0.475 ± 0.200 vs. 0.541 ± 0.220, p = 0.069), but the results were not statistically significant. Positive correlations among adropin and androstenedione levels were observed in the PCOS group (r = 0.27, p = 0.025). Conclusions: Women with PCOS have a different metabolic profile in comparison to women without this syndrome. We did not observe a statistically significant difference in adropin concentration between the PCOS and the healthy control group. Therefore, more studies regarding adropin in PCOS are needed. (Endokrynol Pol 2019; 70 (2): 151-156)

Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies in reproductive-aged women. The pathogenesis of this syndrome is not yet fully understood. Previous studies indicate the coexistence of low-grade chronic inflammation and PCOS. Toll-like receptors (TLRs) play a key role in the inflammatory reactions. They induce an innate immune response when in contact with pathogen-associated molecular patterns (PAMP). TLRs expression on several cell types has been described, including immune cells, epithelial and endothelial cells, adipocytes, pancreatic beta-cells and ovarian tissue. The stimulation of TLRs triggers signaling pathways, which in turn leads to proinflammatory cytokines production, including IL-6 and TNF alpha. Elevated concentrations of these cytokines were also observed in patients with PCOS. Currently, there are few studies about the role of TLRs in the pathogenesis of PCOS. Women with this syndrome are more frequently diagnosed with metabolic disorders, such as obesity or insulin resistance (IR). The substances released from adipose tissue, including free fatty acids, contribute to the increased activation of the two TLRs - 2 and 4. Recent data also confirms their overexpression in women with PCOS. Increased activation and the presence of specific gene polymorphisms for TLR2 and TLR4 is presumed to be a contributor to the development of IR and hyperandrogenism in women with PCOS.

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