Abstract

Background Diaphanous related formin 1 (DIAPH1) is a novel component of advanced glycation end product (AGE) signal transduction that was recently found to participate in diabetes-related disorders, obesity, and androgen hormones. We investigated whether plasma DIAPH1 levels were a potential prognostic predictor for polycystic ovary syndrome (PCOS). Methods The levels of circulating plasma DIAPH1 and indicators of glucose, insulin, lipid metabolism, liver enzymes, kidney function, sex hormones, and inflammation were measured in 75 patients with PCOS and 77 healthy participants. All of the participants were divided into normal-weight (NW) and overweight/obese (OW) subgroups. Statistical analyses were performed with R studio. Results PCOS patients manifested hyperandrogenism, increased luteinizing hormone/follicle-stimulating hormone (LH/FSH), and accumulated body fat and insulin resistance. Plasma DIAPH1 levels were significantly decreased in women with PCOS compared to control participants, and DIAPH1 levels were distinctly reduced in OW PCOS compared to OW control subjects (P < 0.001). DIAPH1 levels correlated with fasting blood glucose (FBG), total cholesterol (TC), the homeostasis model assessment of β-cell function (HOMA-β), and LH/FSH in all participants (FBG: r = 0.351, P < 0.0001; TC: r = 0.178, P = 0.029; HOMA-β: r = −0.211, P = 0.009; LH/FSH: r = −0.172, P = 0.040). Multivariate logistic regression analysis revealed that plasma DIAPH1 levels were an independent risk factor for PCOS. A model containing DIAPH1, BMI, FBG, and testosterone was constructed to predict the risk of PCOS, with a sensitivity of 92.0% and a specificity of 80.9%. A nomogram was constructed to facilitate clinical diagnosis. Conclusions These findings suggest the association of plasma DIAPH1 with glucose metabolism, insulin resistance, and sex hormones and support DIAPH1 as a potential predictive factor for PCOS.

Highlights

  • Polycystic ovary syndrome (PCOS) is a metabolic and reproductive disorder that is characterized by ovulation dysfunction, hyperandrogenism, and polycystic ovary changes, which are commonly accompanied by insulin resistance (IR) and compensatory hyperinsulinemia [1]

  • Because Diaphanous related formin 1 (DIAPH1) participates in the advanced glycation end product (AGE) signaling that aggravates inflammation and IR in polycystic ovary syndrome (PCOS) and hormone reproduction, we examined the potential connection of DIAPH1 with PCOS

  • Glucose and insulin metabolic parameters, including fasting insulin (FINS), hemoglobin A1c (HbA1c), homeostasis model assessment of IR (HOMA-IR), and homeostasis model assessment of β-cell function (HOMA-β), were all significantly higher (94.74%, 0.78%, 100.61%, and 65.31%, respectively) in women with PCOS (P < 0:001), which revealed that PCOS patients had obvious insulin resistance (IR) and compensatory hyperinsulinemia

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Summary

Introduction

Polycystic ovary syndrome (PCOS) is a metabolic and reproductive disorder that is characterized by ovulation dysfunction, hyperandrogenism, and polycystic ovary changes, which are commonly accompanied by insulin resistance (IR) and compensatory hyperinsulinemia [1]. Recent studies revealed that elevated levels of advanced glycation end products (AGEs), a group of glycated proteins or lipids after exposure to sugars, represented the inflammatory state in PCOS, which could be aggravated by obesity and hyperinsulinemia [7, 8]. Diaphanous related formin 1 (DIAPH1) is a novel component of advanced glycation end product (AGE) signal transduction that was recently found to participate in diabetes-related disorders, obesity, and androgen hormones. The levels of circulating plasma DIAPH1 and indicators of glucose, insulin, lipid metabolism, liver enzymes, kidney function, sex hormones, and inflammation were measured in 75 patients with PCOS and 77 healthy participants. These findings suggest the association of plasma DIAPH1 with glucose metabolism, insulin resistance, and sex hormones and support DIAPH1 as a potential predictive factor for PCOS

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