Asprosin levels in women with and without the polycystic ovary syndrome: a systematic review and meta-analysis

Figures & data

Figure 1. Flowchart of study selection.

Table 1. Studies comparing circulating asprosin in women with and without polycystic ovary syndrome (PCOS): Authors, study location and period of study, aims of studies, number of participants, age, study design and exclusion criteria, and main findings.

Authors [reference]	Location and period of study. Aims.	Sample size. Age.	Study design and exlusion criteria	Main findings
1. Alan et al. [21]	Location: Izmir, Turkey; June 2017 to January 2018. Aim: To compare asprosin levels in women with and without PCOS, and if there is a link between asprosin and metabolic parameters in PCOS.	Sample size: PCOS = 78; control women n = 78. Age: 18–45 year-old women.	Age and BMI matched case-control study of women. Exclusion criteria: irregular menstrual cycles related to the excess of androgens or other adrenal or thyroid disorders, galactorrhea, breastfeeding, hypertension, impaired glucose tolerance or diabetes mellitus, hyperlipidemia, congestive heart failure or coronary artery disease, liver/renal disorders, malignancy or acute infection, chronic inflammatory and autoimmune diseases, hormonal contraception, or anti-androgen therapy. The consumption of medications for hypertension, dyslipidemia, hyperglycemia, insulin resistance, or obesity were also an exclusion criterion.	Asprosin levels are higher in PCOS patients than in the control group. Women with PCOS had higher insulin, HOMA-IR, triglycerides, LH, total testosterone, free androgen index, and DHEA-S. There were also lower HDL-cholesterol and sex hormone-binding globulin.
2. Ameen et al. [22]	Location: Duhok, Iraq. June 20, 2020, to January 11, 2021. Aim: To study asprosin, metabolic outcomes, and insulin resistance in women with PCOS.	Sample size: PCOS = 75; control women n = 96. Age: 17–44 years.	Cross-sectional study. The control group included women with regular menstrual cycles and without endocrine anomalies. Exclusion criteria: women with hypothyroidism, renal or liver diseases, androgen-secreting tumor, Cushing’s syndrome, congenital adrenal hyperplasia, congestive heart diseases, or use of medications for decreasing hypertension, dyslipidemia, hyperglycemia, or obesity.	Serum asprosin was higher in women with PCOS than in the control group and was positively correlated with BMI, waist circumference, fasting insulin and glucose, HOMA-IR, total cholesterol, and triglycerides.
3. Chang et al. [23]	Location: Kweishan, Taoyuan, Taiwan; 2010–2016. Aim: To study irisin and asprosin levels and metabolic and endocrine characteristics in women with and without PCOS.	Sample size: PCOS = 444, control group = 156. Age: PCOS: 25 ± 0.22 years; control group: 27.42 ± 0.37 years.	A cross sectional study of women with and without PCOS assessing insulin, lipids, irisin, asprosin, steroid hormones, lipids, and clinical endpoints as well as HOMA-IR, and Matsuda index stratified by BMI or the presence of the metabolic syndrome.	The regulation of irisin is altered in PCOS patients, while asprosin is not affected by metabolic changes. Asprosin level was significantly correlated with follicle-stimulating hormone, free testosterone, and total testosterone levels.
4. Deniz et al. [24]	Location: Several centers in Turkey; period of study: no stated. Aim: To investigate the relationship between PCOS and asprosin.	Sample size: PCOS = 30, control group = 30. Age: PCOS = 27.14 ± 3.21; control group = 28.22 ± 2.6 years.	Case-control study matched by age and BMI. Exclusion criteria: lactating women, those receiving hormonal treatment for any disease for at least six months, patients with liver or pancreatic diseases, hyperprolactinemia, Cushing’s syndrome, adrenal hyperplasia, thyroid diseases, impaired glucose tolerance, type 1 or T2DM, or those with chronic medical illness. Furthermore, those using alcohol, tobacco, and its products and women using antiandrogen, antidiabetics, insulin sensitizers, lipid-lowering drugs, glucocorticoids, or other hormonal drugs were also excluded from the study.	There were significant relationships between high LH, androgen, and dyslipidemia, increased asprosin in patients with PCOS. The effect on metabolic parameters was probably due to the action of asprosin on appetite.
5. Guo et al. [25]	Location: Huadong, Qingdao, China; January 2017 to December 2018. Aim: to study asprosin levels and androgens, and correlations with other metabolic indexes.	Sample size: PCOS = 80, controls = 82. Age: PCOS = 34.8 ± 6.3, control group = 35. 9 ± 3.2.	Case-control study matched by age, BMI, and waist circumference. Exclusion criteria: patients with irregular menstrual function, diabetes mellitus, hypertension, coronary heart disease, hyperlipidemia, severe liver and kidney disease, primary hypothyroidism, Cushing syndrome, autoimmunity diseases, chronic infections, psychiatric diseases, or malignant tumors.	In PCOS patients, asprosin levels correlated with BMI, waist circumference, HOMA-IR, and free androgen index. The asprosin level in obese patients is nearly two times higher than in no-obese.
6. Jiang et al. [26]	Location: Jinan, China. Period of study: no stated. Aim: to investigate the relationship between serum asprosin levels and PCOS subtypes.	Sample size: PCOS = 93, controls = 77. Age: total sample 28.48 ± 3.47.	An age-matched case-control study. Exclusion criteria: women with androgen-secreting tumors, thyroid disease, hyperprolactinemia, 21-hydroxylase deficiency, Cushing’s syndrome, congenital adrenal hyperplasia, and abnormal intrauterine cavity. A history of recurrent spontaneous abortion, intake of antidiabetic drugs, antiandrogens, oral contraceptives, insulin sensitizers, glucocorticoids, and ovulation induction agents were also excluded.	Asprosin levels were no significant difference between the PCOS and control group. In the PCOS group, asprosin was negatively correlated with BMI, LH, testosterone, basal antral follicles, insulin, HOMA-IR, and triglycerides. Correlations were not significant after adjusting for BMI.
7. Li et al. [27]	Location: Chongqing, China; February 2017 to December 2018. Aim: To investigate the association of asprosin with metabolic profiles, sex-related hormones, or inflammation in PCOS, T2DM and healthy women.	Sample size: PCOS = 41, controls 66 healthy women. Age: PCOS 22.68 ± 5.66: control group 37.02 ± 8.16 years.	Cross-sectional study. Exclusion criteria: patients with androgen-secreting tumors, hyperprolactinemia, 21-hydroxylase deficiency, Cushing’s syndrome, congenital adrenal hyperplasia, thyroid disease, abnormal intrauterine cavity, a history of recurrent spontaneous abortion, or unilateral oophorectomy.	Asprosin was higher in PCOS patients than in healthy women but lower than in T2DM patients, and it was positively correlated with glucose, glycated hemoglobin, HOMA-IR, and testosterone. The BMI-categorized subgroups of PCOS women showed correlations of asprosin with metabolic profiles and sex-related hormones.
8. Liu et al. [28]	Location: Hangzhou, China; December 2018 to December 2019. Aim: To investigate the association between serum asprosin level and insulin resistance in women with PCOS.	Sample size: PCOS = 213, control group 213. Age: PCOS: 25.58 ± 4.82, control group: 25.35 ± 4.50.	Age and BMI matched case-control study. Exclusion criteria: Women with menstrual disorders related to hyperandrogenism, thyroid disease, pregnancy or breastfeeding, hypertension, glucose intolerance or diabetes mellitus, coronary heart failure, liver or kidney diseases, acute infections, chronic inflammation, and autoimmune diseases, malignant diseases, oral contraceptives and/or antiandrogen treatments.	Serum asprosin, glucose, insulin, triglycerides, LH, total testosterone, and DHEA-S in the PCOS group were significantly higher than in the control group. Asprosin levels correlated with BMI, fasting glucose and insulin levels, insulin resistance index, and C-reactive protein in PCOS patients.

Seven studies [21–24, 26–28] followed the Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Criteria [21–24, 26–28], and one study [25] followed the Recommendations from the Endocrinology Expert Group of the Obstetric and Gynecology Branch of the Chinese Medical Association.

Table 2. Pooled effects reported as mean differences (MDs) or standardized MDs (SMDs) and 95% confidence interval (CI), Z score and p-values, and heterogenity (I ²) in women with and without polycystic ovary syndrome.

Outcomes (Figures)	Included studies	Participants (PCOS / Control)	MD or SMD [95% CI]	Z score (p value)	I^2 (%)
Age (Figure 2A)	8	1050 / 796	MD −2.40 [−2.46 to −2.33]	76.79 (< 0.0001)	98
Body mass index (Figure 2B)	8	1050 / 796	MD 1.41 [−0.07 to 2.89]	1.86 (0.06)	95
Asprosin (Figure 2C)	8	1050 / 796	SMD 2.57 [1.64 to 3.50]	5.41 (< 0.0001)	98
Insulin (Figure 2D)	8	1050 / 796	SMD 2.73 [1.18 to 4.28]	3.46 (0.0005)	99
HOMA-IR (Figure 2E)	7	837 / 583	SMD 2.70 [0.85 to 4.55]	2.86 (0.004)	99
Glucose (Figure 2F)	8	1050 / 796	SMD 0.27 [−0.05 to 0.58]	1.66 (0.10)	90
Luteinizing hormone (Figure 3A)	7	975 / 700	SMD = 2.33 [0.60 to 4.06]	2.64 (0.008)	99
Total testosterone (Figure3B)	7	975 / 680	SMD = 4.06 [1.89 to 6.22]	3.67 (0.0002)	100
Dehydroepiandrosterone sulfate (Figure 3C)	6	934 / 635	SMD = 2.38 [0.37 to 4.40]	2.32 (0.02)	100
Sex hormone-binding globulin (Figure 3D)	3	371 / 373	SMD = −3.36 [−4.92 to −1.80]	4.21 (0.0001)	98
Follicle-stimulating hormone (Figure 3 E)	7	975 / 700	SMD = −1.11 [−259 to 0.36]	1.48 (0.14)	99
Estradiol (Figure 3F)	7	762 / 487	SMD = 0.62 [−0.59 to 1.84]	1.01 (0.31)	99
HDL-cholesterol (Figure 4A)	8	1050 / 796	SMD = −0.85 [−1.69 to −0.01]	1.98 (0.05)	98
Total cholesterol (Figure 4B)	8	1050 / 796	SMD = 0.84 [−0.28 to 1.96]	1.47 (0.14)	99
LDL-cholesterol (Figure 4C)	7	975 / 700	SMD = 1.10 [−0.18 to 2.37]	1.69 (0.09)	99
Triglycerides (Figure 4D)	8	1050 / 796	SMD = 1.20 [0.13 to 2.27]	2.20 (0.03)	99

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Chang CL, Huang SY, Hsu YC, et al. The serum level of irisin, but not asprosin, is abnormal in polycystic ovary syndrome patients. Sci Rep. 2019;9(1):6447.

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Data statement

The present meta-analysis was based on published articles. All summary data generated during this study are included in this published article. Raw data used for the analyses are available presented in the original reviewed articles.