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General Comment |
FOund in ovarian cDna library.
NCBI Summary:
Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of this gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease. [provided by RefSeq, Jul 2008]
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Comment |
Plasma sclerostin levels are associated with nutritional status and insulin resistance but not hormonal disturbances in women with polycystic ovary syndrome. Wyskida K et al. (2020) The aim of this study was to evaluate the circulating sclerostin levels with nutritional status, insulin resistance and hormonal disturbances in women with polycystic ovary syndrome (PCOS). The cross-sectional study involved 98 PCOS inpatients (20 normal weight, 17 overweight and 61 obese) with stable body mass. Body composition was assessed by bioimpedance method in addition to anthropometric measurements (body mass and height). Serum/plasma concentrations of glucose, insulin (with the calculation of homeostatic model assessment insulin resistance-HOMA-IR), estradiol, total testosterone, sex hormone-binding globulin (SHBG) and sclerostin were measured. Free androgen index (FAI) and estradiol/testosterone index were calculated. Plasma sclerostin levels were significantly higher in obese 0.61 (interquartile range 0.53-0.77) ng/mL] than in overweight [0.53 (0.49-0.57) ng/mL] and normal weight [0.49 (0.42-0.54) ng/mL] groups. Plasma sclerostin levels were significantly higher in the subgroup with insulin resistance [0.65 (interquartile range 0.53-0.77) vs. 0.52 (0.46-0.58) ng/mL; p < 0.001], while similar concentrations were observed in subgroups with FAI below and above median. Plasma sclerostin levels variability were explained by BMI (r = 0.40), the percentage of body fat (r = 0.40) and HOMA-IR values (r = 0.34) in multivariable models. Circulating sclerostin levels in women with PCOS are related to nutritional status and insulin resistance, but not to sex hormone disturbances.//////////////////
Changes of serum sclerostin and Dickkopf-1 levels during the menstrual cycle. A pilot study. [Liakou CG et al. (2016) Studies in postmenopausal women have identified sclerostin as a strong candidate for mediating estrogen effects on the skeleton. The effects of estradiol on sclerostin and Dickkopf-1 in younger women remain unclear. The main purpose of this study is to investigate the impact of estradiol and gonadotrophins fluctuations during the menstrual cycle on circulating sclerostin and Dickkopf-1 levels and the possible relationship of sclerostin and Dickkopf-1 with changes in N-terminal propeptide of type 1 collagen and C-telopeptide of collagen cross-links. Fourteen healthy premenopausal Caucasian women, with regular menses, aged 33.6 ± 4.5 years participated. After the first day of menstruation and every-other-day up to the next menses, fasting serum estradiol, luteinizing hormone, follicle-stimulating hormone, sclerostin, Dickkopf-1, N-terminal propeptide of type 1 collagen, and C-telopeptide of collagen cross-links levels were measured in peripheral blood. Participants completed dietary questionnaires and the International physical activity questionnaire during the cycle. Neither sclerostin nor Dickkopf-1 levels changed significantly across the menstrual cycle (p = 0.18 and p = 0.39, respectively), while N-terminal propeptide of type 1 collagen and C-telopeptide of collagen cross-links levels presented cyclic variation (p < 0.001 and p = 0.004, respectively). Baseline sclerostin (29.23 ± 10.62 pmol/L) positively correlated with N-terminal propeptide of type 1 collagen (r = 0.71, p < 0.01) and C-telopeptide of collagen cross-links (r = 0.63, p < 0.05), while Dickkopf-1 (4.82 ± 2.23 pmol/L) correlated positively with N-terminal propeptide of type 1 collagen (r = 0.56, p < 0.05). Mid-cycle E2 levels presented significant negative association with the percent decrease of C-telopeptide of collagen cross-links at all-time points during the luteal period (r = -0.60 to -0.68, p < 0.05-0.01). Circulating sclerostin and Dickkopf-1 levels do not change across the menstrual cycle and do not demonstrate any relationship with estradiol in premenopausal women. Further investigation is needed concerning the role of sclerostin and Dickkopf-1 on bone turnover in young estrogen-sufficient women.//////////////////
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