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The aim of this study is to determine the serum levels of visfatin in patients with polycystic ovary syndrome (PCOS) and to understand its correlations with other metabolic and hormonal parameters. Thirty-seven patients with PCOS and 30 women without concomitant disease were included in this study. Serum visfatin levels were similar in patients with PCOS and control group. Visfatin levels were higher in normal weight PCOS when compared with obese PCOS, but it did not reach statistical significance. Visfatin levels correlated negatively with fasting blood glucose, total cholesterol (TC), low-density lipoprotein (LDL) and lipoprotein-a levels in PCOS patients. CRP levels increased both in obese PCOS and in obese controls. Plasma visfatin levels had no correlation with homeostasis model assessment-insulin resistance and fasting insulin levels, but the negative correlation between plasma visfatin levels and lipoprotein-a, fasting plasma glucose, TC and LDL levels may indicate a role for visfatin in cardiovascular disease independent of insulin resistance.
Department of Obstetrics and Gynecology , Istanbul , Turkey.
This article was published in the following journal.
Name: Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology
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This study was designed to evaluate insulin resistance and plasma levels of visfatin and resistin in obese and non-obese patients with polycystic ovary syndrome (PCOS). A total of 37 premenopausal PCO...
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An inherited autosomal dominant trait characterized by abnormally elevated levels of total serum THYROXINE; (T4) in euthyroid patients with abnormal SERUM ALBUMIN that binds T4 with enhanced affinity. The serum levels of free T4, free T3, and TSH are normal. It is one of several T4 abnormalities produced by non-thyroid disorder. This condition is due to mutations of the ALB gene on CHROMOSOME 4.
An inherited autosomal recessive trait, characterized by peripheral resistance to THYROID HORMONES and the resulting elevation in serum levels of THYROXINE and TRIIODOTHYRONINE. This syndrome is caused by mutations of gene THRB encoding the THYROID HORMONE RECEPTORS BETA in target cells. HYPOTHYROIDISM in these patients is partly overcome by the increased thyroid hormone levels.
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