Evidence of mononuclear cell preactivation in the fasting state in polycystic ovary syndrome.
Evidence of mononuclear cell preactivation in the fasting state in polycystic ovary syndrome.
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DOI:
10.1016/j.ajog.2014.06.044
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发表时间:
2014-12
影响因子:
9.8
通讯作者:
Minium, Judi
中科院分区:
文献类型:
--
作者:
Gonzalez, Frank;Kirwan, John P.;Rote, Neal S.;Minium, Judi
We evaluated mononuclear cell (MNC) preactivation in women with Polycystic Ovary Syndrome (PCOS) by examining the effect of in vitro lipopolysaccharide (LPS) exposure on cytokine release in the fasting state. Twenty women with PCOS (10 lean, 10 obese) and 20 weight-matched controls (10 lean, 10 obese) volunteered for study participation. Tumor necrosis factor-α (TNF α) and interleukin-6 (IL-6) release was measured from mononuclear cell isolated from fasting blood samples and cultured in the presence and absence of lipopolysaccharide. Plasma IL-6 was measured from the same fasting blood samples. Insulin sensitivity was derived from an oral glucose tolerance test using the Matsuda index and truncal fat was measured by dual energy x-ray absorptiometry. The percent change from baseline in TNFα and IL-6 release from mononuclear cell following lipopolysaccharide exposure was increased (pitalic>0.04) in lean and obese women with PCOS and obese controls compared with lean controls. Plasma IL-6 was increased (pbold>0.02) in obese women with PCOS compared with lean women with PCOS, which in turn was increased (p<0.02) compared with lean controls. The mononuclear cell -derived TNFα and IL-6 responses from mononuclear cell were negatively correlated with insulin sensitivity (p<0.03) and positively correlated with testosterone (p<0.03) and androstenedione (p<0.006) for the combined groups. Plasma IL-6 was positively correlated with percent truncal fat (p<0.008). In PCOS, increased cytokine release from mononuclear cell following lipopolysaccharide exposure in the fasting state reveals the presence of mononuclear cell preactivation. Importantly, this phenomenon is independent of obesity and may contribute to the development of insulin resistance and hyperandrogenism in PCOS. In contrast, the source of plasma IL-6 elevations in PCOS may be excess adiposity.
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影响因子:
5.8
作者:
Ciampelli, M;Leoni, F;Lanzone, A
通讯作者:
Lanzone, A
影响因子:
5.8
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通讯作者:
Kirwan, JP
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Fauser, Bart C. J. M.;Tarlatzis, Basil C.;Barnhart, Kurt
通讯作者:
Barnhart, Kurt
影响因子:
5.8
作者:
Gonzalez, Frank;Sia, Chang Ling;Minium, Judi
通讯作者:
Minium, Judi
影响因子:
9.8
作者:
Gonzalez, Frank;Rote, Neal S.;Minium, Judi;Kirwan, John P.
通讯作者:
Kirwan, John P.