Evidence of mononuclear cell preactivation in the fasting state in polycystic ovary syndrome

Frank González, John P. Kirwan, Neal S. Rote, Judi Minium

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

OBJECTIVE: 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. STUDY DESIGN: 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 cells isolated from fasting blood samples and cultured in the presence and absence of LPS. 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. RESULTS: The percent change from baseline in TNF-α and IL-6 release from MNC following LPS exposure was increased (P <.04) in lean and obese women with PCOS and obese controls compared with lean controls. Plasma IL-6 was increased (P <.02) in obese women with PCOS compared with lean women with PCOS, which in turn was increased (P <.02) compared with lean controls. The MNC-derived TNF-α and IL-6 responses from MNCs were negatively correlated with insulin sensitivity (P <.03) and positively correlated with testosterone (P <.03) and androstenedione (P <.006) for the combined groups. Plasma IL-6 was positively correlated with percentage truncal fat (P <.008). CONCLUSION: In PCOS, increased cytokine release from MNCs following LPS exposure in the fasting state reveals the presence of MNC 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.

Original languageEnglish (US)
Pages (from-to)635.e1-635.e7
JournalAmerican Journal of Obstetrics and Gynecology
Volume211
Issue number6
DOIs
StatePublished - Dec 1 2014

Fingerprint

Polycystic Ovary Syndrome
Fasting
Interleukin-6
Lipopolysaccharides
Insulin Resistance
Tumor Necrosis Factor-alpha
Fats
Cytokines
Hyperandrogenism
Androstenedione
Adiposity
Glucose Tolerance Test
Testosterone
Obesity
X-Rays
Weights and Measures

Keywords

  • inflammation
  • lipopolysaccharide
  • mononuclear cell preactivation

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Evidence of mononuclear cell preactivation in the fasting state in polycystic ovary syndrome. / González, Frank; Kirwan, John P.; Rote, Neal S.; Minium, Judi.

In: American Journal of Obstetrics and Gynecology, Vol. 211, No. 6, 01.12.2014, p. 635.e1-635.e7.

Research output: Contribution to journalArticle

González, Frank ; Kirwan, John P. ; Rote, Neal S. ; Minium, Judi. / Evidence of mononuclear cell preactivation in the fasting state in polycystic ovary syndrome. In: American Journal of Obstetrics and Gynecology. 2014 ; Vol. 211, No. 6. pp. 635.e1-635.e7.
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AB - OBJECTIVE: 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. STUDY DESIGN: 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 cells isolated from fasting blood samples and cultured in the presence and absence of LPS. 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. RESULTS: The percent change from baseline in TNF-α and IL-6 release from MNC following LPS exposure was increased (P <.04) in lean and obese women with PCOS and obese controls compared with lean controls. Plasma IL-6 was increased (P <.02) in obese women with PCOS compared with lean women with PCOS, which in turn was increased (P <.02) compared with lean controls. The MNC-derived TNF-α and IL-6 responses from MNCs were negatively correlated with insulin sensitivity (P <.03) and positively correlated with testosterone (P <.03) and androstenedione (P <.006) for the combined groups. Plasma IL-6 was positively correlated with percentage truncal fat (P <.008). CONCLUSION: In PCOS, increased cytokine release from MNCs following LPS exposure in the fasting state reveals the presence of MNC 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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