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Evidence of proatherogenic inflammation in polycystic ovary syndrome.
Metabolism. 2009 Jul; 58(7):954-62.M

Abstract

Women with polycystic ovary syndrome (PCOS) have chronic low-level inflammation that can increase the risk of atherogenesis. We measured circulating proatherogenic inflammatory mediators in women with PCOS (8 lean: body mass index, 18-25 kg/m(2); 8 obese: body mass index, 30-40 kg/m(2)) and weight-matched controls (8 lean, 8 obese). Blood samples were obtained fasting and 2 hours after glucose ingestion to measure interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemotactic protein-1 (MCP-1), C-reactive protein (CRP), matrix metalloproteinase-2, plasminogen activator inhibitor-1 (PAI-1), and activated nuclear factor kappaB in mononuclear cells. Truncal fat was determined by dual-energy x-ray absorptiometry. Fasting MCP-1 levels were elevated in lean women with PCOS compared with lean controls (159.9 +/- 14.1 vs 121.2 +/- 5.4 pg/mL, P < .02). Hyperglycemia failed to suppress matrix metalloproteinase-2 in lean women with PCOS compared with lean controls (1.7 +/- 1.2 vs -4.8 +/- 1.6 pg/mL, P < .002). Among women with PCOS, obese individuals exhibited higher fasting sICAM-1 (16.1 +/- 0.8 vs 10.5 +/- 1.0 ng/mL, P < .03) and PAI-1 (6.1 +/- 0.7 vs 3.4 +/- 0.8 ng/mL, P < .03) levels. Trend analysis revealed higher (P < .005) IL-6, sICAM-1, CRP, PAI-1, systolic and diastolic blood pressures, triglycerides, fasting insulin, and homeostasis model assessment of insulin resistance index in women with PCOS compared with weight-matched controls, and the highest levels in the obese regardless of PCOS status. Fasting MCP-1 levels correlated with activated nuclear factor kappaB during hyperglycemia (P < .05) and androstenedione (P < .004). Truncal fat correlated with fasting IL-6 (P < .004), sICAM-1 (P < .006), CRP (P < .0009), and PAI-1 (P < .02). We conclude that both PCOS and obesity contribute to a proatherogenic state; but in women with PCOS, abdominal adiposity and hyperandrogenism may exacerbate the risk of atherosclerosis.

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Authors+Show Affiliations

González F
Department of Obstetrics and Gynecology, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA. gonzalez.frank@mayo.edu
Rote NS
No affiliation info available
Minium J
No affiliation info available
Kirwan JP
No affiliation info available

MeSH

Absorptiometry, PhotonAdultAndrogensAtherosclerosisC-Reactive ProteinChemokine CCL2Electrophoretic Mobility Shift AssayFemaleGlucose Tolerance TestHumansIntercellular Adhesion Molecule-1Interleukin-6Matrix Metalloproteinase 2NF-kappa BObesityPlasminogen Activator Inhibitor 1Polycystic Ovary SyndromeYoung Adult

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

19375763

Citation

González, Frank, et al. "Evidence of Proatherogenic Inflammation in Polycystic Ovary Syndrome." Metabolism: Clinical and Experimental, vol. 58, no. 7, 2009, pp. 954-62.
González F, Rote NS, Minium J, et al. Evidence of proatherogenic inflammation in polycystic ovary syndrome. Metabolism. 2009;58(7):954-62.
González, F., Rote, N. S., Minium, J., & Kirwan, J. P. (2009). Evidence of proatherogenic inflammation in polycystic ovary syndrome. Metabolism: Clinical and Experimental, 58(7), 954-62. https://doi.org/10.1016/j.metabol.2009.02.022
González F, et al. Evidence of Proatherogenic Inflammation in Polycystic Ovary Syndrome. Metabolism. 2009;58(7):954-62. PubMed PMID: 19375763.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evidence of proatherogenic inflammation in polycystic ovary syndrome. AU - González,Frank, AU - Rote,Neal S, AU - Minium,Judi, AU - Kirwan,John P, PY - 2008/09/22/received PY - 2009/02/03/accepted PY - 2009/4/21/entrez PY - 2009/4/21/pubmed PY - 2009/7/14/medline SP - 954 EP - 62 JF - Metabolism: clinical and experimental JO - Metabolism VL - 58 IS - 7 N2 - Women with polycystic ovary syndrome (PCOS) have chronic low-level inflammation that can increase the risk of atherogenesis. We measured circulating proatherogenic inflammatory mediators in women with PCOS (8 lean: body mass index, 18-25 kg/m(2); 8 obese: body mass index, 30-40 kg/m(2)) and weight-matched controls (8 lean, 8 obese). Blood samples were obtained fasting and 2 hours after glucose ingestion to measure interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemotactic protein-1 (MCP-1), C-reactive protein (CRP), matrix metalloproteinase-2, plasminogen activator inhibitor-1 (PAI-1), and activated nuclear factor kappaB in mononuclear cells. Truncal fat was determined by dual-energy x-ray absorptiometry. Fasting MCP-1 levels were elevated in lean women with PCOS compared with lean controls (159.9 +/- 14.1 vs 121.2 +/- 5.4 pg/mL, P < .02). Hyperglycemia failed to suppress matrix metalloproteinase-2 in lean women with PCOS compared with lean controls (1.7 +/- 1.2 vs -4.8 +/- 1.6 pg/mL, P < .002). Among women with PCOS, obese individuals exhibited higher fasting sICAM-1 (16.1 +/- 0.8 vs 10.5 +/- 1.0 ng/mL, P < .03) and PAI-1 (6.1 +/- 0.7 vs 3.4 +/- 0.8 ng/mL, P < .03) levels. Trend analysis revealed higher (P < .005) IL-6, sICAM-1, CRP, PAI-1, systolic and diastolic blood pressures, triglycerides, fasting insulin, and homeostasis model assessment of insulin resistance index in women with PCOS compared with weight-matched controls, and the highest levels in the obese regardless of PCOS status. Fasting MCP-1 levels correlated with activated nuclear factor kappaB during hyperglycemia (P < .05) and androstenedione (P < .004). Truncal fat correlated with fasting IL-6 (P < .004), sICAM-1 (P < .006), CRP (P < .0009), and PAI-1 (P < .02). We conclude that both PCOS and obesity contribute to a proatherogenic state; but in women with PCOS, abdominal adiposity and hyperandrogenism may exacerbate the risk of atherosclerosis. SN - 1532-8600 UR - https://www.unboundmedicine.com/medline/citation/19375763/Evidence_of_proatherogenic_inflammation_in_polycystic_ovary_syndrome_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0026-0495(09)00091-2 DB - PRIME DP - Unbound Medicine ER -