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. 2017 Mar 1;102(3):810-821.
doi: 10.1210/jc.2016-2692.

Discovery of Novel Lipid Profiles in PCOS: Do Insulin and Androgen Oppositely Regulate Bioactive Lipid Production?

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Free PMC article

Discovery of Novel Lipid Profiles in PCOS: Do Insulin and Androgen Oppositely Regulate Bioactive Lipid Production?

Shengxian Li et al. J Clin Endocrinol Metab. .
Free PMC article

Abstract

Context: Polycystic ovary syndrome (PCOS) is a complex syndrome showing clinical features of an endocrine/metabolic disorder, including hyperinsulinemia and hyperandrogenism. Polyunsaturated fatty acids (PUFAs) and their derivatives, both tightly linked to PCOS and obesity, play important roles in inflammation and reproduction.

Objective: This study aimed to investigate serum lipid profiles in newly diagnosed patients with PCOS using lipidomics and correlate these features with the hyperinsulinemia and hyperandrogenism associated with PCOS and obesity.

Design and setting: Thirty-two newly diagnosed women with PCOS and 34 controls were divided into obese and lean subgroups. A PCOS rat model was used to validate results of the human studies.

Main outcome measures: Serum lipid profiles, including phospholipids, free fatty acids (FFAs), and bioactive lipids, were analyzed using gas chromatography-mass spectrometry (MS) and liquid chromatography-MS.

Results: Elevation in phosphatidylcholine and a concomitant decrease in lysophospholipid were found in obese patients with PCOS vs lean controls. Obese patients with PCOS had decreased PUFA levels and increased levels of long-chain saturated fatty acids vs lean controls. Serum bioactive lipids downstream of arachidonic acid were increased in obese controls, but reduced in both obese and lean patients with PCOS vs their respective controls.

Conclusions: Patients with PCOS showed abnormal levels of phosphatidylcholine, FFAs, and PUFA metabolites. Circulating insulin and androgens may have opposing effects on lipid profiles in patients with PCOS, particularly on the bioactive lipid metabolites derived from PUFAs. These clinical observations warrant further studies of the molecular mechanisms and clinical implications of PCOS and obesity.

Figures

Figure 1.
Figure 1.
Pathways whereby bioactive lipid mediators are generated from phospholipids and FAs. AA is C20:4; DHA is C22:6; LA is C18:2. ALA, alpha linolenic acid C18:3α; DGLA, dihomo-γ-linolenic acid C18:3γ; DPA, docosapentaenoic acid C22:5; EPA, eicosapentaenoic acid C20:5; Lpcat, lysophosphatidylcholine acyltransferase; LT, leukotriene; LX, lipoxin; PLA2, phospholipase A2; P450epo, cytochrome P450 epoxygenase; RVD, resolvin D; RVE, resolvin E; TXA2, thromboxane A2.
Figure 2.
Figure 2.
Serum saturated long-chain fatty acids in lean and obese patients and patients with PCOS. *P < 0.05 compared with LC; #P < 0.05 compared with OB; &P < 0.05 compared with LP.
Figure 3.
Figure 3.
Serum bioactive lipids derived from AA, eicosapentaenoic acid (EPA), DHA, and LA. AA is C20:4; DHA is C22:6; EPA is C20:5; LA is C18:2. *P < 0.05 compared with LC; #P < 0.05 compared with OB; &P < 0.05 compared with LP. LT, leukotriene; LTB4, leukotriene B4; LX, lipoxin; LXA4, lipoxin A4; PGFM, prostaglandin F metabolite; PGI2, prostacycline I2; P450epo, cytochrome P450 epoxygenase; 15d-PGJ2, 15-deoxy-Δ12,14-prostaglandin J2.
Figure 4.
Figure 4.
Lipid metabolites derived from AA, eicosapentaenoic acid (EPA), DHA, and LA in rat serum. AA is C20:4; DHA is C22:6; EPA is C20:5; LA is C18:2. *P < 0.05 compared with CON; #P < 0.05 compared with HF. LTB4 leukotriene B4; LXA4, lipoxin A4; PGFM, prostaglandin F metabolite; PGI2, prostacycline I2; P450epo, cytochrome P450 epoxygenase; RVD, resolvin D; RVE, resolvin E; 15d-PGJ2, 15-deoxy-Δ12,14-prostaglandin J2.

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