Human Endogenous Metabolite

In order to distinguish between IR PCOS and controls, lysophosphatidylcholine 18:2 (1-Linooleoyl-2-Hydroxy-sn-glycero-3-PC) is used. In IR PCOS plasma, there were notable decreases in phosphocholine (PCs) and hemolytic PC (18:2) levels as well as an increase in trilaurin levels [1]. One of the main classes of glycerophospholipids in human plasma is called lysophosphatidylcholine (LPC), and it has been linked to type 2 diabetes, insulin resistance, inflammation, and obesity [2].

Lipid pathways involving LPC 18:2. Phosphatidylcholine in plasma membranes and lipoproteins is converted to LPC 18:2 by phospholipase A2. LPC 18:2 can be converted back to phosphatidylcholine by lipophosphatidylcholine (LPC) transferase. Endothelial lipase can convert phosphatidylcholine in HDL to LPC 18:2. LPC 18:2 can also be generated in the synthesis of cholesteryl esters from phosphatidylcholine and cholesterol. LPC 18:2 has specific activity as a ligand for G protein-coupled receptors or can be converted by autotaxin to lysophosphatidic acid (LPA) 18:2. LPA 18:2 can potentially interact with LPA receptors 1–6 [1].

The study subjects consisted of 504 participants, aged ≥50 years, in the Baltimore Longitudinal Study of Aging (BLSA) who were seen between January 2006 and December 2008 (“baseline”) and had at least two or more follow-up visits after baseline up to June 2014. The study design was aimed at studying the cross-sectional association of plasma metabolites with walking speed and to identify baseline metabolites that predicted differential decline of gait speed over follow-up. Participants were assessed at an in-patient study clinic for follow-up visits every 1–4 years, with more frequent follow-up for older participants. They underwent 2.5 days of medical, physiological, and psychological exams. Gait speed was measured over a 6-month course. The participants asked to walk at their usual pace. The time to complete the walk was converted into gait speed (m/s). The better performance of two trials was used for the analysis.[1]

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All of the PCOS patients and health subjects were recruited from Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Guangzhou, China, from January 2013 to October 2013. The informed consent letters have been obtained from all the participants prior to inclusion in this study. This study was approved by the Medical Ethical Committee of Sun Yat-Sen Memorial Hospital. According to the Rotterdam criteria, PCOS diagnosis was made in patients that present at least two out of the three following clinical traits: (a) oligo- and/or anovulation; (b) clinical and/or biochemical hyperandrogenism, e.g., acne, hirsutism and androgenic alopecia; and (c) PCO (presence of more than 12 follicles in each ovary with the diameter of 2–9 mm, and/or increase in ovary size more than 10 cm3). Patients with IR were diagnosed by oral glucose tolerance test (OGTT) and met the following criterias, (a) plasma fasting glucose concentration <6.1 mmol/L; (b) 2 h after glucose load between 7.8 and 11.1 mmol/L in OGTT assay; (c) fasting insulin level >12 mU/L; and (d) 2-h insulin level in OGTT assay >80 mU/L. The clinical subjects were excluded with any of the following condition, including (a) age <20 or >40 years; (b) current pregnant, delivery or miscarriage within the preceding 3 months; (c) congenital adrenal hyperplasia, androgen-secreting tumors, and other diseases with hyperandrogenism; (d) cardiovascular diseases; and (e) androgenic drug or sex steroid therapy. The control subjects were recruited from health women who visited the hospital for routine checkup with matching ages, regular menstrual cycles, normal androgen levels, no PCO and no IR. According to the above mentioned inclusion/exclusion criteria, a total of 40 PCOS patients, i.e., 21 patients with IR (IR PCOS) and 19 patients without IR (non-IR PCOS), and 19 health participants were included in the present study.[2]

[1]. Targeted Metabolomics Shows Low Plasma Lysophosphatidylcholine 18:2 Predicts Greater Decline of Gait Speed in Older Adults: The Baltimore Longitudinal Study of Aging. J Gerontol A Biol Sci Med Sci. 2019;74(1):62-67.
[2]. UHPLC/Q-TOFMS-based plasma metabolomics of polycystic ovary syndrome patients with and without insulin resistance. J Pharm Biomed Anal. 2016;121:141-150.

1-linoleoyl-sn-glycero-3-phosphocholine is a lysophosphatidylcholine 18:2 in which the acyl group at position 1 is (9Z,12Z)-octadecadienoyl. It has a role as a mouse metabolite. It is a lysophosphatidylcholine(18:2/0:0) and a linoleoyl-sn-glycero-3-phosphocholine. It is functionally related to a linoleic acid.
1-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine has been reported in Drosophila melanogaster, Vitis vinifera, and other organisms with data available.

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Background: Gait speed is an important measure of lower extremity physical performance in older adults and is predictive of disability and mortality. The biological pathways involved in the decline of lower extremity physical performance are not well understood. We used a targeted metabolomics approach to identify plasma metabolites predictive of change in gait speed over time.
Methods: Gait speed was measured at baseline and over median follow-up of 50.5 months in 504 adults, aged ≥50 years, who had two or more study visits in the Baltimore Longitudinal Study of Aging (BLSA). Plasma metabolites were measured using targeted mass spectrometry (AbsoluteIDQ p180 Kit, Biocrates).
Results: Of 148 plasma metabolites (amino acids, biogenic amines, hexoses, glycerophospholipids) measured, eight were significantly associated with gait speed at baseline, independent of age and sex: hexoses (r = -0.148, p < .001), [sphingomyelin (SM) 16:1 (r = -0.091, p = .0009), SM 18:0 (r = -0.085, p = .002), SM 18:1 (r = -0.128, p < .0001], phosphatidylcholine aa 32:3 (r = -0.088, p = .001), lysophosphatidylcholine (LPC) 17:0 (r = 0.083, p = .003), LPC 18:1 (r = 0.089, p = .001), and LPC 18:2 (r = 0.104, p < .0001). Adjusting for baseline age, sex, and chronic diseases, baseline plasma LPC 18:2 was an independent predictor of the rate of change of gait speed over subsequent follow-up (p = .003). No other plasma metabolites were significantly associated longitudinal changes of gait speed over time.
Conclusions: Low plasma LPC 18:2, which has previously been shown to predict impaired glucose tolerance, insulin resistance, type 2 diabetes, coronary artery disease, and memory impairment, is an independent predictor of decline in gait speed in older adults.[1]

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Polycystic ovary syndrome (PCOS), characterized with menstrual irregularities, hyperandrogenism and ovulatory abnormalities, is usually companied with insulin resistance (IR) and accounts for one of the most prevalent reproductive dysfunction of premenopausal women. Despite accumulating investigations, diagnostic standards of this pathological condition remain obscure. The aim of present study is to characterize the plasma metabolic characteristics of PCOS patients with and without IR, and subsequently identify the potential biomarkers for the diagnosis of PCOS and its IR complication. A total of 59 plasma samples from eligible healthy controls (CON, n=19), PCOS patients without IR (non-IR PCOS, n=19) and PCOS patients with IR (IR PCOS, n=21) were profiled by an ultra high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UHPLC/Q-TOFMS) followed by multivariate statistical analysis. Compared to the healthy controls, significant decrease in the levels of phosphocholines (PCs) and lyso PC (18:2)/LPC 18:2, and increase in trilauric glyceride level were observed in the plasma of IR PCOS. Meanwhile, the significant increase in the levels of saturated fatty acids (palmitic acid and stearic acid) and decanoylcarnitine, and decrease in PC (36:2) and PS (36:0) were found in non-IR PCOS patients. Trilauric glyceride and decanoylcarnitine were identified as the potential biomarkers with the highest sensitivity and specificity for the diagnosis of PCOS patients with and without IR, respectively. Furthermore, based on these alterations of metabolites, MetPA network pathway analysis suggested a profound involvement of the abnormalities of glycerophospholipid, glycerolipid and fatty acid metabolisms in the pathogenesis of PCOS and IR complications. Collectively, LC-MS-based metabolomics provides a promising strategy for complementary diagnosis of PCOS and its IR complication and offers a new insight to understand their pathogenesis mechanisms.

C26H50NO7P

519.65

519.332

22252-07-9

Lysophosphatidylcholine 18:2-d9

11005824

White to light yellow oil

5.982

1

7

24

35

623

1

CCCCC/C=C\C/C=C\CCCCCCCC(=O)OC[C@H](COP(=O)([O-])OCC[N+](C)(C)C)O

SPJFYYJXNPEZDW-FTJOPAKQSA-N

InChI=1S/C26H50NO7P/c1-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-20-26(29)32-23-25(28)24-34-35(30,31)33-22-21-27(2,3)4/h9-10,12-13,25,28H,5-8,11,14-24H2,1-4H3/b10-9-,13-12-/t25-/m1/s1

[(2R)-2-hydroxy-3-[(9Z,12Z)-octadeca-9,12-dienoyl]oxypropyl] 2-(trimethylazaniumyl)ethyl phosphate

22252-07-9; LPC 18:2; lyso PC (18:2); lysophosphatidylcholine 18:2; LPC(18:2/0:0); 1-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine; 1-Linoleoyl-sn-glycero-3-phosphorylcholine; PC(18:2(9Z,12Z)/0:0); 1-linoleoyl-phosphatidylcholine; 1-Linoleoylglycerophosphocholine;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO :~100 mg/mL (~192.44 mM)

Solubility in Formulation 1: 2.5 mg/mL (4.81 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.5 mg/mL (4.81 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (4.81 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)