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-glycerol-3-phosphate choline is a lysophosphatidylcholine 18:2, with an acyl group at position 1 being (9Z,12Z)-octadecadienoyl. It is a mouse metabolite. It is a lysophosphatidylcholine (18:2/0:0) and linoleoyl-sn-glycerol-3-phosphate choline. It is functionally related to linoleic acid. 1-(9Z,12Z-octadecadienoyl)-sn-glycerol-3-phosphate choline has been reported in Drosophila melanogaster, grapes, and other organisms with relevant data. Background: Walking speed is an important indicator of lower limb physical function in older adults and can predict disability and mortality. The biological pathways of lower limb motor function decline are not fully understood. We employed targeted metabolomics to identify plasma metabolites that predict changes in walking speed over time. Methods: In the Baltimore Longitudinal Study of Aging (BLSA), baseline gait rate was measured in 504 adults aged ≥50 years, and gait rate was measured over a median follow-up period of 50.5 months. All adults attended at least two study visits. Plasma metabolites were determined using targeted mass spectrometry (AbsoluteIDQ p180 kit, Biocrates). Results: Of the 148 plasma metabolites (amino acids, biogenic amines, hexoses, and glycerophospholipids) measured, 8 were significantly correlated with baseline walking speed, independent of age and sex: hexose (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). After adjusting for baseline age, sex and chronic disease, baseline plasma LPC 18:2 was an independent predictor of the rate of change in walking speed during subsequent follow-up (p = .003). No other plasma metabolites were significantly associated with longitudinal changes in walking speed. Conclusion: Low plasma LPC 18:2 levels (previous studies have shown that they can predict impaired glucose tolerance, insulin resistance, type 2 diabetes, coronary artery disease and memory decline) are an independent predictor of declining walking speed in older adults. [1] Polycystic ovary syndrome (PCOS), characterized by menstrual irregularities, hyperandrogenemia and ovulation abnormalities, often accompanied by insulin resistance (IR), is one of the most common reproductive disorders in premenopausal women. Despite the accumulation of research, the diagnostic criteria for this pathological condition remain unclear. This study aimed to analyze the plasma metabolic characteristics of patients with and without insulin resistance in polycystic ovary syndrome (PCOS) and to further identify potential biomarkers for diagnosing PCOS and its insulin resistance complications. UHPLC/Q-TOFMS was used to analyze 59 plasma samples from healthy controls (CON, n=19), PCOS patients without insulin resistance (non-IR PCOS, n=19), and PCOS patients with insulin resistance (IR PCOS, n=21), followed by multivariate statistical analysis. Compared with healthy controls, PCOS patients showed significantly lower levels of phosphocholine (PC) and lysophosphatidylcholine (lyso PC) in their plasma. Elevated (18:2)/LPC 18:2 levels and elevated trilaurate levels were observed in the plasma of patients with insulin-resistant PCOS (IR PCOS). Meanwhile, significantly elevated levels of saturated fatty acids (palmitic acid and stearic acid) and decanoylcarnitine were found in non-insulin-resistant PCOS patients, while decreased levels of PC (36:2) and PS (36:0). Trilaurate and decanoylcarnitine were identified as potential biomarkers with the highest sensitivity and specificity for diagnosing PCOS patients with and without insulin resistance, respectively. Furthermore, based on these metabolite changes, MetPA network pathway analysis revealed that abnormalities in glycerophospholipid, glyceride, and fatty acid metabolism are closely related to the pathogenesis of PCOS and its insulin resistance complications. In conclusion, metabolomics based on liquid chromatography-mass spectrometry (LC-MS) provides a promising strategy for the auxiliary diagnosis of PCOS and its insulin resistance complications, and offers a new perspective for understanding its pathogenesis.

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.)