Palmitic acid

Manufactured by Merck Group

Sourced in United States, Germany, China, United Kingdom, Sao Tome and Principe, France, Italy, Macao, Canada, Japan, India, Australia, Panama, Ireland, Hungary, Switzerland

Palmitic acid is a saturated fatty acid with the chemical formula CH3(CH2)14COOH. It is a colorless, odorless solid at room temperature. Palmitic acid is a common constituent of animal and vegetable fats and oils.

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Lab products found in correlation

Oleic acid, by Merck Group (182 mentions) Stearic acid, by Merck Group (107 mentions) Linoleic acid, by Merck Group (81 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (68 mentions) Bovine serum albumin (bsa), by Merck Group (56 mentions) Myristic acid, by Merck Group (38 mentions) Palmitoleic acid, by Merck Group (32 mentions) Lauric acid, by Merck Group (28 mentions) Dimethyl sulfoxide (dmso), by Merck Group (23 mentions) Methanol, by Merck Group (23 mentions) Linolenic acid, by Merck Group (23 mentions) Arachidonic acid, by Merck Group (22 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (18 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (18 mentions) Penicillin, by Thermo Fisher Scientific (18 mentions) Oil red o, by Merck Group (16 mentions) Streptomycin, by Thermo Fisher Scientific (16 mentions) Fatty acid free bovine serum albumin, by Merck Group (15 mentions) Fatty acid free bsa, by Merck Group (15 mentions) Insulin, by Merck Group (15 mentions)

656 protocols using palmitic acid

Palmitic Acid and Insulin Treatment of HTR-8/SVneo Cells

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Human HTR-8/SVneo cells gifted by Professor Yanling Wang from the Institute of Zoology of Chinese Academy of Sciences were cultured in RPMI-1640 complete medium (10% fetal bovine serum, 1% double antibody) placed in a 37°C cell culture incubator at 5% CO₂. When the cells reached approximately 90% confluency, they were digested with 0.25% trypsin, and 1:2 split passages were continued and the cells were grown to logarithmic growth phase.
Palmitic acid (Sigma, St Louis, USA) powder was dissolved in 0.1 M NaOH at 70°C to form a 100 nM Palmitic acid mother liquor, and then RPMI-1640 complete medium was added to prepare a 5 mM stock solution that was stored at −20°C. When in use, the Palmitic acid solution was heated in a water bath at 55°C for 15 min, following by cooling at room temperature. Cells in Palmitic acid treatment group were treated with different concentrations of Palmitic acid (0.1, 0.25, 0.5, 0.75, and 1.0 μM), and those in insulin-treated group were treated with different concentrations of insulin (0.05, 0.25, 0.5, 1.0, and 1.5 μM) (Sigma, St Louis, USA); Cells in both groups were then cultured for 24 h.

Guan C.Y., Tian S., Cao J.L., Wang X.Q., Ma X, & Xia H.F. (2020). Down-Regulated miR-21 in Gestational Diabetes Mellitus Placenta Induces PPAR-α to Inhibit Cell Proliferation and Infiltration. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 13, 3009-3034.

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Metabolic Syndrome Modeling in Liver Slices

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Williams medium E with Glutamax (Invitrogen, Bleiswijk, the Netherlands), supplemented with gentamycin (50 mg/mL; Invitrogen), was used as control medium. To mimic metabolic syndrome, supraphysiological concentrations of glucose (Merck, Darmstadt, Germany), fructose (Merck, Darmstadt, Germany), human insulin (Sigma-Aldrich, St. Louis, MO, USA), and palmitic acid (Sigma-Aldrich, St. Louis, MO, USA) were added to the medium. The experimental concentrations (Table 1) were based on human serum concentrations [5 (link),6 (link),7 (link),11 (link),32 (link),33 (link)] and in vivo rodent portal vein concentrations [38 (link),39 (link),40 (link)].
palmitic acid was solubilized using bovine serum albumin (BSA; Sigma-Aldrich, St. Louis, MO, USA). palmitic acid was briefly dissolved in 0.1 M sodium hydroxide (Merck, Darmstadt, Germany) at 70 °C, and then mixed with preheated BSA solution at 55 °C. The same concentration of BSA (0.04%), without palmitic acid, was added to media not containing palmitic acid. This concentration of BSA had no effect on PCLS viability.

Prins G.H., Luangmonkong T., Oosterhuis D., Mutsaers H.A., Dekker F.J, & Olinga P. (2019). A Pathophysiological Model of Non-Alcoholic Fatty Liver Disease Using Precision-Cut Liver Slices. Nutrients, 11(3), 507.

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Glucose and Palmitic Acid Cell Culture

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After pretreatment, the cells were grown in medium, including 50 mM D-glucose (Sigma Aldrich, St. Louis, MO, USA) and/or 0.5 mM palmitic acid (Sigma Aldrich), for 48 h. Glucose solution of 1 M was prepared by dissolving glucose in PBS. Then an appropriate amount of glucose solution was added to the prewarmed (37 °C) medium. The final concentration of glucose in medium was 50 mM. The glucose medium was filtered with 0.2 M sterile filter (Sartorius, Goettingen, Germany) before treatment. The medium containing fatty acid was prepared by combining palmitic acid (PA) with bovine serum albumin (BSA) (Sigma Aldrich). BSA was dissolved in PBS to make a 20% (w/v) BSA solution. Then 0.0056 g palmitic acid (Sigma Aldrich) was dissolved in 1 mL double-distilled water containing 100 μL 1N NaOH to make fresh 20 mM PA solution each time by incubating at 70 °C in a water bath for 15~30 min. palmitic acid was immediately added to prewarmed (37°C) 20% BSA solution in the required amount, and then the mixture was added to prewarmed (37°C) medium. The final concentration of PA in medium was 0.5 mM, and the molar ratio of PA to BSA was 2:1. The medium containing PA was filtered to treat the cells.

Wang S., Jung S, & Ko K.S. (2022). Effects of Amino Acids Supplementation on Lipid and Glucose Metabolism in HepG2 Cells. Nutrients, 14(15), 3050.

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Palmitic Acid Metabolism and ROS

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Palmitic acid (Sigma–Aldrich, St Louis, MO, USA) was dissolved in 0.01 mM NaOH at 90°C for 10 min. Then, the clear solution was complexed with 5% fatty acid‐free bovine serum albumin (BSA; Sigma–Aldrich) and shaken gently at 37°C for 2 h. The complexed Palmitic acid solution was added to the cell culture medium to obtain the indicated final Palmitic acid concentration. N‐Acetyl‐L‐cysteine (NAC; Sigma–Aldrich) dissolved in phosphate‐buffered saline (PBS) was added to the culture medium, and the final concentration was 5 mM. To determine the ROS levels, the cells were stained with 10 μM 2',7'‐dichlorofluorescin diacetate (Sigma–Aldrich) dissolved in PBS for 30 min in the dark at 37°C. The ROS generation from mitochondria was evaluated by a Mitochondrial ROS Detection Kit (Cayman Chemical, Ann Arbor, MI, USA). The fluorescence was measured with a FlexStation 3 (Molecular Devices, San Jose, CA, USA).

Pan X., Mizukami H., Hara Y., Yamada T., Yamazaki K., Kudoh K., Takeuchi Y., Sasaki T., Kushibiki H., Igawa A, & Hakamada K. (2022). Diabetes mellitus impacts on expression of DNA mismatch repair protein PMS2 and tumor microenvironment in pancreatic ductal adenocarcinoma. Journal of Diabetes Investigation, 14(1), 132-144.

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Palmitic Acid and Thapsigargin Treatment Protocol

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Palmitic acid (#P0500, dissolved in ethanol) and thapsigargin (#T9033, dissolved in DMSO) were from Sigma-Aldrich. Prior to treatment Palmitic acid was bound to fatty acid free bovine serum albumin (A7030, Sigma-Aldrich) by first dissolving BSA in DMEM (without supplements) at 20 % (w/v) concentration and then adding 10x Palmitic acid to the solution. The solution was then placed on a shaker at 42°C for 30 minutes to allow for binding of Palmitic acid to BSA. The BSA/Palmitic acid solutions were then diluted 1:10 with DMEM and final concentration of 5 % BGS, 1 % Penicillin/streptomycin and 2 % BSA. For the dose range of Palmitic acid from 200–600 μM the molar ratio range of Palmitic acid to BSA was 0.83:1 – 2:1, with the ratio for the 400 μM Palmitic acid being 1.33:1. thapsigargin and vehicle treatments were prepared in similar medium (DMEM with 5 % BGS, 1 % penicillin/streptomycin and 2 % BSA).

Jäntti M.H., Jackson S., Kuhn J., Parkkinen I., Sree S., Hinkle J., Jokitalo E., Deterding L, & Harvey B.K. (2022). Palmitate and thapsigargin have contrasting effects on ER membrane lipid composition and ER proteostasis in neuronal cells. Biochimica et biophysica acta. Molecular and cell biology of lipids, 1867(11), 159219.

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Evaluating Magnolol's Impact on Hepatic Steatosis

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Human hepatoma cell line HepG2 was obtained from American Type Culture Collection (ATCC, Manassas, VA, USA) and cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco Life Technologies, Grand Island, NY, USA) containing 10% fetal bovine serum at 37 °C in a humidified atmosphere containing 5% CO₂. Cellular steatosis was induced by treatment with 0.3 mM palmitic acid (PA) (Sigma-Aldrich, St. Louis, MO, USA) conjugated with serum-free bovine albumin for 24 h. HepG2 cells were divided into the following four groups (n = 5 for each group): (1) Ctrl group: cells were treated with 0.1% DMSO; (2) MG group: cells were treated with magnolol (8 μg/mL); (3) PA group: cells were treated with 0.3 mM palmitic acid for 24 h; and (4) PA+MG group: cells were pretreated with magnolol (8 μg/mL) for 6 h before PA exposure.

Kuo N.C., Huang S.Y., Yang C.Y., Shen H.H, & Lee Y.M. (2020). Involvement of HO-1 and Autophagy in the Protective Effect of Magnolol in Hepatic Steatosis-Induced NLRP3 Inflammasome Activation In Vivo and In Vitro. Antioxidants, 9(10), 924.

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Isolating and Treating Murine Hepatocytes

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Hepatocytes were isolated from male C57BL/6 mice by a two-step (collagenase B and pronase E) perfusion method under ketamine/xylazine anesthesia as described previously (24 (link)). The isolated hepatocytes were seeded in collagen-coated culture dishes at a density of 2^*10∧5 cells/ml and cultured in Dulbecco's modified Eagle's medium (HyClone, Logan, UT, USA) supplemented with 10% fetal bovine serum (Gibco, Carlsbad, CA, USA) and 1% (v/v) penicillin-streptomycin at 37°C in 5% CO2 incubator for 48 h. The hepatocytes were then serum-starved for 6 h, followed by treatment with adiponectin (APN; 10 μg/ml, Biovendor, Nycodenz) for 2 h prior to 300 μmol/ml palmitic acid (PA; Sigma, St. Louis, MO) exposure for 24 h. Palmitic acid was conjugated to 2% BSA and dissolved in DMEM, 2%BSA was added as control in untreated group. For the inhibition experiment, the hepatocytes were treated with AMPK inhibitor (compound C, 10 μm/M; Sigma) 2 h prior to adiponectin treatment. The treated hepatocytes and culture supernatant were collected for subsequent analyses.

Dong Z., Zhuang Q., Ye X., Ning M., Wu S., Lu L, & Wan X. (2020). Adiponectin Inhibits NLRP3 Inflammasome Activation in Nonalcoholic Steatohepatitis via AMPK-JNK/ErK1/2-NFκB/ROS Signaling Pathways. Frontiers in Medicine, 7, 546445.

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Modulating Cell Line Responses to Inflammatory Stimuli

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The LX-2 and HepG2 cell lines were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA). These cells were cultured in DMEM (BI, Israel) supplemented with 10% fetal bovine serum (FBS, BI) and 1% penicillin/streptomycin at 37°C with 5% CO 2 . In the experimental groups, LX-2 cells were exposed to ST2825 (10 µM) (MedChemExpress, USA) for 2 h, and then were challenged with TLR1/2 agonist (Pam3CSK4, 100 ng/mL), TLR4 agonist (LPS, 1 mg/mL) and palmitic acid (400 µM) (Sigma, USA) respectively for 24 h. In the control groups, LX-2 cells were directly challenged with TLR1/2 agonist (Pam3CSK4, 100 ng/mL), TLR4 agonist (LPS, 1 mg/mL) and palmitic acid (400 µM) (Sigma, USA) respectively for 24 h. To induce excessive lipid accumulation, HepG2 cells were cultured in DMEM medium with 20 µM AKT inhibitor (CSNpharm, USA) for 24h, then 400 µM palmitic acid and 200 ng/mL recombinant protein OPN (Cloud-Clone Corp, China) for 24h [32] .

Li Y., Wei M., Yuan Q., Liu Y., Tian T., Hou L, & Zhang J. (2022). MyD88 in hepatic stellate cells promotes the development of alcoholic fatty liver via the AKT pathway. Journal of molecular medicine (Berlin, Germany), 100(7).

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Synthesis of Diols-Derived Compounds

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Compounds 10 & 11 were synthesized from diols 8 & 9 respectively according to the protocol reported for PDIM A synthesis (42 (link), 43 (link)). Compound 8 (10 mg, 53.11 μmol), palmitic acid (40.9 mg, 159.33 μmol, 3.0 eq, Sigma-Adrich), DCC (43.8 mg, 212.44 μmol, 4.0 eq) and DMAP (26.0 mg, 212.44 μmol, 4.0 eq) were dissolved in dry DCM (0.5 mL) and the resulting mixture was stirred at 25 °C for 48 hours under nitrogen. Compound 9 (10 mg, 41.08 μmol), palmitic acid (31.6 mg, 123.24 μmol, 3.0 eq, Sigma-Aldrich), DCC (33.9 mg, 164.32 μmol, 4.0 eq) and DMAP (20.1 mg, 163.32 μmol, 4.0 eq) were dissolved in dry DCM (0.5 mL) and the resulting mixture was stirred at 25 °C for 48 hours under nitrogen. For both reactions, the solvent was removed under reduced pressure and the product was purified by silica gel chromatography with hexanes/ethyl ether (50:1, v/v) to obtain compound 10 (30 mg, 85.0% yield) or 11 (16.9 mg, 57.1% yield) as a white wax.

Touchette M.H., Bommineni G.R., Delle Bovi R.J., Gadbery J.E., Nicora C.D., Shukla A.K., Kyle J.E., Metz T.O., Martin D.W., Sampson N.S., Miller W.T., Tonge P.J, & Seeliger J.C. (2015). Diacyltransferase Activity and Chain Length Specificity of Mycobacterium tuberculosis PapA5 in the Synthesis of Alkyl Beta-Diol Lipids. Biochemistry, 54(35), 5457-5468.

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Inflammatory Mediator Modulation Protocol

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ILG was purchased from AK Scientific Inc. (Union City, CA, USA) and Sigma-Aldrich (St. Louis, MO, USA). Pioglitazone was purchased from Funakoshi (Tokyo, Japan). ILG and pioglitazone were dissolved in dimethyl sulfoxide (DMSO). Recombinant mouse TNF-α, IL-4, and IFN-γ were purchased from R & D Systems (Minneapolis, MN, USA). Human insulin was purchased from Eli Lilly (Indianapolis, IN, USA). LPS from E. coli O55:B5, lipid A from Salmonella minnesota, palmitic acid, TDM, ATP, and thioglycolate were purchased from Sigma-Aldrich. palmitic acid was conjugated to bovine serum albumin (BSA, Sigma-Aldrich) to increase solubility. BAY11-7082 was purchased from InvivoGen (San Diego, CA, USA). PD98059 was purchased from Merck Millipore (Darmstadt, Germany).

Watanabe Y., Nagai Y., Honda H., Okamoto N., Yamamoto S., Hamashima T., Ishii Y., Tanaka M., Suganami T., Sasahara M., Miyake K, & Takatsu K. (2016). Isoliquiritigenin Attenuates Adipose Tissue Inflammation in vitro and Adipose Tissue Fibrosis through Inhibition of Innate Immune Responses in Mice. Scientific Reports, 6, 23097.

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