Sodium palmitate

Manufactured by Merck Group

Sourced in United States, United Kingdom

Sodium palmitate is a white, waxy solid that is commonly used in laboratory settings. It is a salt of palmitic acid, a saturated fatty acid. Sodium palmitate has various applications in research and analytical processes, but no further details on its intended use will be provided.

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Lab products found in correlation

Sodium oleate, by Merck Group (26 mentions) Bovine serum albumin (bsa), by Merck Group (24 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (13 mentions) Palmitate, by Merck Group (10 mentions) Fatty acid free bsa, by Merck Group (6 mentions) Oleic acid, by Merck Group (6 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (6 mentions) Oil red o, by Merck Group (5 mentions) Thapsigargin, by Merck Group (4 mentions) Fatty acid free bovine serum albumin, by Merck Group (4 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (4 mentions) Tnf α, by Merck Group (3 mentions) Antimycin a, by Merck Group (3 mentions) Sodium pyruvate, by Merck Group (3 mentions) Phosphate buffered saline (pbs), by Merck Group (3 mentions) Oleate, by Merck Group (3 mentions) Penicillin, by Thermo Fisher Scientific (3 mentions) Streptomycin, by Thermo Fisher Scientific (3 mentions) Bodipy fl c16, by Thermo Fisher Scientific (3 mentions) Dimethyl sulfoxide (dmso), by Merck Group (3 mentions)

Spelling variants of this product

Palmitate (284 citations) Sodium palmitate (PA) (7 citations) Sodium palmitate (P9767) (4 citations) U-13C16-Sodium Palmitate (2 citations)

128 protocols using sodium palmitate

Palmitate-BSA Conjugate for Cancer Study

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Sodium Palmitate (Millipore Sigma, #P9767) was heated to 70 C for 30 minutes in autoclaved H 2 O. Aqueous solution of Sodium Palmitate was added dropwise to free fatty acid (FFA)-stripped BSA solution and heated at 37 C for 2 hours to nalize conjugation to a 6:1 molar ratio of palmitate to BSA. Prior to cell treatment stock solutions of either FFA stripped BSA (vehicle control) or Palmitate: BSA (6:1 molar ratio) were heated to 37 C and added to 2% charcoal-stripped FBS media. MCF7 and MCF7/TamR cells were seeded in six-well plates at a density of 350,000/well and allowed to adhere for 24 hours. 10% FBS DMEM media was replaced with 2% charcoal-stripped FBS media containing either BSA, Palmitate:BSA, TVB-3166, TVB-3166 + BSA, or TVB-3166 + Palmitate:BSA. Additionally, cells were pretreated with 1,2-Bis(2-Aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA) (Millipore Sigma Aldrich, #A4926) for 60 minutes (20 µM) prior to the addition of TVB-3166 (200 nM) for 72 hours.

Gruslova A., McClellan B., Balinda H.U., Viswanadhapalli S., Alers V., Sareddy G.R., Huang T., Garcia M., deGraffenried L., Vadlamudi R.K, & Brenner A.J. (2021). FASN inhibition as a potential treatment for endocrine-resistant breast cancer. Breast cancer research and treatment, 187(2).

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Palmitate-BSA Conjugation and Calcium Signaling

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Sodium Palmitate (Millipore Sigma, #P9767) was heated to 70 C for 30 minutes in autoclaved H 2 O. Aqueous solution of Sodium Palmitate was added dropwise to free fatty acid (FFA)-stripped BSA solution and heated at 37 C for 2 hours to finalize conjugation to a 6:1 molar ratio of palmitate to BSA. Prior to cell treatment stock solutions of either FFA stripped BSA (vehicle control) or Palmitate: BSA (6:1 molar ratio) were heated to 37 C and added to 2% charcoal-stripped FBS media. MCF7 and MCF7/TamR cells were seeded in six-well plates at a density of 350,000/well and allowed to adhere for 24 hours. 10% FBS DMEM media was replaced with 2% charcoal-stripped FBS media containing either BSA, Palmitate:BSA, TVB-3166, TVB-3166 + BSA, or TVB-3166 + Palmitate:BSA. Additionally, cells were pretreated with 1,2-Bis(2-Aminophenoxy)ethane-N,N,N′,N′tetraacetic acid (BAPTA) (Millipore Sigma Aldrich, #A4926) for 60 minutes (20 µM) prior to the addition of TVB-3166 (200 nM) for 72 hours.

Gruslova A., McClellan B., Balinda H., Viswanadhapalli S., Alers V., Sareddy G.R., Perfit M.R., deGraffenried L.A., Vadlamudi R.K., & Brenner A. (2021). FASN Inhibition as a Potential Treatment for Endocrine-Resistant Breast Cancer.

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Mitochondrial Respiration Modulation

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NTZ, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), antimycin A, 2,4-DNP, oligomycin, and sodium palmitate were obtained from Sigma. Z-VAD-FMK was obtained from Selleckchem. Tizoxanide (TZ) was obtained from MedChem Express. Cidofovir was obtained from Gilead Sciences Inc. DL-mevalonolactone was obtained from TCI Chemicals. sodium palmitate was conjugated to fatty acid free BSA (Sigma) according to the Seahorse Bioscience protocol.

Hickson S.E., Margineantu D., Hockenbery D.M., Simon J.A, & Geballe A.P. (2018). Inhibition of vaccinia virus replication by nitazoxanide. Virology, 518, 398-405.

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Preparation of Sodium Palmitate and Oleate Solution

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A 5 mM stock solution of sodium palmitate (Sigma-Aldrich) was prepared by dissolving the fatty acid salt in 10% BSA (Sigma-Aldrich, fraction V, fatty acid-free) in Krebs buffer by continuous stirring for ∼4 h in a 37 °C water bath. The stock solution was then diluted by Krebs buffer to obtain the final concentration of 0.5 mM sodium palmitate. To prepare a 2:1 mixture of palmitate and oleate (final fatty acid concentration: 0.5 mM), sodium palmitate was dissolved first, followed by the addition of the proper amount of sodium oleate (Sigma-Aldrich).

Zhu L., Almaça J., Dadi P.K., Hong H., Sakamoto W., Rossi M., Lee R.J., Vierra N.C., Lu H., Cui Y., McMillin S.M., Perry N.A., Gurevich V.V., Lee A., Kuo B., Leapman R.D., Matschinsky F.M., Doliba N.M., Urs N.M., Caron M.G., Jacobson D.A., Caicedo A, & Wess J. (2017). β-arrestin-2 is an essential regulator of pancreatic β-cell function under physiological and pathophysiological conditions. Nature Communications, 8, 14295.

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Ferroptosis Pathway Modulation Assay

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TVB-3664 (FASNi) or the inactive isomer (TVB-2632) were from Sagimet Biosciences (San Mateo, CA). ML162 (#20455) or Ferrostatin-1 (#17729) were from Cayman. ARS-1620 (HY-U00418) and Liproxstatin-1 (HY-12726) were from MedChemExpress. 16:0–18:1 PC (hereafter PC #850457P), Sodium palmitate (#P9767) and N-Acetyl-L-cysteine (#A7250) were from Millipore-Sigma. CellROX™ Green Reagent (#C10444) was from Thermo Fischer Scientific.

Bartolacci C., Andreani C., Vale G., Berto S., Melegari M., Crouch A.C., Baluya D.L., Kemble G., Hodges K., Starrett J., Politi K., Starnes S.L., Lorenzini D., Raso M.G., Solis Soto L.M., Behrens C., Kadara H., Gao B., Wistuba I.I., Minna J.D., McDonald J.G, & Scaglioni P.P. (2022). Targeting de novo lipogenesis and the Lands cycle induces ferroptosis in KRAS-mutant lung cancer. Nature Communications, 13, 4327.

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Overexpression of CRTC1 in MIN6 Cells

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MIN6 cells were obtained from AddexBio (San Diego, CA, USA), cultured between passages 11–25 and maintained in culture as previously described [58 (link)]. In detail, MIN6 were cultured in DMEM (cat. 5671, Sigma-Aldrich, St. Louis, MO, USA) supplemented with L-Glutamine 1%, Antibiotic/Antimicotic 1% (A5955, Sigma-Aldrich, St. Louis, MO, USA), FBS 15% (cat. ECS0180L, Euroclone, Milan, Italy), sodium pyruvate 1% (cat. ECM0542D, Euroclone, Milan, Italy) and β-Mercaptoethanol 50 µM. MIN6 were transfected with CRTC1 overexpressing plasmid (EX-Mm18750-Lv183) or with control plasmid (EX-EGFP-Lv151) (both from Genecopoeia, Rockville, MD, USA) through Lipofectamine 2000 transfection reagent. Lipotoxic stress was induced by using 0.5 mM of sodium palmitate (Sigma-Aldrich, St. Louis, MO, USA) or with EtOH 0.5% as a control treatment for 48 h as previously described [59 (link)]. Pro-inflammatory stress was induced by a cytokines mix composed of IL-1β (5 ng/mL, cat. I5271, Sigma-Aldrich, St. Louis, MO, USA), TNFα (30 ng/mL, cat. T7539) and IFNγ (10 ng/mL, cat. 485MI- R&D System, Minneapolis, MN, USA) for 24 h. Oxidative stress was induced using H₂O₂ (cat. H1009, Sigma-Aldrich, St. Louis, MO, USA) at 100 µM for 90 min.

Grieco G.E., Brusco N., Fignani D., Nigi L., Formichi C., Licata G., Marselli L., Marchetti P., Salvini L., Tinti L., Po A., Ferretti E., Sebastiani G, & Dotta F. (2022). Reduced miR-184-3p expression protects pancreatic β-cells from lipotoxic and proinflammatory apoptosis in type 2 diabetes via CRTC1 upregulation. Cell Death Discovery, 8, 340.

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Metabolic Profiling of Immune Cells

Cited 1 time

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Chicken γ globulin (CGG; Sigma-Aldrich), 4-Hydroxy-3-nitrophenylacetyl (NP)-conjugates and detection reagents were as described^{35 (link)}. All antibodies used in this study are described in detail in the Nature Research Reporting Summary and in Supplementary Table 1. DAPI was from BD Biosciences and Streptavidin (CAS no. 9013–20.1) was from Sigma-Aldrich. Ghost Dye Violet 510 was from Tonbo Biosciences. Peanut agglutinin (PNA) was purchased from Vector laboratories (lot ZD0814) and conjugated Alexa Fluor 700 in our laboratory. 2-NBDG (N13195 or Cayman #11046), BODIPYTM FL C12 (D-3822; for in vitro metabolite uptake) and BODIPYTM FL C16 (D-3821; for in vivo metabolite uptake) were from Life Technologies. (+)- Etomoxir sodium salt (CAS no. 828934-41-4) and Thioridazine hydrochloride (CAS no. 130-61-0) were from Cayman Chemicals. Sodium Palmitate (Sigma, P9767) was conjugated to ultra-fatty acid-free bovine serum albumin (BSA; Roche) following the Seahorse Bioscience protocol as described^{53 (link)}.

Weisel F.J., Mullett S.J., Elsner R.A., Menk A.V., Trivedi N., Luo W., Wikenheiser D., Hawse W.F., Chikina M., Smita S., Conter L.J., Joachim S.M., Wendell S.G., Jurczak M.J., Winkler T.H., Delgoffe G.M, & Shlomchik M.J. (2020). Germinal center B cells selectively oxidize fatty acids for energy while conducting minimal glycolysis. Nature immunology, 21(3), 331-342.

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Palmitate-Induced Microglial Stress Response

Cited 3 times

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In a separate cohort, young (n=6) and aged (n=6) chow-fed male rats were euthanized and hippocampal and amygdalar microglia were isolated and plated as described above. A 100x concentration of sodium palmitate (Sigma, P9767) was reconstituted in molecular biology grade water and heated to 70°C for ~ 5 min before being diluted 1:10 in DMEM + 10% FBS heated to 37 °C. Palmitate was further diluted 1:10 to the working concentration upon delivery to the wells. Microglia were incubated with palmitate (50, 100, and 500μM) or vehicle for 2 h at 37 °C, 5% CO2. These doses were chosen in accordance with previous studies that treated microglia, astrocytes, or neurons with palmitate (Duffy et al., 2015b (link); Frago et al., 2017 (link); Hidalgo-Lanussa et al., 2017 (link); Listenberger et al., 2001b (link); Sergi et al., 2018 (link); Tse and Belsham, 2018 (link); Wang et al., 2012 (link); Yanguas-Casás et al., 2018 (link)) and are consistent with a physiological range of plasma palmitic acid levels (Abdelmagid et al., 2015 (link)). Following treatment, the plate was centrifuged at 1000×g for 10 min at 4 °C to pellet cells and cells washed 1× in ice-cold PBS and centrifuged at 1000×g for 10 min at 4 °C. Cell lysis/homogenization, DNase treatment, and cDNA synthesis were performed as described above.

Butler M.J., Cole R.M., Deems N.P., Belury M.A, & Barrientos R.M. (2020). Fatty food, fatty acids, and microglial priming in the adult and aged hippocampus and amygdala. Brain, behavior, and immunity, 89, 145-158.

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Hypoxia Modulation of Insulin and FFA Effects

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Early passage (passages 3–4) HK-2 cells were grown to 80% confluence and made quiescent by serum starvation for 24 h. Cells were then exposed to hypoxia (1% O₂, 5% CO₂, 94% nitrogen gas) for 24 h in a hypoxia workstation (Hirasawa Works, Tokyo, Japan) or remained in the CO₂ incubator used for routine culture (normoxia). An oxygen sensor was used to ensure that the oxygen concentration inside the workstation was maintained at 1% throughout the experiments (MC-8G-S, Iijima electronics corporation, Aichi, Japan). Cells were further supplemented with 1 μM human insulin (Sigma Aldrich) or 0.3 mM FFA. The FFA stock solution consisted of 6.35 mM sodium palmitate (Sigma Aldrich) and 12.7 mM sodium oleate (Sigma Aldrich) in FFA-free bovine serum albumin (BSA) (1.8 mM) as previously described48 (link)49 (link). Cells were divided into six groups: (1) cells without insulin or FFA in normoxia (normal O₂ concentration of 20%), (2) cells without insulin or FFA in hypoxia, (3) cells with insulin in normoxia, (4) cells with insulin in hypoxia, (5) cells with FFA in normoxia and (6) cells with FFA in hypoxia. After incubation for 24 h, cells were collected using TRIzol reagent (Invitrogen, Carlsbad, CA) to perform real-time RT-PCR.

Futatsugi K., Tokuyama H., Shibata S., Naitoh M., Kanda T., Minakuchi H., Yamaguchi S., Hayashi K., Minamishima Y.A., Yanagita M., Wakino S, & Itoh H. (2016). Obesity-induced kidney injury is attenuated by amelioration of aberrant PHD2 activation in proximal tubules. Scientific Reports, 6, 36533.

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Palmitate-BSA Preparation Protocol

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Sodium palmitate (P9767; Sigma-Aldrich) was prepared by diluting a 200 mM stock solution in 70% ethanol into 10% fatty acid–free, low-endotoxin bovin serum albumin (BSA) (A-8806; Sigma-Aldrich; adjusted to pH 7.4) by heating at 50 °C. The palmitate-BSA stock solution was filtered using a 0.22-µm low-protein binding filter (Millipore, Billerica, MA, USA). Sodium palmitate was added at 0.5 mM. BSA/70% ethanol (10%) was used as vehicle in control cells.

De Cicco P., Maisto M., Tenore G.C, & Ianaro A. (2020). Olive Leaf Extract, from Olea europaea L., Reduces Palmitate-Induced Inflammation via Regulation of Murine Macrophages Polarization. Nutrients, 12(12), 3663.

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