A biochemical reagent called palmitic acid (sodium) can be utilized in life science research as an organic compound or biological material.

Absorption, Distribution and Excretion
Rat liver slices were incubated with 14C-labeled sodium palmitate at 37°C for 120 minutes. Lipid fractions were extracted and separated by chromatography. After 5 minutes, palmitate reached maximum incorporation into the phospholipid fraction. 14C-1-palmitate was injected into rabbit fetuses in utero. Radioactivity in the fetal liver, blood, carcass, and placenta was measured. Total specific activity was highest in plasma early on, but maximum incorporation occurred in the liver later. Phospholipid incorporation was faster. Metabolism/Metabolites Metabolism of radiolabeled acetone, acetate, or palmitate was investigated in pregnant and non-pregnant guinea pigs. Fasting pregnant and non-pregnant guinea pigs were cardiacally injected with 14C-labeled acetone, sodium acetate, or sodium palmitate, respectively. The dose range was 0.4 to 2.2 mg/kg body weight. Exhaled carbon dioxide was collected and its radioactivity was measured. The carbon-14 content in lipids and the total acetone bodies in blood and urine were determined. …In the sodium palmitate treatment group, the specific activity of carbon dioxide in pregnant guinea pigs was twice that of the control group. The carbon-14 content in liver lipids in the non-pregnant group was twice that of the pregnant group. The authors concluded that pregnant guinea pigs utilize carbon-14 more for biosynthesis than for carbon dioxide excretion, while the opposite is true for non-pregnant guinea pigs. Adipocytes isolated from rat epididymal adipose tissue were incubated with albumin-bound carbon-14 palmitate. The amount of carbon-14 incorporated into carbon dioxide and glycerides was determined. Some evidence suggests that the exogenous palmitate library is in isotopic equilibrium with the intracellular precursors of these metabolic processes. Precautions were taken to minimize the dilution of the exogenous palmitate library by cellularly released fatty acids. The carbon dioxide produced by 1-carbon-14 palmitate was three times that produced by 16-carbon-14 palmitate. Octate enhanced the differential oxidation of palmitic acid carbon and inhibited the oxidation of palmitic acid, but had no similar effect on esterification. Glucose increased palmitate esterification in the cells of both starved and starved rats. Insulin enhanced this effect of glucose. The effect of glucose on palmitate oxidation is more complex and depends on glucose concentration. Esterification accounts for 99% of fatty acid metabolic flux, and the ways in which glucose, insulin, or starvation affects palmitate esterification and oxidation suggest that factors controlling esterification may act as secondary effects to alter oxidation, but the reverse is not true. It is speculated that oxidation and esterification compete for a single intracellular precursor, possibly extramitochondrial long-chain fatty acyl-CoA. /palmitate/

Interactions
Upper body obesity is associated with insulin resistance, hypertension, and endothelial dysfunction. The authors investigated the forearm vascular function response to vasodilator (endothelium-dependent and endothelium-independent) and vasoconstrictor stimulation in eight normotensive, upper body/visceral obese men with a family history of hypertension and eight age-matched non-obese men… Body composition and insulin regulation of free fatty acid (FFA) and glucose metabolism were also measured. Forearm blood flow was measured before and during brachial artery infusion of acetylcholine (Ach), sodium nitroprusside (NTP), and blockade of angiotensin II (±nitric oxide synthase (NO)) synthase with N(G)-monomethyl-L-arginine (L-NMMA). On another day, we measured basal and insulin-regulated glucose ((3-(3)H)glucose) and free fatty acid ((9,10-(3)H)palmitate) turnover. Obese men exhibited a stronger vasoconstrictive response to angiotensin II than non-obese men (P<0.05), while endothelium-dependent vasodilation responses were similar. The slope of the angiotensin II dose-response curve was significantly correlated with basal plasma palmitate concentration. Visceral obesity men showed significantly reduced basal and insulin-mediated glucose disposal rates, while free fatty acid turnover was significantly increased. No differences were found in endothelium-independent vasodilation, nor were there any relationships between vascular reactivity and palmitate and glucose kinetics or body composition. Angiotensin II-stimulated forearm vasoconstriction was enhanced in viscerally obese men with normal blood pressure. /Palmitate/

[1]. Antitumor activity of palmitic acid found as a selective cytotoxic substance in a marine red alga. Anticancer Res. 2002 Sep-Oct;22(5):2587-90.

[2]. Expression of Notch family is altered in non‑alcoholic fatty liver disease. Mol Med Rep. 2020 Sep;22(3):1702-1708.

common saturated fatty acid found in fats and waxes, including olive oil, palm oil, and human lipids.

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Mechanism of Action
Vascular dysfunction is a major complication of metabolic disorders such as diabetes and obesity. This study aimed to determine whether inflammatory responses exist in the vascular system of diet-induced obese mice, and whether Toll-like receptor 4 (TLR4), a key mediator of innate immunity, is involved in these responses. Mice lacking TLR4 (TLR4^(-/-)) and wild-type (WT) control mice were fed a low-fat (LF) control diet or a high-saturated-fat (HF) diet, respectively, for 8 weeks. Compared with mice fed the LF diet, both genotypes of mice fed the HF diet showed similar increases in body weight, body fat percentage, and serum insulin and free fatty acid (FFA) levels. In the aortic lysate of wild-type (WT) mice fed a high-fat diet, vascular inflammatory markers upstream (IKK-β activity) and downstream (ICAM protein and IL-6 mRNA expression) of the transcriptional regulator NF-κB were elevated, and this effect was associated with cellular insulin resistance and impaired insulin-stimulated endothelial nitric oxide synthase (eNOS). Conversely, although the increase in body fat in TLR4(-/-) mice was comparable to that in wild-type mice, no vascular inflammation or impaired insulin responsiveness was observed in aortic samples from TLR4(-/-) mice fed the same high-fat diet. Incubation of wild-type mouse aortic explants or cultured human microvascular endothelial cells with saturated fatty acid palmitate (100 mol/L) also activated IKK-β, inhibited insulin signaling transduction, and blocked insulin-stimulated NO production. Subsequent confirmation indicated that these effects were dependent on the activation of TLR4 and NF-κB. These findings indicate that the TLR4 signaling pathway is a key mediator of the detrimental effects of palmitate on endothelial NO signaling, and for the first time demonstrate that TLR4 plays a crucial role in the mechanism by which diet-induced obesity triggers vascular inflammation and insulin resistance. /Palmitrate/
Insulin stimulates pancreatic β-cells to secrete and synthesize itself. Although the exact molecular mechanisms are unclear, alterations in β-cell insulin signaling have been considered a potential link between insulin resistance and impaired release, as observed in non-insulin-dependent diabetes mellitus. However, insulin resistance is also associated with elevated levels of plasma free fatty acids (FFA), which are well-known regulators of pancreatic insulin secretion. Based on this information, we investigated the effects of FFA on pancreatic insulin receptor signaling. Exposure of pancreatic islet cells to palmitate upregulated multiple insulin-inducible activities, including tyrosine phosphorylation of the insulin receptor and pp185. This is the first time that short-term exposure to 100 μM palmitate in these cells can activate early steps in insulin receptor signaling. 2-Bromopalmitate (a carnitine palmitoyl-CoA transferase-1 inhibitor) did not affect the effects of this fatty acid. Serunine (an acylation inhibitor) eliminated the effects of palmitate on insulin receptor protein levels and phosphorylation. This result supports the view that protein acylation may be an important mechanism by which palmitate regulates the insulin signaling pathway in rat pancreatic islet cells. Accumulation of long-chain fatty acids in the heart is thought to play a role in the development of heart failure and diabetic cardiomyopathy. Multiple animal models have shown increased lipid accumulation in cardiomyocytes, suggesting a link between lipid accumulation, cardiomyocyte death, and cardiomyopathy development. This review summarizes how fatty acid accumulation promotes the occurrence or progression of heart failure by initiating apoptosis. Long-chain saturated fatty acids induce apoptosis by producing reactive intermediates. The production of reactive intermediates occurs concurrently with the de novo synthesis of ceramides, but ceramide production is not essential for cell death. Cardiomyocyte dysfunction and death caused by reactive intermediates produced from long-chain saturated fatty acids may be involved in the pathogenesis of human heart disease. /Long-chain fatty acids/

C16H31NAO2

278.41

278.222

408-35-5

Palmitic acid;57-10-3;Palmitic acid-13C16 sodium;2483736-17-8;Palmitic acid-d31 sodium;467235-83-2;Palmitic acid-d31;39756-30-4;Palmitic acid-1-13C;57677-53-9;Palmitic acid-d2;62689-96-7;Palmitic acid-d3;75736-53-7;Palmitic acid-13C16;56599-85-0;Palmitic acid-d4;75736-49-1;Palmitic acid-13C;287100-87-2;Palmitic acid-13C sodium;201612-54-6;Palmitic acid-d3 sodium;347841-37-6;Palmitic acid-1,2,3,4-13C4;287100-89-4;Palmitic acid-15,15,16,16,16-d5;285979-77-3;Palmitic acid-13C2;86683-25-2;Palmitic acid-d2-1;62690-28-2;Palmitic acid-9,10-d2;78387-70-9

2735111

White to off-white solid powder

340.6ºC at 760mmHg

270 °C

154.1ºC

4.217

0

2

14

19

184

0

CCCCCCCCCCCCCCCC(=O)[O-].[Na+]

GGXKEBACDBNFAF-UHFFFAOYSA-M

InChI=1S/C16H32O2.Na/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16(17)18;/h2-15H2,1H3,(H,17,18);/q;+1/p-1

sodium;hexadecanoate

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, 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: 11.11 mg/mL (39.91 mM)
H2O: < 0.1 mg/mL

Solubility in Formulation 1: ≥ 1.11 mg/mL (3.99 mM) (saturation unknown) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (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 11.1 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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 (Please use freshly prepared in vivo formulations for optimal results.)