一种称为棕榈酸（钠）的生化试剂可作为有机化合物或生物材料用于生命科学研究。

Absorption, Distribution and Excretion
Rat liver slices were incubated with (14)C-labeled sodium palmitate for 120 min at 37 °C. Lipid fractions extracted & separated by chromatography. Palmitate was maximally incorporated into phospholipid fractions after 5 min.
(14)C-1-Palmitate was injected into rabbit fetuses in utero. Fetal liver, blood, carcass & placenta checked for radioactivity. Highest total early specific activity in plasma, but later liver displayed most extensive incorporation. Phospholipid incorporation more rapid.

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Metabolism / Metabolites
The metabolism of radiolabeled acetone, acetate, or palmitate was studied in pregnant and nonpregnant guinea-pigs. Fasted pregnant guinea-pigs and guinea-pigs that were not pregnant were injected intracardially with carbon-14 C-(14) labeled acetone, sodium-acetate, or sodium-palmitate. Doses ranged from 0.4 to 2.2 milligrams per kilogram. Expired carbon-dioxide was collected and assayed for radioactivity. C-(14) content of lipids, and blood and urine total acetone bodies were measured. ... In the palmitate treated animals, specific carbon-dioxide activities were twice as great in the pregnant guinea-pigs. Liver lipid C-(14) content of the group that were not pregnant was twice that of the pregnant group. The authors conclude that pregnant guinea-pigs used C-(14) more for biosynthesis than for carbon-dioxide excretion, while the opposite is true for guinea-pigs that were not pregnant.
Fat cells isolated from rat epididymal adipose tissue were incubated with albumin-bound (14)C-palmitate. Incorporation of (14)C into (14)CO2, and glycerides was measured. Some evidence is presented to suggest that the exogenous palmitate pool is in isotopic equilibrium with intracellular precursors for these metabolic processes. Precautions were taken to minimize dilution of the exogenous palmitate pool by fatty acids released from the cells. (14)CO2 production from (1-(14)C)-palmitate was 3 times that from (16-(14)C)-palmitate. Octanoate increased this differential oxidation of palmitate carbons and also inhibited palmitate oxidation without similarly affecting esterification. Glucose increased palmitate esterification in cells from fed or starved rats. Insulin potentiated this effect of glucose. Glucose influenced palmitate oxidation in a more complex manner, dependent upon the glucose concentration. Both the observation that esterification constitutes 99% of the metabolic flux of fatty acid and the manner in which glucose, insulin, or starvation influence palmitate esterification and oxidation suggested that factors controlling esterification may alter oxidation as a secondary effect, but not vice versa. It is suggested 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/ examined forearm vascular function in response to vasodilator (endothelium-dependent and endothelium-independent) and vasoconstrictor stimuli in 8 normotensive, upper body/viscerally obese men with a positive family history of hypertension and 8 age-matched nonobese 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 infusions of acetylcholine (Ach), sodium nitroprusside (NTP), and angiotensin II (+ / - nitric oxide synthase (NO)) synthase blockade with N(G)-monomethyl L-arginine (L-NMMA). On a separate day, baseline and insulin-regulated glucose ((3-(3)H)glucose) and FFA ((9,10-(3)H)palmitate) turnover were measured. The vasoconstrictor response to angiotensin II was greater (P<0.05) in obese men than in nonobese men, whereas endothelium-dependent vasodilation was similar. The slope of the angiotensin II dose-response curve correlated significantly with the basal plasma palmitate concentration. Basal and insulin-mediated glucose disposal was significantly reduced and FFA turnover significantly increased in viscerally obese men. No differences in endothelium-independent vasodilation or relationships between vascular responsivity and palmitate and glucose kinetics or body composition were found. Angiotensin II-stimulated forearm vasoconstriction is increased in viscerally obese normotensive men. /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.

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

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Mechanism of Action
Vascular dysfunction is a major complication of metabolic disorders such as diabetes and obesity. The current studies were undertaken to determine whether inflammatory responses are activated in the vasculature of mice with diet-induced obesity, and if so, whether Toll-Like Receptor-4 (TLR4), a key mediator of innate immunity, contributes to these responses. Mice lacking TLR4 (TLR4(-/-)) and wild-type (WT) controls were fed either a low fat (LF) control diet or a diet high in saturated fat (HF) for 8 weeks. In response to HF feeding, both genotypes displayed similar increases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared with mice on a LF diet. In lysates of thoracic aorta from WT mice maintained on a HF diet, markers of vascular inflammation both upstream (IKK-beta activity) and downstream of the transcriptional regulator, NF-kappa-B (ICAM protein and IL-6 mRNA expression), were increased and this effect was associated with cellular insulin resistance and impaired insulin stimulation of endothelial nitric oxide synthase (eNOS). In contrast, vascular inflammation and impaired insulin responsiveness were not evident in aortic samples taken from TLR4(-/-) mice fed the same HF diet, despite comparable increases of body fat mass. Incubation of either aortic explants from WT mice or cultured human microvascular endothelial cells with the saturated FFA, palmitate (100 mol/L), similarly activated IKK-beta, inhibited insulin signal transduction and blocked insulin-stimulated NO production. Each of these effects was subsequently shown to be dependent on both TLR4 and NF-kappa-B activation. These findings identify the TLR4 signaling pathway as a key mediator of the deleterious effects of palmitate on endothelial NO signaling, and are the first to document a key role for TLR4 in the mechanism whereby diet-induced obesity induces vascular inflammation and insulin resistance. /Palmitate/
Insulin stimulates its own secretion and synthesis by pancreatic beta-cells. Although the exact molecular mechanism involved is unknown, changes in beta-cell insulin signalling have been recognized as a potential link between insulin resistance and its impaired release, as observed in non-insulin-dependent diabetes. However, insulin resistance is also associated with elevated plasma levels of free fatty acids (FFA) that are well known modulators of insulin secretion by pancreatic islets. This information led us to investigate the effect of FFA on insulin receptor signalling in pancreatic islets. Exposure of pancreatic islets to palmitate caused up-regulation of several insulin-induced activities including tyrosine phosphorylation of insulin receptor and pp185. This is the first evidence that short exposure of these cells to 100 microM palmitate activates the early steps of insulin receptor signalling. 2-Bromopalmitate, a carnitine palmitoyl-CoA transferase-1 inhibitor, did not affect the effect of the fatty acid. Cerulenin, an acylation inhibitor, abolished the palmitate effect on protein levels and phosphorylation of insulin receptor. This result supports the proposition that protein acylation may be an important mechanism by which palmitate exerts its modulating effect on the intracellular insulin signalling pathway in rat pancreatic islets.
Accumulation of long-chain fatty acids in the heart has been proposed to play a role in the development of heart failure and diabetic cardiomyopathy. Several animal models with increased cardiomyocyte lipid accumulation suggest a link between the accumulation of lipid, cardiomyocyte cell death and the development of cardiomyopathy. In this review, we discuss the mechanism through which fatty acid accumulation may contribute to the development or progression of heart failure by initiation of apoptotic cell death. Long-chain saturated fatty acids induce apoptosis through a mechanism involving the generation of reactive intermediates. Reactive intermediate production occurs in concert with de novo ceramide synthesis, but ceramide production is not required for cell death. Cardiomyocyte dysfunction and death from reactive intermediates generated by long-chain saturated fatty acids may contribute to 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

283-290 °C(lit.)

154.1ºC

4.217

40.13

0

2

14

19

184

0

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

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

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

配方 1 中的溶解度: ≥ 1.11 mg/mL (3.99 mM) (饱和度未知) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 11.1 mg/mL澄清的DMSO储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80 +，混匀；然后加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。