Role Of Palmitic Acid Research Articles

The Role of Palmitic Acid in the Co-Toxicity of Bacterial Metabolites to Endothelial Cells.

Metabolic endotoxemia most often results from obesity and is accompanied by an increase in the permeability of the intestinal epithelial barrier, allowing co-absorption of bacterial metabolites and diet-derived fatty acids into the bloodstream. A high-fat diet (HFD) leading to obesity is a significant extrinsic factor in developing vascular atherosclerosis. In this study, we evaluated the effects of palmitic acid (PA) as a representative of long-chain saturated fatty acids (LCSFA) commonly present in HFDs, along with endotoxin (LPS; lipopolysaccharide) and uremic toxin indoxyl sulfate (IS), on human vascular endothelial cells (HUVECs). HUVECs viability was measured based on tetrazolium salt metabolism, and cell morphology was assessed with fluorescein-phalloidin staining of cells' actin cytoskeleton. The effects of simultaneous treatment of endothelial cells with PA, LPS, and IS on nitro-oxidative stress in vascular cells were evaluated quantitatively with fluorescent probes. The expression of vascular cell adhesion molecule VCAM-1, E-selectin, and occludin, an essential tight junction protein, in HUVECs treated with these metabolites was evaluated in Western blot. PA, combined with LPS and IS, did not influence HUVECs viability but induced stress on actin fibers and focal adhesion complexes. Moreover, PA combined with LPS significantly enhanced reactive oxygen species (ROS) production in HUVECs but decreased nitric oxide (NO) generation. PA also considerably increased the expression of VCAM-1 and E-selectin in HUVECs treated with LPS or IS but decreased occludin expression. Palmitic acid enhances the toxic effect of metabolic endotoxemia on the vascular endothelium.

The role of palmitic acid in pulmonary surfactant systems by Langmuir monolayer study: Lipid–peptide interactions

Palmitic acid (PA) has been widely used as an useful and effective additive to pulmonary surfactants (PS) such as Survanta and Surfaxin. Moreover, PA has well-known biological and physicochemical properties, and its simple chemical structure allows its manufacture at low cost. However, the role and significance of PA in PS formulations are still controversial. In the present study, the PS model preparation containing PA has been investigated to clarify its additional effect (molecular recognition and interaction in particular) employing the Langmuir monolayer technique. The elucidation of the PA effect is performed by comparison with the data from its analogue (or homologue) lipids; i.e. three fatty acids and four fatty alcohols. The surface pressure (π)-molecular area (A) and surface potential (ΔV)−A isotherms for the eight DPPC/fatty lipid systems containing a PS model peptide (Hel 13-5) have been measured. In addition, the morphology and phase behavior are examined with in situ fluorescence and ex situatomic force microscopy. As a result, it is found that a balance between the hydrophilicity of the headgroup and the hydrophobicity of the tail group in the lipids is an important factor in pulmonary functions. In particular, the dissociation degree of the fatty acids, which depends on the pH or the surface pH, strongly affects their electrostatic interaction with positively charged Hel 13-5. The chain length is also significant and the carbon number 16 is found to be most appropriate. The present molecular-level information on the interaction between the lipids and Hel 13-5 in the presence of DPPC indicates that PA takes on a hydrophile–lipophile balance suitable for the PS preparation.

The twists and turns of sphingolipid pathway in glucose regulation

Palmitic acid is a saturated fat found in foods that lead to obesity, cardiovascular disease, and Type II diabetes. It is linked to the development of resistance to insulin stimulation in muscle, liver and other organs involved in glucose metabolism, which, in turn, underlines the onset of Type II diabetes. The cellular and molecular mechanisms of this insulin resistance are complex and not completely understood. This article is focused on the role of palmitic acid as a precursor in the synthesis of sphingolipids, a class of lipid molecules that participate in cellular stress response. Recent evidence had indicated that increased dietary supply of palmitate can stimulate the rate of sphingolipid synthesis in “lean” tissues and generate excessive amounts of sphingolipid metabolites that have a negative effect on the insulin signaling cascade. Many experimental results point to the existence of a causative link between sphingolipid synthesis, insulin response, and hyperglycemia. It is not yet clear, however whether ceramides or glycosphingolipids are involved as both have been implicated to be inhibitors of the insulin signaling cascade. Evidence for a coordinated regulation of sphingolipid and tri/diacylglycerol metabolism complicates further the delineation of a single mechanism of sphingolipid effect on glucose homeostasis.

Role of palmitic acid on the isolation and properties of halorhodopsin

Purified halorhodopsin was isolated from Halobacterium halobium as previously vescribed (Duschl, A. et al. (1988) J. Biol. Chem. 263, 17016–17022). Two purple bands were eluted from phenyl-Sepharose column, indicating the presence of differently retained halorhodopsin forms; the absorption spectra of the two halorhodopsin bands in the dark were not different. By gas chromatography/mass spectrometry we could iventify palmitate (which is only a minor lipid component of archaeal cells) among lipids associated with purple fractions. Typically the palmitate content of the first eluted band was higher than that of the second, indicating a correlation between the palmitate content and the retention time; from one to two fatty acid molecules per halorhodopsin molecule were present vepending on the fraction analysed. Very little or no palmitate was released from venaturated halorhodopsin. By adding palmitate to buffers used in the phenyl-Sepharose chromatography, only one sharp purple band was collected, corresponding to the less retained halorhodopsin fraction. Pentavecanoic fatty acid could also affect the halorhodopsin chromatography. Chromatography of halorhodopsin in the presence of β-mercaptoethanol showed only one band, corresponding to the more retained halorhodopsin form. The two halorhodopsin fractions had different photoreactivity; the less retained halorhodopsin fraction (at higher palmitate content) showed an higher rate of vecay of the absorbance at 570 nm upon illumination. By following the vecay of the absorbance at 570 nm upon addition of alkali in the dark, we found that the two halorhodopsin fractions had different p K a values of veprotonation.

The role of palmitic acid in pulmonary surfactant: enhancement of surface activity and prevention of inhibition by blood proteins

The surface activity of two surfactant preparations, Lipid Extract Surfactant (LES) and Survanta, was examined during adsorption and dynamic compression using a pulsating bubble surfactometer. At low surfactant phospholipid concentrations (1–2.5 mg/ml), Survanta reduces surface tension at minimum bubble radius faster than LES: however, with continued pulsation LES obtains a lower surface tension. Addition of surfactant-associated protein A (SP-A) to LES significantly reduces the time required to reduce surface tension. Survanta is completely unresponsive to the addition of SP-A in that no further reduction of surface tension is observed. Addition of various blood components has been previously shown to inactivate surfactants in vitro. Addition of fibrinogen to Survanta causes an increase in surface tension when measured in the absence of calcium. When assayed in the presence of calcium, inhibition by fibrinogen is not observed possibly due to aggregation of this protein. Albumin and α-globulin strongly inhibit Survanta at physiological serum concentrations both in the presence and absence of calcium. The surface activity of Survanta is also inhibited by lysophosphatidylcholine (lyso-PC). The role of palmitic acid in the surface activity of pulmonary surfactant was examined by adding palmitic acid to LES. At low phospholipid concentrations addition of palmitic acid (10% w/w of the surfactant phospholipid) greatly enhances the surface activity of LES. Maximal enhancement of surface activity and adsorption was observed at or above 7.5% added palmitic acid (w/w of surfactant lipid). LES supplemented with palmitic acid is more resistant to inhibition by fibrinogen, albumin, α-globulin and lyso-PC than LES alone, however, the counteraction of blood protein inhibition is not as pronounced as that observed with SP-A.

Differences in cellular fatty acids and lipid composition inClostridium pasteurianum under nitrogen-and non-nitrogen-fixing conditions

Clostridium pasteurianum total cellular saturated fatty acids increased through its growth cycle from 81% to 91% but varied significantly in the composition under nitrogen- and non-nitrogen-fixing conditions. During ammonia-assimilating growth, palmitic acid decreased from 67.7% to 43.5% by late log while marked increases in shorter chain saturated fatty acids (C15:0 and below) and a long chain saturated C22:0 occured. In contrast, under N2-fixing growth conditions, palmitic acid increased from 45.5% to 84.3% by late log, representing nearly the total amound of saturated fatty acids found inC. pasteurianum. The total cellular lipid concentration decreased as the culture aged. irrespective of the nitrogen sources; however, the phospholipid concentration increased significantly during N2-fixing growth as compared with a 50% decrease during ammonia-assimilating conditions. The implication of these differences and possible role of palmitic acid and phospholipids inC. pasteurianum nitrogen fixation process are discussed.