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PubMed2001

Palmitic acid opens a novel cyclosporin A-insensitive pore in the inner mitochondrial membrane.

An assortment of agents can induce mitochondria to undergo a permeability transition, which results in the inner mitochondrial membrane becoming nonselectively permeable to small (<1500 Da) solutes. This mitochondrial permeability transition (MPT) is characterized by a strict dependence on matrix Ca2+ and sensitivity to cyclosporin A (CsA). However, it is becoming increasingly clear that other experimental conditions can elicit increases in mitochondrial permeability that are distinct from this classic MPT. For example, butylated hydroxytoluene (BHT; Sokolove, P. M., and Haley, L. M. (1996) J. Bioenerg. Biomembr. 28, 199-206) and signal peptides (Sokolove, P. M., and Kinnally, K. W. (1996) Arch. Biochem. Biophys. 336, 69-76) promote increases in mitochondrial permeability that are CsA-insensitive. It has been suggested (Gudz, T., Eriksson, O., Kushnareva, Y., Saris, N.-E., and Novgorodov, S. A. (1997) Arch. Biochem. Biophys. 342, 143-156) that BHT might be opening a CsA-insensitive pore by increasing phospholipase A2 activity and thereby producing an accumulation of free fatty acids and lysophospholipids. We have therefore examined the effect of the saturated free fatty acid, palmitic acid (PA), on the permeability of isolated rat liver mitochondria. The following results were obtained: (1) In the absence of additional triggers, PA (20-60 microM) induced concentration-dependent, CsA-insensitive mitochondrial swelling. (2) Swelling required mitochondrial energization. (3) PA-induced swelling was fast and occurred without a lag. (4) Both Ca2+ and Sr2+ supported PA-induced swelling; the site of cation action was the matrix. (5) EGTA and BSA were potent inhibitors of PA-induced swelling. (6) PA opened a pore rather than disrupting mitochondrial membrane structure. (7) The pore opened by PA closed spontaneously. These results suggest that palmitic acid promotes a nonclassic permeability increase that is clearly distinguishable from the occurrence of the MPT.

Animals↗
PubMed1983

Effects of postdecapitation ischemia on the metabolism of [14C]arachidonic acid and [14C]palmitic acid in the mouse brain.

The effect of postdecapitation ischemia on the labeling of the free fatty acid pool and their incorporation in lipids was examined during the first 10 min after decapitation in mouse brain that had been injected intracerebrally with either [1-14C]arachidonic acid or [1-14C]palmitic acid. One min after decapitation, animals injected with labeled arachidonic acid exhibited a greatly reduced incorporation of label in brain phospholipids, diglycerides, and triglycerides. When radioactive palmitic acid was used, brain lipids exhibited considerably less inhibition of label. However, a similar degree of inhibition was observed 10 min after decapitation with both fatty acids. At this time, free arachidonic acid had decreased 84% as compared to the 24% decrease observed in the controls, and about 77% of the free palmitic acid remained in the free fatty acid fraction as compared with 30% in the controls. This decreased labeling may reflect ATP shortage that affects the fatty acid activation-reacylation reactions or the enzymes involved. Alternatively, the enhanced endogenous free arachidonic acid may compete with the radiolabeled arachidonic acid resulting in an inhibition of lipid labeling. Inhibition of label may have been greater in radiolabeled arachidonic acid than palmitic because of the larger accumulation of the former endogenous fatty acid during early ischemia.

Animals↗
PubMed1996

Dietary linoleic acid increases and palmitic acid decreases hepatic LDL receptor protein and mRNA abundance in young pigs.

The present study was conducted to determine the effects of dietary fatty acids on hepatic LDL receptor (LDLr) protein abundance and mRNA levels. Sixty pigs were randomized into 10 groups and fed corn-soybean meal diets containing three cholesterol levels (0.25%, 0.5%, and 1.0%, w/w) with no added fat, or fats rich (30% of calories) in palmitic acid or linoleic acid. A control group was fed the base diet with no added fat. After 30 days, plasma LDL-cholesterol (LDL-C) levels increased as the dietary cholesterol increased (P < 0.05); however, there was no significant effect of either fatty acid. Dietary fatty acids, however, had distinctly different effects on hepatic LDLr protein (analyzed by ELISA) and mRNA (analyzed by Northern blot) abundance. When pigs consumed diets containing 0.25% cholesterol, linoleic acid increased hepatic LDLr protein 40% whereas palmitic acid reduced it 40% (P < 0.05). These changes in LDLr protein abundance were accompanied by parallel changes in hepatic LDLr mRNA; linoleic acid increased LDLr mRNA 2-fold (P < 0.01), whereas palmitic acid decreased it 60% (P < 0.01). The differential effects of fatty acids on LDLr expression were only observed at 0.25% cholesterol, suggesting that higher intakes of cholesterol have a dominant and repressive effect on regulation of LDLr expression. Cholesterol intake increased hepatic total cholesterol levels (P < 0.01) while dietary fatty acids had no effect on hepatic sterols. In summary, our results indicate that dietary linoleic acid and palmitic acid have markedly different effects on hepatic LDLr protein abundance that are mediated by differential effects on LDLr mRNA and protein levels. Further studies are needed to fully elucidate the molecular mechanisms by which fatty acids regulate LDLr mRNA and protein levels.

Aging↗
PubMed1983

Partial synthesis and physical properties of cerebroside sulfate containing palmitic acid or alpha-hydroxy palmitic acid.

Chromatographically pure galactosylceramide I3-sulfate (cerebroside sulfate (CBS)) containing palmitic acid or D-2-hydroxypalmitic acid has been prepared by the acylation of galactosylsphingosine I3-sulfate obtained from the saponification of bovine brain sulfatides. Optically pure D-2-hydroxypalmitic acid was obtained by adapting literature methods for the synthesis of the racemic acid and its resolution. The thermotropic behavior of the two synthetic CBSs were compared to each other and to the corresponding components in natural CBS, obtained by fractionation of bovine brain sulfatides, in order to determine the contribution of the hydroxy fatty acid to intermolecular hydrogen bonding between molecules of the lipid. The gel to liquid crystalline phase transition temperature (Tc) of the hydroxy fatty acid (HFA) synthetic form is 53.2 degrees C, 3 degrees higher than that of the non-hydroxy fatty acid (NFA) form at low concentrations of Na+ or K+. A similar difference was found for the HFA and NFA forms of natural CBS. The enthalpy of the NFA synthetic form is 8.5 kcal/mol, about 30% greater than that of the HFA form. The difference in Tc between the NFA and HFA forms is abolished as the Na+ or K+ concentration increases but the difference in enthalpy persists. Increasing cation concentration, over the range 0.01-2 M, increases Tc more than for an acidic phospholipid, phosphatidylglycerol, probably due to increased intermolecular hydrogen bonding as the charged sulfate is shielded. K+ causes a 3-4 degrees C greater increase in Tc relative to that produced by Na+ while K+ and Na+ have similar effects on phosphatidylglycerol.

Animals↗
PubMed2004

Regulation of CYP2E1 by ethanol and palmitic acid and CYP4A11 by clofibrate in primary cultures of human hepatocytes.

CYP2E1 and CYP4A11 are cytochrome P450 enzymes that are regulated by physiological conditions including diabetes and fasting. In addition, the xenochemical clofibrate has been reported to induce both rodent CYP2E1 and CYP4A. These findings suggest similar modes of regulation. Also in common to both enzymes is the ability to metabolize fatty acids such as laurate and arachidonic acid. Here, we used primary cultures of human hepatocytes to determine if certain xenochemicals could regulate CYP2E1 and CYP4A11. Ethanol significantly (p < 0.05) increased expression of CYP2E1 mRNA by 216 +/- 32% of control, but did not alter CYP4A11 mRNA accumulation (145 +/- 22% of control). In contrast, hepatocytes exposed to ethanol exhibited only a slight elevation in CYP2E1 protein (122 +/- 13% of control) and a negligible effect on CYP4A11 protein. Clofibrate significantly (p < 0.05) enhanced both CYP4A11 mRNA and protein by 239 +/- 30% and 154 +/- 10% of control, respectively, but did not increase CYP2E1. Because rodent CYP4A is reportedly regulated by fatty acids through peroxisome proliferator activated receptor alpha (PPARalpha) and CYP2E1 is induced by high fat diets, we examined the effects of a medium chain fatty acid, palmitate on CYP2E1 mRNA content. Palmitic acid significantly (p < 0.05) increased CYP2E1 mRNA to 326 +/- 57% of control. Collectively, results presented here identify agents that enhance CYP2E1 and CYP4A11 at the transcription level and suggest that fatty acids may represent a similar mode of regulation for these P450 enzymes. The lack of induction of CYP2E1 protein by ethanol in human hepatocytes indicates that for certain P450 enzymes, isolated hepatocytes may not be an adequate tool for predicting in vivo responses.

Adolescent↗
PubMed2003

Palmitic acid incorporation into intramuscular acylglycerols depends on both total and unbound to albumin palmitic acid concentration.

Palmitic acid incorporation into the intramuscular acylglycerols in rat skeletal muscles of different fiber types was investigated at various total and unbound to albumin concentrations by means of the hind-limb perfusion technique. It was found that at simultaneously increasing total and unbound to albumin palmitic acid concentrations in the perfusion medium the incorporation of palmitic acid into acylglycerols increased. However, when the concentration of palmitic acid not bound to albumin was kept constant and the total palmitic acid concentration was increased, the incorporation also increased although markedly less than under former conditions. The increase was most apparent in the muscles composed of slow-twitch oxidative and fast-twitch oxidative-glycolytic fibers where fatty acid uptake is the greatest. These findings suggest that fatty acid incorporation into intramuscular acylglycerols depends not only on the unbound to albumin fatty acid concentration but also, to some extent, on the total fatty acid concentration.

Animals↗
PubMed1998

Palmitic acid is associated with halorhodopsin as a free fatty acid. Radiolabeling of halorhodopsin with 3H-palmitic acid and chemical analysis of the reaction products of purified halorhodopsin with thiols and NaBH4.

Halorhodopsin, isolated from Halobacterium salinarium cells incubated with tritiated palmitic acid, co-elutes with labeled palmitate in phenylsepharose CL-4B chromatography. Halorhodopsin-bound 3H-palmitate is not readily displaced by prolonged exposure to a large excess of detergents and by re-chromatography of radiolabeled halorhodopsin on phenylsepharose. On other hand, the association of labeled palmitate with purified halorhodopsin is not resistant to denaturation induced either by isopropanol/hexane or by SDS gel electrophoresis. We have tested the hypothesis that tightly associated palmitate is bound to halorhodopsin through a thioester bond, which is unstable in denaturing conditions. Using GC/MS, we have analysed the reaction products of native halorhodopsin with specific thioester reagents, thiols and NaBH4, which are inactive on free fatty acids. The results of this analytical approach indicate that there is no thioester bond between halorhodopsin and palmitic acid and that palmitic acid is associated with halorhodopsin as a free fatty acid.

Bacteriorhodopsins↗
PubMed1992

Arachidonic and palmitic acid utilization in aged rat brain areas.

We have previously demonstrated that the arachidonic acid (20:4) incorporation into brain lipids differs according to the age of the animals used and the experimental conditions adopted. These differences led to a further investigation of arachidonic acid uptake in both aged and adult rat brains, its transformation into CoA derivatives, its incorporation into diacyl-glycerols and polar lipids, and finally its oxidation to CO2. These metabolic parameters were then compared with those obtained after using the saturated fatty acid palmitate (16:0). In both cases slices or mitochondria from different brain areas of 24-month-old and 4-month-old rats were examined. The results obtained indicate that the uptake of the fatty acids into cells is not modified by age. However, the successive metabolic transformations of the acids are altered to a considerable extent. In particular, in 24-month-old animals (compared with 4-month-old rats) there is a significant decrease of 20:4 in its incorporation into lipids as well as its oxidation to CO2, while arachidonoyl-CoA content increases by about 50%. This increased amount of CoA derivative, which has a potent detergent effect, may interfere with membrane structure and affect membrane physiological functions. Furthermore, because the free arachidonate pool is maintained in a dynamic equilibrium with its esterified forms, the final result may be a perturbation of this equilibrium.

Aging↗
PubMed2002

Metabolic fate of long-chain unsaturated fatty acids and their effects on palmitic acid metabolism and gluconeogenesis in bovine hepatocytes.

The objectives were to determine the metabolic fate of different long-chain fatty acids, and their effects on palmitic acid metabolism and gluconeogenesis in bovine hepatocytes. Hepatocytes were isolated from four ruminating calves and exposed in suspension for 3 h to one of the following treatments: 1 mM palmitic acid (1C16), 2 mM palmitic acid (2C16), or 1 mM palmitic acid plus either 1 mM oleic (C18:1), linoleic (C18:2), linolenic (C18:3), eicosapentaenoic (C20:5), or docosahexaenoic acid (C22:6). Oxidation of [1-(14)C]palmitic acid or one of the [1-(14)C]-labeled treatment fatty acids to CO2 or incorporation into cellular triglycerides (TG), phospholipids, cholesterol, and cholesterol esters were measured. Rates of oxidation to CO2 were 3- to 4-fold higher for C22:6 than for other fatty acids, with the exception of C20:5, which had intermediate rates of oxidation to CO2. In general, treatments 2C16 and C18:1 yielded the highest rates of incorporation into most cellular lipids, whereas the polyunsaturated fatty acids were poor substrates for incorporation into cellular lipids. The most pronounced change was a large reduction of polyunsaturated fatty acid incorporation into cellular TG compared to 1C16, 2C16, and C18:1. The unsaturated fatty acids also influenced palmitic acid metabolism. The addition of C20:5 yielded the highest rates of palmitic acid oxidation to CO2 followed by addition of C18:1 and C22:6. Treatments containing polyunsaturated fatty acids decreased palmitic acid metabolism to TG and total cellular lipids compared with treatments 2C16 and C18:1. Rates of gluconeogenesis from propionate were significantly higher for the treatment containing C18:1. Long-chain fatty acids vary in their routes of metabolism and influence palmitic acid metabolism and gluconeogenesis in bovine hepatocytes.

Animals↗
PubMed1989

Effect of alpha-1-acid glycoprotein, albumin and palmitic acid on the brain and salivary gland extraction of warfarin in rats.

The effect of plasma protein binding of warfarin on its transfer into the brain and salivary gland was investigated using alpha-1-acid glycoprotein and human serum albumin (HSA) in combination or not with palmitic acid. The tissue extraction of [14C] warfarin relative to [3H]water was determined by intracarotid injection technique in male Wistar rats. The tissue extraction of warfarin varied inversely with the concentration of added serum protein, (HSA and alpha-1-acid glycoprotein), and addition of palmitic acid to HSA diminished the extraction. The fraction of drug uptaked by tissue (tissue available fraction) was always dramatically greater than the in vitro free drug fraction, and this was interpreted as an enhanced in vivo drug dissociation from the binding protein. The fraction of drug uptake by salivary gland was closer to the in vitro free fraction than the fraction of drug uptake by brain tissue. The addition of palmitic acid to HSA induced parallel changes in the in vitro free fraction of warfarin and in the brain tissue or salivary gland extraction of warfarin. These data indicate that a part of protein-bound warfarin (as determined in vitro) is available for tissue extraction via an enhanced in vivo dissociation of the drug-protein complex in the tissue microcirculation. The in vitro data were fitted to a saturable model of binding whereas the in vivo data could satisfactorily fit a model dealing with a nonsaturable model of binding, and this is probably the result of the several-fold increase in the in vivo dissociation constant.

Animals↗
PubMed2000

Effects of exchanging 4%en between dietary stearic and palmitic acid on hamster plasma lipoprotein metabolism.

This study was designed to determine whether the exchange of specific fatty acids (palmitic (16:0) for stearic (18:0)), would exert differential effects on plasma and lipoprotein lipids, when diets contained approximately 30%en from fat with adequate levels of linoleic acid (18:2). Thirty-two male Golden Syrian hamsters were fed isocaloric purified diets with comparable amounts of 18:2 (approximately 10.5%en). The 18:0-rich diet (50% cocoa butter, 41% safflower oil, 9% sunflower oil) provided 4.8%en 16:0 and 5.3%en from 18:0, while the 16:0-rich diet (59% palm oil, 36% safflower oil, 5% olive oil) provided 8.7%en from 16:0 and 1.2%en from 18:0, resulting in a 16:0/18:0 exchange of approximately 4%en. Both diets contained negligible amounts of lauric and myristic acid (< 0.2%en), approximately 9.5%en from oleic acid and 77 mg cholesterol/1000 kcal. Animals were fed their respective diets for 4 weeks at which point various lipid and lipoprotein parameters were measured. There were no significant difference between dietary groups for any of the measured parameters, which included body weights, food consumption, plasma lipids, lipoprotein lipid and apoprotein concentrations, as well as lipoprotein compositions. Additionally, estimated diameters of various lipoprotein particles were not affected by the fatty acid exchanges employed. Thus these data suggest that when total fat is restricted to 30%en and 18:2 levels are approximately 10%en, a 4%en exchange between 16:0 and 18:0 (representing intakes of approximately 9 g/d/2000 kcal diet) produces comparable plasma lipids.

Animals↗
PubMed1995

[A study on the effect of cortisol and progesterone on cytosolic arachidonic and palmitic acid concentrations in cultured human myometrial cells].

Glucocorticoids inhibit prostaglandin synthesis in several cell types, presumably by inhibiting arachidonic acid deacylation from phospholipids. We studied the effects of cortisol (F) and progesterone (P) on fatty acid release from cultured human myometrial cells. Confluent monolayer cultures of myometrial cells were adapted to steroids containing medium for 24 hours and the intracellular arachidonic acid and palmitic acid concentrations were determined. In the presence of fetal calf serum (FCS), the palmitic acid concentrations significantly decreased after the addition of 10(-7)M F. In the absence of FCS, the concentrations of both fatty acids were markedly increased after the addition of F. During oxytocin stimulation, the arachidonic acid concentration did not change but the palmitic acid concentration decreased slightly after the addition of F. A similar evaluation was done with P. The palmitic acid concentration decreased slightly after the addition of 10(-5)M P in the presence of FCS but increased markedly in the absence of FCS. During stimulation with oxytocin, the fatty concentrations of fatty acids decreased significantly in a dose-dependent manner. These results suggest that both F and P are implicated as regulatory factors in the activation of arachidonic acid cascade.

Arachidonic Acid↗
PubMed1977

Modification of the binding of sulphamidochlorobenzoic acid to human albumin by palmitic acid contamination of albumin.

Palmitic acid a common contaminant of albumin preparations, competitively inhibits the binding of sulphamidochlorobenzoicacid (SCBA) to human albumin thus decreasing its observed affinity. The effect of palmitic acid depends on its concentration, i.e. the purity and concentration of the albumin preparation used. The correct value for SCBA affinity was obtained by correcting the experimental data according to the palmitic acid concentration by use of a multiligand analysis method.

Albumins↗
PubMed1994

Effect on blood lipids, coagulation, and fibrinolysis of a fat high in myristic acid and a fat high in palmitic acid.

The hypothesis that myristic acid (C14:0) has a stronger cholesterol-increasing potential than does palmitic acid is based on very few experimental observations. A randomized, strictly controlled dietary study was therefore designed to investigate the effect of a synthetic fat that was high in myristic acid, and palm oil, which is high in palmitic acid, on lipoproteins and hemostatic variables. Twelve men were served two diets (40% of energy as fat) with 41% of fat as myristic (diet M) or palmitic acid (diet P) for 3 wk with 1 mo between the two dietary schedules. Plasma HDL cholesterol was 8% higher with diet M than with diet P: 1.10 +/- 0.06 (mean +/- SEM) vs 1.01 +/- 0.05 mmol/L (P < 0.006). Diet M raised factor VII coagulant (F VIIc) activity to 98% (77-117%) vs 96% (71-109%) (medians and ranges) after diet P (P = 0.02). Total and LDL-cholesterol concentrations did not differ between the diets. In conclusion, the myristic acid test fat was not more cholesterolemic than was palm oil, but it did induce a minor rise in F VIIc activity.

Adult↗