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At least 19 recordsLinked to original sources
PubMed1979

Amniotic fluid lecithin/sphingomyelin ratio, palmitic acid, palmitic acid/stearic acid ratio, total cortisol, creatinine, and percentage of lipid-positive cells in assessment of fetal maturity and fetal pulmonary maturity: a comparison.

Lecithin/sphingomyelin (L/S) ratio, creatinine, percentage of lipid-positive cells, palmitic acid, palmitic acid/stearic acid (P/S) ratio, and total cortisol were analyzed as tests for fetal maturity and fetal pulmonary maturity in 164 samples of amniotic fluid from 121 patients. Fifty samples were taken within 72 hours of delivery. The best tests for fetal maturity (37 weeks) with differential percentages were L/S ratio, palmitic acid, and P/S ratio. In the assessment of fetal pulmonary maturity, we studied an additional 174 samples in which only L/S ratio, creatinine, and lipid-positive cells were analyzed. All tests showed a high predictive value of an immature (positive) result was much less for all six parameters; the three best tests were total cortisol (33%), lipid-positive cells (26%) and L/S ratio (14%).

Amniotic Fluid↗
PubMed1996

Metabolic fate of oleic acid, palmitic acid and stearic acid in cultured hamster hepatocytes.

Unlike other saturated fatty acids, dietary stearic acid does not appear to raise plasma cholesterol. The reason for this remains to be established, although it appears that it must be related to inherent differences in the metabolism of the fatty acid. In the present study, we have looked at the metabolism of palmitic acid and stearic acid, in comparison with oleic acid, by cultured hamster hepatocytes. Stearic acid was taken up more slowly and was poorly incorporated into both cellular and secreted triacylglycerol. Despite this, stearic acid stimulated the synthesis and secretion of triacylglycerol to the same extent as the other fatty acids. Incorporation into cellular phospholipid was lower for oleic acid than for palmitic acid and stearic acid. Desaturation of stearic acid, to monounsaturated fatty acid, was found to be greater than that of palmitic acid. Oleic acid produced from stearic acid was incorporated into both triacylglycerol and phospholipid, representing 13% and 6% respectively of the total after a 4 h incubation. Significant proportions of all of the fatty acids were oxidized, primarily to form ketone bodies, but by 8 h more oleic acid had been oxidized compared with palmitic acid and stearic acid.

Analysis of Variance↗
PubMed2003

Saturated free fatty acids, palmitic acid and stearic acid, induce apoptosis by stimulation of ceramide generation in rat testicular Leydig cell.

In men, obesity has generally been associated with reduced plasma testosterone levels and with elevation of the plasma free fatty acids (FFAs). In this study, we investigated the effects of saturated FFAs including palmitic acid (PA) and stearic acid (SA), and polyunsaturated FFA arachidonic acid (AA) on the survival of rat testicular Leydig cell cultured in vitro. PA and SA markedly suppressed Leydig cell survival in a time- and dose-dependent manner. In contrast, AA stimulated the cell proliferation at 5-10 times of physiological concentration. The suppressive effect of PA and SA on cell survival was caused by apoptosis evidenced by DNA ladder formation and Annexin V-EGFP/propidium iodide staining of the cells. The apoptotic effect of PA was possibly mediated by ceramide generation because it could be completely blocked by ceramide synthase inhibitor fumonisin B1 and exogenous ceramide itself could directly induce apoptosis in vitro. Surprisingly, the apoptosis induced by PA could be partly prevented by AA. These results indicate that PA and SA induce apoptosis in testicular Leydig cells by ceramide production and these apoptotic effects may be a possible mechanism for reproductive abnormalities in obese men, and AA can partly prevent the apoptotic effect induced by saturated FFA.

Animals↗
PubMed1988

Modification of CaCo-2 cell membrane fatty acid composition by eicosapentaenoic acid and palmitic acid: effect on cholesterol metabolism.

Membrane fatty acid composition of CaCo-2 cells was modified by incubating the cells for 8 days in medium containing 100 microM eicosapentaenoic acid or palmitic acid. The effect of membrane fatty acid changes on cholesterol metabolism was then studied. Cells incubated with eicosapentaenoic acid had significant changes in membrane fatty acid composition with an accumulation of 20:5 and 22:5 and a reduction in monoenoic fatty acids compared to cells grown in palmitic acid. Intracellular cholesteryl esters could not be detected in CaCo-2 cells grown in the presence of the n-3 polyunsaturated fatty acid. In contrast, cells incubated with the saturated fatty acid contained 2 micrograms/mg protein of cholesteryl esters. Cells grown in eicosapentaenoic acid, however, accumulated significantly more triglycerides compared to cells modified with palmitic acid. The rate of oleic acid incorporation into triglycerides was significantly increased in cells incubated with eicosapentaenoic acid. CaCo-2 cells modified by eicosapentaenoic acid had lower rates of HMG-CoA reductase and ACAT activities compared to cells modified with palmitic acid. The incorporation of the two fatty acids into cellular lipids also differed. Palmitic acid was predominantly incorporated into cellular triglycerides, whereas eicosapentaenoic acid was preferentially incorporated into phospholipids with 60% of it in the phosphatidylethanolamine fraction. The data indicate that membrane fatty acid composition is significantly altered by growing CaCo-2 cells in eicosapentaenoic acid. These modifications in membrane fatty acid saturation are accompanied by a decrease in the rates of cholesterol synthesis and cholesterol esterification.

Adenocarcinoma↗
PubMed2000

Myristic acid, unlike palmitic acid, is rapidly metabolized in cultured rat hepatocytes.

This study was designed to examine and compare the metabolism of myristic and palmitic acids in cultured rat hepatocytes. [1-(14)C]-Labeled fatty acids were solubilized with albumin at 0.1 mmol/L in culture medium. Incubation with 24-hr cultured hepatocytes was carried out for 12 hr. Myristic acid was more rapidly (P < 0.05) taken up by the cells than was palmitic acid (86.9 +/- 0.9% and 68.3 +/- 5.7%, respectively, of the initial radioactivity was cleared from the medium after 4 hr incubation). Incorporation into cellular lipids, however, was similar after the same time (33.4 +/- 2.8% and 34.9 +/- 9.3%, respectively, of initial radioactivity). In the early phase of the incubation (30 min), myristic acid was more rapidly incorporated into cellular triglycerides than was palmitic acid (7.4 +/- 0.9% and 3.6 +/- 1.9%, respectively, of initial radioactivity). However, after 12 hr incubation, the radioactivity of cellular triglycerides, cellular phospholipids, and secreted triglycerides was significantly higher with palmitic acid as precursor. Myristic acid oxidation was significantly higher than that of palmitic acid (14.9 +/- 2.2% and 2.3 +/- 0.6%, respectively, of the initial radioactivity was incorporated into the beta-oxidation products after 4 hr). Myristic acid was also more strongly elongated to radiolabeled palmitic acid (12.2 +/- 0.8% of initial radioactivity after 12 hr) than palmitic acid was to stearic acid (5.1 +/- 1.3% of initial radioactivity after 12 hr). The combination of elongation and beta-oxidation results in the rapid disappearance of C14:0 in hepatocytes whereas C16:0 is esterified to form glycerolipids. This study provides evidence that myristic acid is more rapidly metabolized in cultured hepatocytes than is palmitic acid.

Journal Article↗
PubMed1994

Impact of myristic acid versus palmitic acid on serum lipid and lipoprotein levels in healthy women and men.

The cholesterol-raising effect of dietary saturated fatty acids is largely accounted for by lauric, myristic, and palmitic acids. Dairy fat is a major source of myristic acid, and palm oil is especially rich in palmitic acid. Myristic acid is suspected of being much more cholesterolemic than palmitic acid, but direct comparisons have been lacking. We therefore fed 36 women and 23 men three diets that differed from each other in palmitic, oleic, and myristic acid content by about 10% of total energy. We used palm oil, high-oleic acid sunflower oil, and a specially produced high-myristic acid fat to achieve these differences. Each diet was consumed for 3 weeks in random order. Mean serum cholesterol was 4.53 mmol/L on the high-oleic acid diet, 4.96 mmol/L on the palmitic acid diet, and 5.19 mmol/L on the myristic acid diet (P < .0001 for all comparisons). Myristic acid raised low-density lipoprotein (LDL) cholesterol by 0.11 mmol/L, high-density lipoprotein (HDL) cholesterol by 0.12 mmol/L, and apolipoprotein (apo) A-I by 7.2 mg/dL relative to palmitic acid; increases relative to oleic acid were 0.50 mmol/L for LDL cholesterol, 0.15 mmol/L for HDL cholesterol, 6.0 mg/dL for apoB, and 8.9 mg/dL for apoA-I (P < .01 for all comparisons). The HDL cholesterol and apoA-I levels on the palmitic and oleic acid diets were the same. None of the responses differed significantly between woman and men. Myristic acid and palmitic acid both caused high LDL cholesterol and apoB levels and low HDL to LDL ratios.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Opposite effects on cholesterol metabolism and their mechanisms induced by dietary oleic acid and palmitic acid in hamsters.

The effects of dietary oleic acid on cholesterol metabolism were investigated and compared with those of palmitic acid in hamsters. Addition of 5% oleic acid to a 0.1% cholesterol-supplemented diet decreased plasma total cholesterol, very low density lipoprotein (VLDL) cholesterol, and low density lipoprotein (LDL) cholesterol, increased hepatic LDL receptor activity, and decreased plasma cholesteryl ester transfer protein (CETP) activity in comparison with 0.1% cholesterol alone. In contrast, addition of 5% palmitic acid to a 0.1% cholesterol-supplemented diet increased total cholesterol and LDL-cholesterol, increased plasma CETP activity, and suppressed hepatic LDL receptor activity to a greater extent than 0.1% cholesterol alone. Neither oleic acid nor palmitic acid altered hepatic microsomal 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase activity, but oleic acid increased hepatic microsomal cholesterol 7 alpha-hydroxylase activity. These results suggest that dietary oleic acid inhibits the increases in total, VLDL-, and LDL-cholesterol induced by dietary cholesterol by preventing both LDL receptor suppression and increased CETP activity, whereas dietary palmitic acid augments the cholesterol-induced increases in total and LDL-cholesterol by both further suppression of LDL receptor activity and further stimulation of CETP activity.

Animals↗
PubMed1992

Comparison of effects of lauric acid and palmitic acid on plasma lipids and lipoproteins.

The effects of lauric acid (C12:0) on plasma lipids and lipoproteins were compared with the effects of palmitic acid (C16:0) and oleic acid (C18:1) in a metabolic-diet study of 14 men by using liquid-formula diets fed for 3 wk each in random order. Lauric acid was supplied in a synthetic high-lauric oil, palmitic acid was provided by palm oil and oleic acid in oleic-rich sunflower seed oil. The high-lauric oil resulted in higher concentrations of plasma total cholesterol (4.94 +/- 0.75 mmol/L [mean +/- SE]) and LDL cholesterol (3.70 +/- 0.57 mmol/L) when compared with high-oleic sunflower oil (4.44 +/- 0.54 and 3.31 +/- 0.44 mmol/L, respectively), but did not raise total and LDL cholesterol concentrations as much as did palm oil (5.17 +/- 0.65 and 3.93 +/- 0.51 mmol/L, respectively). No differences were noted in plasma triglycerides or HDL cholesterol. Lauric acid raises total and LDL cholesterol concentrations compared with oleic acid, but is not as potent for increasing cholesterol concentrations as is palmitic acid.

Adult↗
PubMed1998

Lower arachidonic acid content and preferential beta-oxidation of arachidonic acid over palmitic acid in tumour cell lines as compared to normal lymphoid cells.

In several studies certain polyunsaturated fatty acids (PUFA) have been shown to be selectively tumouricidal or suppressive of tumour cell proliferation. The mechanism behind this phenomenon likely involves peroxidation of the PUFA and generation of free radicals to which tumour cells seem to be more sensitive than normal cells. In this report we have measured the total lipid content in separated lymphoid cells and several tumour cell lines, among which, T-cell leukaemia, monocytic leukaemia, melanoma, fibrosarcoma, lung carcinoma and colon adenocarcinoma are included. Generally these tumour cell lines contain only one half to one third of the relative amount of arachidonic acid (AA) as compared to freshly prepared lymphocytes and monocytes or lymphocytes kept in culture. Furthermore, when we measured the beta-oxidation in long term incubation of [1-14C] AA and compared it with that of [1-14C] palmitic acid we found that several of the tumour cell lines showed a preference for AA over palmitic acid in the tumour cell lines whereas the opposite was observed for normal lymphoid cells.

Arachidonic Acid↗
PubMed1985

Synthesis of chain elongated-desaturated fatty acids from palmitic acid by liver and brain microsomes during the development of the pig.

Rates of chain elongation-desaturation of C16:0 were compared for liver and brain microsomes in fetal, neonatal and postnatal piglets. Rates of chain elongation of C16:0 were greatest in liver in the postnatal period. For all developmental periods examined, the amount of chain elongated fatty acid of C20 or greater chain length exceeded the amount of C18 precursors synthesized from C16:0. These observations suggest that chain elongation of fatty acids occurs during the latter part of gestation at rates equivalent to that observed in the early postnatal period.

Aging↗
PubMed1986

Direct identification of palmitic acid as the lipid attached to p21ras.

p21v-H-ras, the transforming protein of Harvey murine sarcoma virus, contains a covalently attached lipid. Using thin-layer chromatography, we identified the acyl group as the 16-carbon saturated fatty acid palmitic acid. No myristic acid was detected in fatty acids released from in vivo-labeled p21v-H-ras. The p21v-K-ras protein encoded by Kirsten sarcoma virus was also palmitylated. The processing and acylation of p21v-K-ras however differed from that of p21v-H-ras. Three forms of [3H]palmitic acid-labeled p21ras proteins were detected in Kirsten sarcoma virus-transformed cells. This contrasted with Harvey sarcoma virus, in which two forms of p21v-H-ras contained palmitic acid. Analysis by partial proteolysis of p21v-H-ras labeled with [3H]palmitic acid suggested that all of the lipid found in intact p21v-H-ras was located in the C-terminal region. On sodium dodecyl sulfate-polyacrylamide gels, p21v-H-ras labeled with [3H]palmitic acid migrated slightly ahead of the majority of p21v-H-ras. Of the mature forms of p21v-H-ras, apparently only a subpopulation contains palmitic acid.

Animals↗
PubMed1981

Salicylic acid stimulation of palmitic acid oxidation by rat skeletal muscle mitochondria.

The effects of salicylic acid on palmitic acid oxidation were studied using rat skeletal muscle mitochondria. Salicylic acid, in concentrations that exerted no effect on mitochondrial coupling (0.1 mM), significantly stimulated mitochondrial palmitic acid oxidation, with maximal stimulation occurring at subsaturating concentrations of substrate. In the same preparation, salicylate had no effect on the oxidation of palmitoylcarnitine or palmitoyl-CoA. Salicylate appears to augment the initial step of palmitic acid oxidation by lowering the apparent Michaelis constant (Km) of long chain fatty acid: CoASH ligase (AMP) (EC 6.2.1.3) for palmitic acid.

Animals↗
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↗