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PubMed1994

N-terminal fatty acylation of the alpha-subunit of the G-protein Gi1: only the myristoylated protein is a substrate for palmitoylation.

The alpha-subunit of the G-protein Gi1 carries two fatty acyl moieties covalently bound to its N-terminal region: myristic acid is linked to glycine-2 and palmitic acid is linked to cysteine-3. Using site-directed mutagenesis on a cDNA construct of alpha i1 we have generated an alpha i1-G2A mutant, carrying alanine instead of glycine at position 2, and alpha i1-C3S mutant, in which serine replaced cysteine-3 and a double mutant with both substitutions (alpha i1-G2A/C3S). These constructs were individually expressed by transfection in Cos-7 cells, and incorporation of fatty acids into the various mutants was compared with wild-type alpha i1 monitoring metabolic labelling with [3H]palmitate or [3H]myristate. The disruption of the palmitoylation site in alpha i1-C3S did not influence myristoylation, whereas prevention of myristoylation in alpha i1-G2A also abolished palmitoylation. Co-translational myristoylation is thus an absolute requirement for alpha i1 to be post-translationally palmitoylated. The non-palmitoylated alpha i1-C3S showed reduced membrane binding to the same extent as the non-myristoylated/non-palmitoylated alpha i1-G2A and alpha i1-G2A/C3S mutants, indicating that the attachment of palmitic acid is necessary for proper interaction with the membrane.

Acylation↗
PubMed1989

Influence of non-esterified fatty acids on respiratory control of reconstituted cytochrome-c oxidase.

Bovine heart cytochrome-c oxidase was reconstituted in liposomes (asolectin) and the activity measured in the presence and absence of uncoupler at increasing concentrations of non-esterified fatty acids. Palmitic and stearic acids resulted in a decrease of about 40% in the respiratory control ratio at a concentration of 1 microM, when measured using a spectrophotometric procedure but not with a polarographic assay method. At higher fatty acid concentrations no further change was found. A 50% decrease in respiratory control was determined when the enzyme was reconstituted in pure phosphatidylcholine containing 2% cardiolipin. The respiratory control of reconstituted cytochrome-c oxidase from bovine liver was not influenced by fatty acids.

Animals↗
PubMed1987

Partitioning of polar fatty acids into lymph and portal vein after intestinal absorption in the rat.

We tested the hypothesis that fatty acids destined for the portal vein after intestinal absorption would be diverted into lymph when infused along with a saturated long-chain fatty acid. Thoracic fistula rats were infused intraduodenally with either linolenic (18:3), lauric (12:0), or decanoic (10:0) acid, or with each fatty acid in combination with 5 mM palmitic acid (16:0), in micellar solutions of taurocholate (10 mM) and 2-mono-oleoylglycerol. Lymphatic transport of linolenic acid was enhanced by co-absorption with palmitic acid: when 0.1 mM linolenic acid was infused alone, 32 +/- 8% of that absorbed and transported beyond the mesentery was carried in lymph. The addition of palmitic acid to the infusate increased the percentage transported in lymph to 56 +/- 10% (P less than 0.005). The increment was due to enhanced intracellular re-esterification of linolenate into triacylglycerol. When 5 mM linolenic acid was infused, the comparable figures for lymphatic transport were 55 +/- 2% for linolenate infused alone and 66 +/- 6% for linolenate infused with palmitate (P less than 0.005). In contrast, the predominantly portal venous transport of lauric and decanoic acids was unaffected by co-absorption with palmitate. We conclude that the partitioning of long-chain fatty acids between portal blood and lymph is dependent on the luminal milieu, in addition to polarity of the fatty acid and the rate of absorption. Unsaturated long-chain fatty acids have a substantial portal transport under conditions which simulate normal food ingestion.

Animals↗
PubMed1992

Fatty acids are precursors of alkylamines in Deinococcus radiodurans.

Deinococcus radiodurans contains novel phospholipids of which the structures of three have been previously described. These three lipids contain both fatty acids and alkylamines. Both the fatty acid and alkylamine constituents were found to be composed of a mixture of species, of which C15, C16, and C17 saturated and monounsaturated alkyl chains predominated. Alkylamines contained a relatively higher proportion of saturated species. Progression of bacterial growth through the mid-log to stationary phases was accompanied by an increase in the proportions of C15 and C17 alkyl chains in both fatty acid and alkylamine constituents. Radiolabeled palmitic acid was found to be rapidly incorporated into both fatty acid and alkylamine components of phosphatidylglyceroylalkylamine, which is the precursor of the more-complex phosphoglycolipids found in major amounts in D. radiodurans. After culturing D. radiodurans in the presence of a mixture of palmitic acids labeled with 14C and 3H in the 1 and 9,10 positions, respectively, the same 14C/3H ratio was recovered in both fatty acid and alkylamine constituents, strongly suggesting that alkylamines are derived from intact fatty acids rather than by a de novo pathway. The results identify a novel product of fatty acid metabolism which has not to date been observed in any other organism.

Alkylation↗
PubMed1984

Fatty acylation of proteins during development of sea urchin embryos.

Developing embryos of the sea urchin, Strongylocentrotus purpuratus, incorporate [3H]palmitic acid into at least 20 proteins. The [3H]palmitic acid associated with these proteins is released by alkaline hydrolysis or by treatment with hydroxylamine but not by extensive extraction with chloroform:methanol, indicating that the fatty acids are covalently attached to protein. The finding that the fatty acid is released by hydroxylamine or beta-mercaptoethanol at neutral or even slightly acidic pH suggests that this moiety may be attached to the polypeptide via a thiol ester bond. Concanavalin A-agarose chromatography and endo-beta-N-acetylglucosaminidase H digestion revealed that 14 of the proteins containing covalently linked fatty acid also contain at least one asparagine-linked oligosaccharide chain. With one exception, all of the fatty acylated proteins are tightly associated with membranes. The rate of incorporation of [3H]palmitic acid into the proteins is developmentally regulated. Between fertilization and the onset of gastrulation (approximately 30 h), embryos exhibit a linear, 5.5-fold increase in the rate of incorporation of fatty acid into polypeptide. Incorporation increases an additional 25% during gastrulation, and then remains constant throughout subsequent development to the pluteus stage (approximately 90 h). These findings demonstrate that the fatty acylation of proteins and glycoproteins is not limited to higher organisms, since it occurs during differentiation and embryonic development of a relatively simple invertebrate.

Acylation↗
PubMed1990

Amiodarone inhibits the mitochondrial beta-oxidation of fatty acids and produces microvesicular steatosis of the liver in mice.

Amiodarone has been shown to produce microvesicular steatosis of the liver in some recipients. We have determined the effects of amiodarone on the mitochondrial oxidation of fatty acids in mice. In vitro, the formation of 14C-acid-soluble beta-oxidation products from [U-14C]palmitic acid by mouse liver mitochondria was decreased by 92% in the presence of 125 microM amiodarone and by 94% in the presence of 125 microM N-desethylamiodarone. Inhibition due to 100 or 150 microM amiodarone persisted in the presence of 5 mM acetoacetate, whereas acetoacetate totally relieved inhibition due to 15 microM rotenone. In vivo, exhalation of [14C]CO2 from [U-14C]palmitic acid was decreased by 31, 40, 58 and 78%, respectively, in mice receiving 19, 25, 50 and 100 mg.kg-1 of amiodarone hydrochloride 1 hr before the administration of [U-14C]palmitic acid. One hour after 100 mg.kg-1, the exhalation of [14C]CO2 from [1-14C]palmitic acid, [1-14C]octanoic acid or [1-14C]butyric acid was decreased by 78, 72 and 53%, respectively. Exhalation of [14C]CO2 from [1-14C]palmitic acid was normal between 6 and 9 hr after administration of 100 mg.kg-1 of amiodarone hydrochloride, but was still inhibited by 71 and 37%, 24 and 48 hr after 600 mg.kg-1. Twenty four hours after the latter dose of amiodarone, hepatic triglycerides were increased by 150%, and there was microvesicular steatosis of the liver. We conclude that amiodarone inhibits the mitochondrial beta-oxidation of fatty acids and produces microvesicular steatosis of the liver in mice.

Amiodarone↗
PubMedDate not supplied

Synthesis and tissue distribution of fluorine-18 labeled trifluorohexadecanoic acids. Considerations in the development of metabolically blocked myocardial imaging agents.

A versatile method for the synthesis of trifluoro fatty acids, potential metabolically blocked myocardial imaging agents, has been developed. Two trifluorohexadecanoic (palmitic) acids have been prepared [6,6,16-trifluorohexadecanoic acid (I) and 7,7,16-trifluorohexadecanoic acid (II)], each of which bears two of the fluorine atoms as a gem-difluoromethylene unit on the fatty acid chain (at C-6 or C-7) and the third at the omega (C-16) position. The metabolic stability of carbon-fluorine bonds suggests the gem-difluoro group may block the beta-oxidation pathway, while the terminal fluorine could be the site for labeling with fluorine-18. The convergent synthetic approach utilizes a 2-lithio-1,3-dithiane derived from 10-undecenal or 9-decenal, which is alkylated with the OBO (oxabicyclooctyl) ester of 5-bromopentanoic acid or 6-bromohexanoic acid, respectively. Hydroboration-oxidation and alcohol protection are followed by halofluorination to convert the 1,3-dithiane system to a gem-difluoro group. The third fluorine is introduced by fluoride ion displacement of a trifluoromethanesulfonate. This synthesis is adapted to the labeling of these trifluoro fatty acids with the short-lived radionuclide fluorine-18 (t1/2 = 110 min), with the third fluorine introduced as fluoride ion in the penultimate step. The radiochemical syntheses proceed in 3-34% radiochemical yield (decay corrected), with an overall synthesis and purification time of 90 min. Tissue distribution studies in rats were performed with I and II, as well as with 16-[18F]fluoropalmitic acid (III), [11C]palmitic acid, and [11C]octanoic acid. The heart uptake of the fluoropalmitic acids decreases with substitution, the 2-min activity level for 16-fluoropalmitic acid being 65% and that for both 6,6,16- and 7,7,17-trifluoropalmitic acids being 30% that of palmitic acid. Fluorine substitution results in some alteration in the retention of activity by the heart: 16-fluoropalmitate actually clears more rapidly than palmitate, but the two trifluoropalmitates (particularly 6,6,16-trifluoropalmitate, I) show somewhat slower clearance of activity, although the improvement of I over palmitate is only modest. There is considerable accumulation of activity in the bone after administration of the fluorine-18 labeled fatty acids, suggestive of metabolic defluorination. These results indicate that fluorine substitution alters the physicochemical properties of the fatty acid so that uptake by the myocardium is diminished. Furthermore, while the gem-difluoro substituents at C-6 and C-7 may block beta-oxidation, the chain-terminal radiofluorine substituent is subject to omega-oxidation that releases it as fluoride ion.

Animals↗
PubMed2001

Validation of deuterium labeled fatty acids for the measurement of dietary fat oxidation: a method for measuring fat-oxidation in free-living subjects.

BACKGROUND: Fatty acid oxidation has frequently been measured using (13)C or (14)C labeled fatty acids. While providing valuable data, the breath test method is hindered by the need for a controlled environment to measure VCO(2) and collect frequent breath samples. Additionally, the CO(2) breath tests require the use of (13)C- or (14)C-acetate to correct for isotope exchange in the TCA cycle. We validated d(31)-palmitic acid for measuring dietary fat oxidation. When oxidized, the deuterium appears as water and mixes with the body water pool providing a cumulative record of fat oxidation. METHODS: The recovery of deuterium from d(31)-palmitic acid at 10 h post-dose was compared to that of (13)CO(2) from [1-(13)C]-palmitic acid in nine subjects (body mass index (BMI)=23.6+/-2.8; percentage body fat (%BF)=22.6+/-5.3; mean+/-s.d.). Subjects were studied at rest. [1-(13)C]-acetate (2 mg/kg) was dosed in a liquid breakfast. On a second day, [1-(13)C]-palmitic acid (10 mg/kg) and d(31)-palmitic acid (15 mg/kg) were dosed with the same liquid breakfast. RESULTS: Recovery of (13)CO(2) from [1-(13)C]-acetate at 10 h post-dose was 53.7+/-10.4%. Recovery of d(31)-palmitic acid was 13.2+/-7.7% (mean+/-s.d.) and [1-(13)C]-palmitic acid recovery was 6.4+/-3.6%. When the (13)C data was corrected for [1-(13)C]-acetate (Na salt) recovery, the mean difference in percentage recovery between the two tracers was 0.5+/-2.8% and cumulative recoveries through 10 h post-dose were highly correlated (y=1.045x - 0.47; r(2)=0.88, P<0.0002). Our data shows both labels to be equivalent in their ability to measure dietary fat oxidation in resting subjects. CONCLUSIONS: The use of deuterium labeled palmitic acid eliminates the need for rigid control over the subjects' environment. Frequent sampling and measurement of VCO(2) are not needed for accurate calculation of percentage recovery of the deuterium label. In addition, the deuterium label has a decreased potential for isotopic exchange compared to (13)C or (14)C, so a recovery correction factor is probably not required.

Adult↗
PubMed1986

Location of long chain fatty acid-binding sites of bovine serum albumin by affinity labeling.

Affinity labeling with palmitic acid was used to identify long chain fatty acid-binding sites of bovine serum albumin. [1-14C]Palmitic acid was activated by esterification with N-ethyl-5-phenyl-isoxazolium-3'-sulfonate (Woodward's Reagent K). The product was purified by chromatography and shown to compete with unesterified fatty acids for binding sites on bovine serum albumin. Activated [14C]palmitic acid coupled covalently to albumin producing [14C]palmitoyl-albumins containing from 0.12 to a maximum of 6.9 mol of attached label per mol of albumin. The presence of the covalently attached affinity label depressed binding of other long chain fatty acids to albumin. Albumin carrying 1 eq. of [14C]palmitate was cleaved using cyanogen bromide, pepsin, and trypsin. Radioactive peptides were isolated by high pressure liquid chromatography. Three peptides accounted for greater than 90% of the label. Residues labeled with [14C]palmitate were identified as Lys-116, Lys-349 and Lys-473, and the relative distribution of label was 10, 45, and 45% respectively, consistent with the presence of two strong binding sites in the COOH-terminal half of albumin and a somewhat weaker site in the NH2-terminal half.

Affinity Labels↗
PubMed2002

Fatty acid and sn-2 fatty acid composition in human milk from Granada (Spain) and in infant formulas.

OBJECTIVE: To investigate differences in fatty acid and sn-2 fatty acid composition in colostrum, transitional and mature human milk, and in term infant formulas. SETTING: Departament de Nutrició i Bromatologia, University of Barcelona, Spain and University Hospital of Granada, Spain. SUBJECTS: One-hundred and twenty mothers and 11 available types of infant formulas for term infants. DESIGN: We analysed the fatty acid composition of colostrum (n=40), transitional milk (n=40), mature milk (n=40) and 11 infant formulas. We also analysed the fatty acid composition at sn-2 position in colostrum (n=12), transitional milk (n=12), mature milk (n=12), and the 11 infant formulas. RESULTS: Human milk in Spain had low saturated fatty acids, high monounsaturated fatty acids and high linolenic acid. Infant formulas and mature human milk had similar fatty acid composition. In mature milk, palmitic acid was preferentially esterified at the sn-2 position (86.25%), and oleic and linoleic acids were predominantly esterified at the sn-1,3 positions (12.22 and 22.27%, respectively, in the sn-2 position). In infant formulas, palmitic acid was preferentially esterified at the sn-1,3 positions and oleic and linoleic acids had higher percentages at the sn-2 position than they do in human milk. CONCLUSION: Fatty acid composition of human milk in Spain seems to reflect the Mediterranean dietary habits of mothers. Infant formulas resemble the fatty acid profile of human milk, but the distribution of fatty acids at the sn-2 position is markedly different.

Colostrum↗
PubMed1985

Response of laying hens to dietary saturated and unsaturated fatty acids in the presence of varying dietary calcium levels.

The response of 33-week-old White Leghorn laying hens to dietary palmitic, oleic, or a 50/50 mixture of oleic and palmitic acids at an 8% inclusion level in the presence of 3, 3.6, or 4.2% dietary calcium was investigated over a 7-week period. There was no significant effect of treatments on egg production and egg weight. Although birds on diets supplemented with oleic acid consumed less feed (P less than .01) than those on diets supplemented with palmitic acid (102 g vs. 114 g), they gained more weight (P less than .01) than birds on diets supplemented with palmitic acid (+105 g vs. -32 g) over the 7-week period. There was no significant effect of the fatty acid treatment on shell quality as estimated by shell deformation. However, increasing the calcium content of the diets reduced feed intake and weight gain (P less than .05) and improved egg shell quality (P less than .05). The fat content of diets supplemented with oleic acid was better utilized than that from diets with an oleic/palmitic mixture, which, in turn, was better utilized than fat from diets supplemented with palmitic acid (P less than .01). Metabolizable energy values of diets followed a trend similar to fat retention and were independent of dietary calcium levels. There were no significant effects of fatty acid supplementation on calcium and magnesium retention, although increasing the calcium content of the diet resulted in a decreased (P less than .01) percentage of calcium retention.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

The binding of L-tryptophan to serum albumins in the presence of non-esterified fatty acids.

Bovine, human and rat serum albumins were defatted and palmitic acid, oleic acid and lauric acid added in various molar ratios. The binding of L-tryptophan to these albumins was measured at 20 degrees C in a 0.138 M salt solution at pH 7.4, by using an ultrafiltration technique, and analysed in terms of n, the number of available tryptophan-binding sites per albumin molecule, with apparent association constant, k. 2. n and k were 0.90 and 2.3x10(-4)M(minus-1) respectively for defatted bovine serum albumin and 0.87 and 9.7x10(-3)M(-minus-1) for human albumin. Addition of palmitic acid did not decrease n until the molar ratio, fatty acid/bovine albumin, approached and exceeded 2. The decrease in k was small and progressive. In contrast, lauric caused a marked decrease in n and k at ratios as low as 0.5. A similar distinction between the effects on n of palmitic acid and oleic acid and those of lauric acid was seen for human albumin. k for human albumin was not significantly affected by fatty acids under the conditions studied. 3. It is concluded that primary long-chain fatty acid sites interact only weakly with the tryptophan site on albumin and that inhibition of tryptophan binding occurs when secondary long-chain sites are occupied. Primary medium-chain fatty acid sites are distinct from primary long-chain sites but may be grouped with secondary long-chain sites. 4. The relationship between free and bound tryptophan in samples of rat plasma (Stoner et al., 1975) is discussed in terms of a similar but limited study of rat albumin.

Animals↗
PubMed1987

Arachidonoyl-coenzyme A synthetase and nonspecific acyl-coenzyme A synthetase activities in purified rat brain microvessels.

Purified rat brain microvessels were prepared to demonstrate the occurrence of acyl-CoA (EC 6.2.1.3) synthesis activity in the microvasculature of rat brain. Both arachidonoyl-CoA and palmitoyl-CoA synthesis activities showed an absolute requirement for ATP and CoA. This activity was strongly enhanced by magnesium chloride and inhibited by EDTA. The apparent Km values for acyl-CoA synthesis by purified rat brain microvessels were 4.0 microM and 5.8 microM for palmitic acid and arachidonic acid, respectively. The apparent Vmax values were 1.0 and 1.5 nmol X min-1 X mg protein-1 for palmitic acid and arachidonic acid, respectively. Cross-competition experiments showed inhibition of radiolabelled arachidonoyl-CoA formation by 15 microM unlabelled arachidonic acid, with a Ki of 7.1 microM, as well as by unlabelled docosahexaenoic acid, with a Ki of 8.0 microM. Unlabelled palmitic acid and arachidic acid had no inhibitory effect on arachidonoyl-CoA synthesis. In comparison, radiolabelled palmitoyl-CoA formation was inhibited competitively by 15 microM unlabelled palmitic acid, with a Ki of 5.0 microM and to a much lesser extent by arachidonic acid (Ki, 23 microM). The Vmax of palmitoyl-CoA formation obtained on incubation in the presence of the latter fatty acids was not changed. Unlabelled arachidic acid and docosahexaenoic acid had no inhibitory effect on palmitoyl-CoA synthesis. Both arachidonoyl-CoA and palmitoyl-CoA synthesis activities were thermolabile. Arachidonoyl-CoA formation was inhibited by 75% after 7 min at 40 degrees C whereas a 3-min heating treatment was sufficient to produce the same relative inhibition of palmitoyl-CoA synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyl Coenzyme A↗
PubMedDate not supplied

Dietary lipids and adipose tissue fatty acids in the marmoset monkey (Callithrix jacchus).

The fatty acid composition of marmoset monkey perirenal fat was examined after long-term feeding of different lipid supplemented diets. Saturated fatty acid supplementation significantly reduced linoleic acid; n-6 polyunsaturated fatty acid (PUFA) supplementation decreased oleic acid but did not reduce the saturated fatty acid content of perirenal fat. Dietary supplementation with fish oil also reduced the level of linoleic acid but increased the level of palmitic acid as well as that of the long-chain n-3 PUFAs. Perirenal fat levels of linoleic acid and docosahexaenoic acid are reliable measures of n-6 and n-3 PUFA intake respectively, but the levels of saturated fatty acids palmitic and stearic do not accurately reflect the marmosets dietary intake.

Adipose Tissue↗
PubMed1998

Individual saturated fatty acids and effects on whole blood aggregation in vitro.

OBJECTIVES: In two studies we have compared the effects of four different saturated fat diets (medium chain fatty acids (MCFA), and lauric, myristic and palmitic acids) with those of a monounsaturated oleic acid diet on in-vitro whole blood aggregation in healthy women and men. DESIGN: Study 1 had a cross-over design with three diet periods of each six weeks, and studied the effects of diets enriched in lauric, palmitic or oleic acids. Study 2 had a parallel design. After a three week oleic acid run-in diet, three groups of subjects were formed which consumed either an MCFA, myristic acid or oleic acid rich diet for six weeks. SUBJECTS: Eighteen women and 14 men in Study 1 and 37 women and 23 men in Study 2. All subjects were healthy and were aged 20-60 y. INTERVENTIONS: The experimental diets were the same in nutrient composition except for on average 8 En% (Study 1) or 10 En% (Study 2) which was provided by either MCFA, lauric acid, myristic acid, palmitic acid or oleic acid. Blood samples were taken at the end of each dietary period. Whole blood platelet aggregation, anticoagulated with recombinant hirudin was assessed after administration of collagen (final concentration (fc): 0.38 microgram/mL) in Study 1 and collagen (fc: 0.22 microgram/mL) or ADP (fc: 1.25 mumol/L) in Study 2. Collagen-induced formation of thromboxane (Tx)A2, measured as thromboxane (Tx)B2, was evaluated in Study 1 only. RESULTS: The aggregation velocity between the saturated fatty acid diets and the monounsaturated fatty acid diet did not differ. TxB2 concentrations measured in collagen activated blood samples, which correlated significantly with aggregation velocity, did not differ between the lauric or the palmitic compared with the oleic acid diet. A stepwise regression analysis indicated that collagen-induced aggregation was negatively correlated with the number of red blood cells. ADP-induced aggregation also correlated negatively with red blood cell count, and positively with platelet count. CONCLUSIONS: The exchange of 7-10 En% from oleic acid for MCFA, lauric, myristic or palmitic acid does not affect in-vitro whole blood aggregation induced by collagen. ADP-induced aggregation is not affected when 10 En% from oleic acid is exchanged for MCFA or myristic acid.

Adenosine Diphosphate↗
PubMed1991

Bradykinin activates a phospholipase D that hydrolyzes phosphatidylcholine in PC12 cells.

In PC12 pheochromocytoma cells whose phospholipids had been prelabelled with [3H]palmitic acid, bradykinin increased the production of [3H]phosphatidic acid. The increase in [3H]phosphatidic acid occurred within 1-2 min. before the majority of the increase in [3H]diacylglycerol. When the phospholipids were prelabeled with [3H]choline, bradykinin increased the intracellular release of [3H]choline. The production of phosphatidic acid and choline suggests that bradykinin was increasing the activity of phospholipase D. Transphosphatidylation is a unique property of phospholipase D. In cells labeled with [3H]palmitic acid, bradykinin stimulated the transfer of phosphatidyl groups to both ethanol and propanol to form [3H]phosphatidylethanol and [3H]phosphatidylpropanol, respectively. The effect of bradykinin on [3H]phosphatidic acid and [3H]phosphatidylethanol formation was partially dependent on extracellular Ca2+. In cells treated with nerve growth factor, carbachol also increased [3H]phosphatidylethanol formation. To investigate the substrate specificity of phospholipase D, cells were labeled with [14C]stearic acid and [3H]palmitic acid, and then incubated with ethanol in the absence or presence of bradykinin. The 14C/3H ratio of the phosphatidylethanol that accumulated in response to bradykinin was almost identical to the 14C/3H ratio of phosphatidylcholine. The 14C/3H ratio in phosphatidic acid and diacylglycerol was higher than the ratio in phosphatidylcholine. These data provide additional support for the idea that bradykinin activates a phospholipase D that is active against phosphatidylcholine. The hydrolysis of phosphatidylcholine by phospholipase D accounts for only a portion of the phosphatidic acid and diacylglycerol that accumulates in bradykinin-stimulated cells: bradykinin evidently stimulates several pathways of phospholipid metabolism in PC12 cells.

Adrenal Gland Neoplasms↗
PubMed1976

Lipid composition and lipid metabolism of Spiroplasma citri.

In a horse serum-based medium containing a full complement of fatty acids, cells of Spiroplasma citri were seen to preferentially incorporate palmitic acid. In the same medium, which had a steryl ester-to-sterol ratio of 3.64, a steryl ester-to-sterol ratio of 0.23 was seen in the cells, cholesterol being preferentially incorporated over cholesteryl ester. Like most other mycoplasmas, S. citri was shown to be unable to synthesize fatty acids or esterify cholesterol. The neutral lipids of S. citri grown in a medium containing horse serum consisted of free cholesterol, cholesteryl ester, free fatty acids, triglycerides and diglycerides. All polar lipids were phospholipids, with no glycolipids detected. These phospholipids, which are characteristic of many mycoplasmas, are phosphatidyl glycerol, diphosphatidyl glycerol, and their lyso derivatives. Sphingomyelin was also incorporated when cells were grown on horse serum. A sterol requirement for the growth of S. citri was confirmed using a serum-free medium supplemented with bovine serum albumin, palmitic acid, and various concentrations of sterols dissolved in Tween 80. The addition of palmitic acid stimulated growth but was not essential for growth. S citri was shown to grow best on cholesterol and beta-sitosterol and was able to grow on stigmasterol and ergosterol to a lesser degree. No growth was obtained using mevalonate, deoxycholate, or taurodeoxycholate as an alternative to sterol. S. citri was also able to grow when palmitic acid was replaced with oleic acid, linoleic acid, or linolenic acid. Alterations in the lipid composition of the growth medium and hence in the lipid composition of S. citri induced changes in the characteristic helical morphology of the cells, concurrent with loss of cell viability. Culture, age, and pH were also factors in determining cell morphology and viability.

Cholesterol↗
PubMed1981

The biological origin of ketotic dicarboxylic aciduria. In vivo and in vitro investigations of the omega-oxidation of C6-C16-monocarboxylic acids in unstarved, starved and diabetic rats.

The conversion of radioactive C6-C16-monocarboxylic acids to urinary adipic, suberic, sebacic and 3-hydroxybutyric acids was investigated in vivo in unstarved, starved and diabetic ketotic rats. Hexanoic, octanoic and decanoic acids were converted to C6-, C6-C8- and C6-C10-dicarboxylic acids, respectively, in fed and 72-h-starved rats. Lauric acid was converted to C6-C8-dicarboxylic acids in starved rats but not in unstarved rats. Decanoic and lauric acids were converted to relatively high amounts of C6-C8-dicarboxylic acids compared with myristic acid in myristic acid in ketotic diabetic rats, while radioactivity from [1-14C]-and [16-(14)] palmitic acid was not incorporated into C6-C8-dicarboxylic acids in diabetic ketotic rats. C6-C12-monocarboxylic acids in hydrolysed rat adipose tissue wee determined by gas-liquid chromatography-mass spectrometry (selected ion monitoring). Decanoic and lauric acids were found in amounts of 7.6-9.1 and 85.9-137.5 micrometers/100 mg tissue, respectively, whereas the amounts of hexanoic and octanoic acids were negligible. It is concluded that the biological origin of the C6-C8-dicarboxylic aciduria seen in ketotic rats are C10-C14-monocarboxylic acids, which are initially omega-oxidised solely or partly as free acids and subsequently beta-oxidised to adipic and suberic acids. The in vitro omega-oxidation of C6-C16-monocarboxylic acids to corresponding dicarboxylic acids in the 100,000 Xg supernatant fraction of rat liver homogenate was measured by selected ion monitoring. 0.09, 0.14, 16.1, 5.8, 7.0 and -6.9% of, respectively, hexanoic, octanoic, decanoic, lauric, myristic and palmitic acid were omega-oxidised to dicarboxylic acids of corresponding chain lengths after 90 min of incubation, when correction for the production of dicarboxylic acids in control assays was made. An in vitro production of C12-C16-dicarboxylic acids was detected in all assays ()including control assays), probably formed from"endogenous' monocarboxylic acids preexistent in the homogenate. Ths "endogenous' production of dicarboxylic acids was inhibited by C10-C16-monocarboxylic acids, where palmitic acid had the strongest effect. In fact, palmitic acid inhibited its own omega-oxidation when added in concentrations above 0.6 mM. Starvation of rats for 72 h did not alter the "endogenous' in vitro production of hexadecanedioic acid.

Animals↗