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PubMed1990

Characterization of FadL-specific fatty acid binding in Escherichia coli.

The product of the fadL gene (FadL) is a central component of the long-chain fatty acid transport system of Escherichia coli. When fatty acid activation is blocked by a mutation in the structural gene for acyl CoA synthetase (fadD) transport is inhibited allowing a FadL-specific fatty acid binding activity to be measured. This binding activity was 4- to 6-fold greater in the fadL+ fadD strain LS6928 when compared to the delta fadLfadD strain LS6929. With long-chain fatty acids, this binding activity was saturable and it was estimated that there were approx. 35,000 FadL-specific oleic acid binding sites per cell in the fadL+ strain LS6928. The FadL-specific fatty acid binding affinity was highest for oleic acid (18:1) and palmitic acid (16:0) giving apparent KD values of 2.3.10(-7) M and 8.8.10(-7) M, respectively. FadL-specific binding affinity of myristic acid (14:0) was nearly an order of magnitude less and no FadL-specific binding of decanoic acid (10:0) could be measured. Two lines of evidence suggest that FadL-fatty acid binding occurs by a hydrophobic interaction: (1) There was a preference for the long-chain substrates oleic acid and palmitic acid; and (2) oleic acid binding activity was not significantly changed over the pH range 5.0 to 8.0. The FadL-specific binding of oleic acid in the fadL+ strain LS6928 could be blocked by preincubation with antisera raised against purified FadL providing a clear correlation between the activity and identity of FadL. The binding activity associated with FadL was measured in vesicles of the outer membrane following passage over the hydrophobic resin Lipidex 1000. The KD of oleic acid binding attributable to FadL in outer membranes vesicles (6.0.10(-7) M) was in close agreement with that determined in whole cells. Overall, these studies demonstrated that FadL binds long-chain fatty acids with a relatively high affinity prior to their transport across the outer membrane.

Bacterial Outer Membrane Proteins↗
PubMed1997

Mechanism of the anti-tumour effect of 2,3,5-trimethyl-6-(3-pyridylmethyl) 1,4-benzoquinone (CV-6504).

2,3,5-Trimethyl-6-(3-pyridylmethyl) 1,4-benzoquinone (CV-6504), an inhibitor of 5-lipoxygenase, effectively suppressed growth of the MAC16 tumour in vivo and prevented the accompanying cachexia, when administered daily at a dose of 10 mg kg(-1). There was a reduction in the tumour concentration of linoleic (LA), arachidonic (AA), oleic, stearic and palmitic acid. In order to elucidate the mechanism of the anti-tumour action, the effect of CV-6504 on the metabolism of AA through the 5-, 12- and 15-lipoxygenase pathways has been determined in cell lines sensitive (MAC16, MAC13, MAC26 and Caco-2) and resistant (A549 and DU-145) to CV-6504. Incubation of all cell lines with [3H]AA led to the appearance of [3H]5-, 12- and 15-HETE. Preincubation of MAC16, MAC13, MAC26 and Caco-2 with 10 microM CV-6504 inhibited the conversion of AA to 5-, 12- and 15-HETE, while in A549 and DU-145 cells there was no effect on metabolism through any lipoxygenase pathway. Two other cell lines, MDA-MB-231 and PC-3, sensitive to growth inhibition by CV-6504, are known to require LA for growth, while DU-145, which was insensitive to growth inhibition by CV-6504, showed no growth response to LA. These results suggest that some tumours are dependent on lipoxygenase metabolites of LA and AA for their continual growth, and interference with this pathway produces a specific growth inhibition.

Animals↗
PubMed2006

Palmitate induced mitochondrial deoxyribonucleic acid damage and apoptosis in l6 rat skeletal muscle cells.

A major characteristic of type 2 diabetes mellitus (T2DM) is insulin resistance in skeletal muscle. A growing body of evidence indicates that oxidative stress that results from increased production of reactive oxygen species and/or reactive nitrogen species leads to insulin resistance, tissue damage, and other complications observed in T2DM. It has been suggested that muscular free fatty acid accumulation might be responsible for the mitochondrial dysfunction and insulin resistance seen in T2DM, although the mechanisms by which increased levels of free fatty acid lead to insulin resistance are not well understood. To help resolve this situation, we report that saturated fatty acid palmitate stimulated the expression of inducible nitric oxide (NO) synthase and the production of reactive oxygen species and NO in L6 myotubes. Additionally, palmitate caused a significant dose-dependent increase in mitochondrial DNA (mtDNA) damage and a subsequent decrease in L6 myotube viability and ATP levels at concentrations as low as 0.5 mM. Furthermore, palmitate induced apoptosis, which was detected by DNA fragmentation, caspase-3 cleavage, and cytochrome c release. N-acetyl cysteine, a precursor compound for glutathione formation, aminoguanidine, an inducible NO synthase inhibitor, and 5,10,15,20-tetrakis(4-sulphonatophenyl) porphyrinato iron (III), a peroxynitrite inhibitor, all prevented palmitate-induced mtDNA damage and diminished palmitate-induced cytotoxicity. We conclude that exposure of L6 myotubes to palmitate induced mtDNA damage and triggered mitochondrial dysfunction, which caused apoptosis. Additionally, our findings indicate that palmitate-induced mtDNA damage and cytotoxicity in skeletal muscle cells were caused by overproduction of peroxynitrite.

Adenosine Triphosphate↗
PubMed2001

A human cellular model for studying the regulation of glucagon-like peptide-1 secretion.

GLP-1 (glucagon-like peptide-1) is a potent insulin secretagogue released from L cells in the intestine. The regulation of GLP-1 secretion has been described both in vivo and in vitro in several animal species, but data from human cellular models are lacking. For this purpose, factors and cell-signaling pathways regulating GLP-1 secretion were investigated in the NCI-H716 human intestinal cell line. After differentiation, these cells homogeneously produced 16.8 pmol GLP-1/mg protein with a basal release of 4.2% during a 2-h incubation period. Nutrients, such as palmitic acid, oleic acid, and meat hydrolysate, stimulated GLP-1 secretion in a dose-dependent manner, as did the cholinergic agonist carbachol and the neuromediator gastrin-releasing peptide. Along with stimulating GLP-1 release, gastrin-releasing peptide, like ionomycin, increased intracellular calcium levels. Activators of PKA and PKC were able to increase GLP-1 secretion in NCI-H716 cells. However, neither PKA activators nor meat hydrolysate increased proglucagon mRNA levels. These findings indicate that the NCI-H716 cell line constitutes a unique model to study the cellular mechanism of GLP-1 secretion in humans and suggest potential interspecies divergence in the regulation of proglucagon gene expression in enteroendocrine cells.

Animals↗
PubMed1976

Effect of cortisone and acth on the phospholipids of human amniotic fluid and lung tissue in early gestation.

Fifteen physically healthy women who received permission for legal abortion on sociomedical grounds in the second trimester of pregnancy were given either cortisone acetate per os or adrenocorticotrophic hormone (ACTH) intramuscularyly for 3 days previous to hysterotomy. Eight other patients served as controls. The phospholipid composition of amniotic fluid, fetal lung washings, and lung tissue was analyzed. In the cortisone group there was a significant increase in the proportion of palmitic acid in the lung tissue lecithins linked to a corresponding decrease in the oleic acid. A similar tendency was observed in the ACTH group, but the changes were not significant. The investigation suggests that the human fetal lung already at this early stage of development is capable of responding to the action of cortisone by a relative increase in the synthesis of dipalmitoyllecithin.

Adrenocorticotropic Hormone↗
PubMed1989

Effect of fatty acids and their derivatives on mitochondrial structures.

Reye's Syndrome (RS) is characterized by encephalopathy, fatty degeneration of viscera and high levels of free fatty acids which are implicated in cellular toxicity. We have examined the effects of octanoic acid (C8:0), palmitic acid (C16:0) and oleic acid (C18:1) on rat liver mitochondrial swelling by spectroscopic and microscopic techniques. Of the fatty acids tested oleic acid had a greater effect than palmitic acid while octanoic acid had no effect. Acyl-CoA derivatives produced greater mitochondrial swelling than either acyl-carnitine or free fatty acids. However, identical amounts of palmitoyl-CoA and oleoyl-CoA were required to produce the same degree of swelling. Addition of carnitine (2mM) to oleoyl-CoA reduced the mitochondrial swelling significantly thus suggesting that the toxicity of the fatty acids may be reduced by conversion to their carnitine derivatives. Twice the concentration of oleoyl-carnitine was required to produce half the maximum swelling as compared to oleoyl-CoA. Ultrastructural profiles of mitochondria treated with oleic acid, oleoyl-CoA and oleoyl-carnitine demonstrated greater swelling with oleoyl-CoA than with oleic acid or oleoyl-carnitine. These results suggest that carnitine may protect the mitochondria from damage by the fatty acids and their acyl-CoA derivatives in Reye's Syndrome.

Acyl Coenzyme A↗
PubMed1995

[Free fatty acids in gallbladder bile].

Using gas chromatography and high performance liquid chromatography (HILC), we examined free fatty acid and lecithin molecular species in gallbladder biles from patients with cholesterol gallstones. Effect of free fatty acids on cholesterol nucleation in model bile was studied by a sensitive cholesterol crystal growth assay. Compared to bile of controls, biles from patients with gallstones had higher total free fatty acid level, more palmitic acid, more stearic acid, more linoleic acid and arachidonic acid. The lecithin pattern was similar in all. After free fatty acids were added to model bile, palmitic acid, oleic, acid, linoleic acid and arachidonic acid had significant effect of pro-nucleating, free fatty acids on non-protein pro-nucleating factor. These data suggest that variations in quantitation and composition of free fatty acids are importanct in the pathogenesis of cholesterol gallstone formation.

Bile↗
PubMed1997

Hepatic microsomal membrane lipidic composition and growth hormone effect in adult male rat: evidence for a 'feminization' process of total phospholipid fatty acid pattern.

Growth hormone (GH) effects on fatty acid composition and on delta5-, delta6-, delta9-desaturase and palmitic acid elongation activities were studied in male rat hepatic microsomes. Sham-operated and hypophysectomized animals were injected with two different dosages of GH, mimicking either the male or female GH secretion pattern. Half the hypophysectomized animals received thyroxine and cortisol in concentrations chosen to compensate for the lack of thyroid hormones and glucocorticoids. GH, administered to sham-operated or to cortisol/thyroxine-treated hypophysectomized rats resulted in an increase in stearic and arachidonic acid proportions, while palmitic acid percentage was decreased. Total monounsaturated fatty acids were dramatically reduced by this treatment. DeltaA-desaturase and palmitic acid elongation activities were increased by GH treatment, while delta9-desaturase activity was decreased. These GH effects on desaturation and elongation activities could explain the modifications in microsomal fatty acid composition. Hypophysectomy markedly altered the fatty acid composition by reducing arachidonic and stearic acid proportions and increasing the linoleic acid proportion, while delta9-, delta5-desaturase and palmitic acid elongation activities were decreased. Restoration of most of the fatty acid proportions to control values was realized in hypophysectomized animals with a cortisol/thyroxine replacement administered alone or together with the low dosage of GH mimicking the male secretion pattern. High GH dosage produces essentially a 'feminization' process of the fatty acid composition of the hepatic microsomal membrane in male rats when compared to that of females.

Animals↗
PubMed1976

Metabolism of erucic acid in the isolated perfused rat heart.

In the present work the uptake and utilization of [14C]erucic acid by the perfused rat heart has been investigated and compared with those of [14C]-palmitic acid. Both fatty acids were found to be taken up by the heart at the same rate. On the other hand, the incorporation of erucic acid into tissue lipid during 30 min perfusion were significantly high and CO2 production low as compared with palmitic acid. Incorporation of erucic acid into diacylglycerol, triacylglycerol and cholesterol ester was considerably higher than that of palmitic acid. During a 30-min period, a large amount of [14C]erucic acid was accumulated in tissue fatty acid fraction. Similarly, relatively high labelling was found in the fatty acid and diacylglycerol fraction during the initial 300 s of perfusion with erucic acid. When [14C]erucic acid and unlabelled palmitic acid was used, the radioactivity was very high in the fatty acid fraction of the heart lipid in comparison with the experiment when [14C]palmitate and unlabelled erucic acid was used. Therefore, erucic acid is poorly oxidized by the heart and is preferentially incorporated into heart lipids. There was relatively high incorporation of [14C]erucic acid into diacylglycerol and addition of unlabelled palmitic acid tended to decrease it, probably converting more diacylglycerol to triacylglycerol. When [14C]palmitic acid and erucic acid were used together, incorporation to triacylglycerol was high and diacylglycerol low. These results, therefore suggest that palmitic acid is a more suitable acyl donor than erucic acid for the C-3 position of triacylglycerol, especially when the diacylglycerol contains erucoyl moieties.

Animals↗
PubMed1995

Biosynthesis and palmitoylation of endothelial nitric oxide synthase: mutagenesis of palmitoylation sites, cysteines-15 and/or -26, argues against depalmitoylation-induced translocation of the enzyme.

The presence of myristoylated endothelial nitric oxide synthase (eNOS) in cytosolic fractions of bovine aortic endothelial cells (BAEC) suggests that N-myristoylation of eNOS is not sufficient for membrane localization. Therefore, we examined if posttranslational palmitoylation was another molecular signal for the membrane attachment of eNOS. Metabolic labeling showed incorporation of [3H]palmitic acid into the membrane-bound, but not the cytosolic, form of eNOS. Fatty acid analysis demonstrated the labeled fatty acid incorporated into eNOS was palmitate, linked via a hydroxylamine-labile thioester bond. Biosynthesis and turnover studies show that the turnover of palmitate is much faster than the protein itself. However, the rates of palmitoylation and depalmitoylation were not affected by bradykinin or ionomycin treatment of BAEC. To examine the contribution of palmitoylation to the membrane association of eNOS, we mutated cysteine-15 and -26. Both mutations markedly diminished palmitoylation of eNOS, but did not significantly alter its membrane association. Additionally, [3H]palmitic acid was not incorporated into nonmyristoylated mutant eNOS (G2A eNOS), suggesting that myristoylation is necessary for subsequent palmitoylation of the enzyme. Taken together, our data imply that palmitoylation does not play a major role in membrane association of eNOS and other amino acid sequences, in conjunction with N-myristoylation, are necessary and sufficient for membrane association of the enzyme.

Animals↗
PubMed2001

Monounsaturated fatty acid diets improve glycemic tolerance through increased secretion of glucagon-like peptide-1.

Diets enriched in monounsaturated fatty acids (MUFA)s have been shown to benefit glycemic control. Furthermore, MUFAs specifically stimulate secretion of the antidiabetic hormone, Glucagon-like peptide-1 (GLP-1) in vitro. To determine whether the MUFA-induced benefit in glycemic tolerance in vivo is due to increased GLP-1 release, lean Zucker rats were pair-fed a synthetic diet containing 5% fat derived from either olive oil (OO; 74% MUFA) or coconut oil (CO; 87% saturated fatty acids; SFA) for 2 weeks. Food intake and body weight gain were similar for both groups over the feeding period. The OO group had improved glycemic tolerance compared with the CO group in both oral and duodenal glucose tolerance tests [area under curve (AUC) 121 +/- 61 vs. 290 +/- 24 mM.120 min, P < 0.05; and 112 +/- 28 vs. 266 +/- 65 mM.120 min, P < 0.05, respectively]. This was accompanied by increased secretion of gut glucagon-like immunoreactivity (gGLI; an index of GLP-1 levels) in the OO rats compared with the CO rats (402 +/- 96 vs. 229 +/- 33 pg/ml at t = 10 min, P < 0.05). Tissue levels of GLP-1 and plasma insulin and glucagon levels were not different between the two groups. To determine the total contribution of GLP-1 to the enhanced glycemic tolerance in OO rats, the GLP-1 receptor antagonist exendin(9-39) (Ex(9-39)) was infused 3 min before a duodenal glucose tolerance test. Ex(9-39) abolished the benefit in glycemic tolerance conferred by OO feeding (OO+Ex(9-39) vs. CO+Ex(9-39), P = NS), and resulted in a deterioration of glycemic tolerance in the OO+Ex(9-39) group when compared with the OO controls (AUC 331 +/- 21 vs. 112 +/- 28 mM.120 min, P < 0.05). To probe the mechanism by which the OO diet enhanced GLP-1 secretion, a GLP-1-secreting L cell line was incubated for 24 h with either 100 microM oleic acid (MUFA) or 100 microM palmitic acid (SFA) and subsequently challenged with GIP, a known stimulator of the L cell. Preexposure to oleic acid but not to palmitic acid significantly increased GIP-induced GLP-1 secretion when compared with controls (55 +/- 12% vs. 34 +/- 9%, P < 0.01). These results demonstrate that the benefit in glycemic tolerance obtained with MUFA diets occurs in association with increased GLP-1 secretion, through a mechanism of enhanced L cell sensitivity. These results suggest that diet therapy with MUFAs may be useful for the treatment of patients with impaired glucose tolerance and/or type 2 diabetes through increased GLP-1 secretion.

Administration, Oral↗
PubMed2001

Palmitic and stearic acids bind Ca2+ with high affinity and form nonspecific channels in black-lipid membranes. Possible relation to Ca2+-activated mitochondrial pores.

A mitochondrial hydrophobic component that forms Ca2+-induced nonspecific ion channels in black-lipid membranes (Mironova et al., 1997) has been purified and its nature elucidated. It consists of long-chain saturated fatty acids--mainly palmitic and stearic. These fatty acids, similar to the mitochondrial hydrophobic component, bind Ca2+ with high affinity in comparison with unsaturated fatty acids, saturated fatty acids with shorter aliphatic chains, phospholipids, and other lipids. Ca2+-binding is inhibited by Mg2+ but not by K+. For palmitic acid, the Kd for Ca2+ was 5 microM at pH 8.5 and 15 microM at pH 7.5, with the Bmax of 0.48 +/- 0.08 mmol/g. This corresponds to one Ca2+ ion for eight palmitic acid molecules. The data of IR spectroscopy confirm that Ca2+ does not form ionic bonds with palmitic and stearic acids under hydrophobic conditions. It has been found that in the presence of Ca2+, palmitic and stearic acids, but not unsaturated FFA induce a nonspecific permeability in black-lipid membranes. Addition of Ca2+ in order to induce the permeability transition, increases the extractable amount of palmitic and stearic acids, the effect being prevented by a phospholipase A2 inhibitor. The possible involvement of palmitic and stearic acids in the mitochondrial nonspecific permeability is discussed.

Animals↗
PubMed2000

Polyunsaturated fatty acids reduce non-receptor-mediated transcellular permeation of protein across a model of intestinal epithelium in vitro.

BACKGROUND: Dietary polyunsaturated fatty acids influence the natural history of intestinal inflammatory diseases. Varying the types of long-chain fatty acids that are exposed to cells alters the physicochemical properties of cell membranes. This study aimed to determine whether such variations alter transcellular and paracellular permeability in intestinal epithelium. METHODS: Monolayers of Caco-2 cells, allowed to differentiate by culturing for 7 days following confluence, were used as the model for intestinal epithelium. Paracellular permeability was assessed by measurement of transepithelial resistance, while transcellular permeability was assessed by the transepithelial flux of horseradish peroxidase. RESULTS: Exposure of the cells to 100 micromol/L of palmitic acid, oleic acid, eicosapentaenoic acid, or linoleic acid, was not toxic to cells (measured by leakage of lactate dehydrogenase), and altered cell membrane fatty acid composition (as measured by gas chromatography). Flux of horseradish peroxidase was significantly affected by 24 h fatty acid exposure (P= 0.038, ANOVA), being decreased by 23 +/- 6% (mean +/- SEM) by eicosapentaenoic acid and 25 +/- 3% by linoleic acid. Oleic acid, palmitic acid and butyrate, had no effect. Transepithelial resistance also varied significantly across the treatment groups (P< 0.001) due to a 28 +/- 5% increase induced by butyrate. The long-chain fatty acids had no effect. CONCLUSIONS: Both omega-3 and omega-6 polyunsaturated fatty acids reduce transcellular, non-receptor-mediated permeation of proteins across differentiated Caco2 cell monolayers, without altering paracellular permeability. Alteration of intestinal barrier function should be considered as a possible mechanism of action of dietary polyunsaturated fatty acids.

Butyrates↗
PubMed1999

Lymphatic absorption of glucose and fatty acids as determined by direct measurement.

BACKGROUND/PURPOSE: Treatment of chylous leaks using enteral feeds supplemented with medium chain triglycerides (MCT) is used widely but often ineffective. Few studies have examined the conventional dogma that MCTs and simple sugars are absorbed directly via the portal system. This study tests the hypothesis that significant absorption of MCTs and simple sugars occurs via the lymphatics. METHODS: A stable, awake rat model with cannulation of the mesenteric lymph duct, portal and jugular veins, and duodenum was used. Venous catheters were infused with saline at 2.5 mL/hr, while the duodenal tube was infused with emulsified fatty acids at 3 mL/hr (0.3% palmitic acid [C16:0] + 0.35% of test nutrient: either Lauric acid [C12:0; n = 5] octanoic acid [C8:0; n = 6] or 3-0-methylglucose, [n = 5].) After 4 hours of stabilization, the animals were given a differentially radiolabeled pulse of palmitic acid plus test nutrient and the subsequent appearance in lymphatic, portal, and jugular systems was measured. Total lymphatic appearance was measured directly; appearance in the portal and jugular systems was measured using the area under the curve method. RESULTS: Results are expressed as mean +/- SD. Palmitic acid: lymphatic absorption (LA), 49.2+/-7.4%; portal venous absorption (PA), 19.8+/-15%; total absorption (TA), 69+/-12.4%. Lauric acid: LA, 32.9+/-6.7%; PA, 7.5+/-2.9%; TA, 40.4+/- 6.3%. Octanoic acid: LA, 5.6+/-2.1%; PA, 27.3+/-6.5%; TA, 32.9+/-4.8%. 3-0 methylglucose: LA, 8.6+/-2.2%; PA 69+/-39%; TA, 76.6+/-39.5. Total lymphatic flow: palmitic plus lauric group, 14+/-2 mL; palmitic plus octanoic, 12.5+/-4.4 mL; palmitic plus 3-0 methylglucose, 12.8+/-2.9 mL. (Total volume measure over 4 hours after giving the radiolabeled pulse.) CONCLUSIONS: The portal venous uptake of the medium chain fatty acid (MCFA), octanoic acid, was not significantly greater than the uptake of the long-chain palmitic acid, but the absorption of lauric acid was less. There are different absorption patterns between different medium-chain fatty acids; however, lymphatic absorption of MCFAs and simple sugars does occur. Total measured absorption of MCFAs is less than that of long-chain fatty acids or sugars. Further work is required to demonstrate the utility of MCT supplementation on nutritional status and lymphatic flow rates in chylous leak syndromes, and to examine the factors that control the results of absorption of fatty acids of varying chain lengths, both in normal and pathological states.

Absorption↗
PubMed2000

Ascorbic acid and ascorbic acid 6-palmitate induced oxidation in egg yolk dispersions.

The oxidation in aqueous dispersions of egg yolk powder and the influence of addition of the proposed antioxidants ascorbic acid and ascorbic acid 6-palmitate indicate that both ascorbic acid and ascorbic acid 6-palmitate propagated the oxidation of egg yolk powder dispersions. Ascorbic acid 6-palmitate was found to be more prooxidative than ascorbic acid. Moreover, it was found that addition of ascorbic acid or ascorbic acid 6-palmitate gave rise to an increase in the amount of free iron Fe(II) in the egg yolk dispersions. It is proposed that ascorbic acid and ascorbic acid 6-palmitate react with the phosvitin-Fe(III) complex found in egg yolk and release Fe(II), which subsequently propagates lipid oxidation. It appears that less oxidation occurs in egg yolk dispersions exposed to high concentrations of peroxy radicals with added ascorbic acid than egg yolk dispersions with added ascorbic acid without exposure to peroxy radicals.

Ascorbic Acid↗
PubMed1994

The role of fatty acid composition and positional distribution in fat absorption in infants.

Fat digestion and absorption in the infant is a multistep process. An initial gastric phase of lipolysis generates modest amounts of diglycerides, monoglycerides, and free fatty acids. These initial digestion products, as well as bile salts, are required for optimal activity of the intestinal phase of lipolysis. Colipase-dependent pancreatic lipase catalyzes the intraduodenal phase of triglyceride digestion in formula-fed infants; in breast-fed infants this process is also mediated by bile salt-stimulated lipase. Triglyceride fatty acid positional distribution may modulate the efficiency of nutrient absorption. Human milk contains palmitic acid (C16:0) primarily in the sn-2 position; infant formula fat blends contain palmitic acid predominantly in the sn-1 and sn-3 positions. Because pancreatic lipase selectively hydrolyzes triglycerides at the sn-1 and sn-3 positions, free fatty acids and 2-monoglycerides are produced. Free palmitic acid, but not 2-monopalmitin (which is efficiently absorbed), may be lost as a calcium-fatty acid soap in the feces. As a result, many infant formulas contain substantial levels of well-absorbed saturated fatty acids of shorter chain lengths (e.g., C12:0) in place of palmitic acid. Means of increasing the proportion of 2-palmitic acid in infant formula may make possible fat blends closer to that of human milk with acceptable absorption characteristics.

Animals↗
PubMed1965

FURTHER STUDIES ON THE LIPID METABOLISM OF THE NORMAL AND VITAMIN B-12 DEFICIENT CHICK EMBRYO.

1. The triglyceride, cholesterol ester and total phospholipid fractions were isolated from the livers and yolk sacs of normal and vitamin B(12)-deficient chick embryos after 13, 15, 17, 19 and 21 days of incubation, and the fatty acid compositions were determined. 2. At all stages of incubation, the concentration of cholesterol ester in the livers of the normal embryos were greater, and on days 15 and 17 the concentrations of triglyceride were considerably less, than the corresponding concentrations in the livers of the deficient embryos. 3. Between day 13 and day 21 of incubation the concentration of oleic acid in the liver triglycerides of the normal embryos increased, whereas the concentrations of palmitic acid and docosahexaenoic acid decreased. Vitamin B(12) deficiency resulted in higher concentrations of palmitic acid in the liver triglycerides on days 15, 17 and 19, higher concentrations of C(18) polyunsaturated acids on days 13 and 15 and lower concentrations of oleic acid on days 13, 15, 17 and 19. 4. At all stages of development, cholesterol oleate accounted for almost 80% of the total liver cholesterol esters in both normal and deficient embryos. 5. As development of the normal embryos progressed, the concentrations of palmitic acid and arachidonic acid in the liver phospholipid decreased, whereas the concentrations of stearic acid and docosahexaenoic acid increased. Vitamin B(12) deficiency resulted in markedly higher concentrations of stearic acid and palmitic acid and markedly lower concentrations of arachidonic acid and docosahexaenoic acid in the liver phospholipids. 6. Vitamin B(12) deficiency did not influence the fatty acid composition of the triglyceride, cholesterol ester and phospholipid fractions either in the yolks of fertile unincubated eggs or in the yolks obtained from eggs that had been incubated for 13, 15, 17, 19 and 21 days.

Animals↗