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PubMed1976

Effects of lactate and glutamine on palmitate metabolism in rat kindey cortex.

Rat renal cortical slices were incubated with [1-(14)C]palmitate bound to 2.5% albumin. The following effects were found: a)1 mM palmitate utilization or oxidation to CO(2) varied according to the concentration of lactate in the media, it increased at 0.8 and 3.2 mM, was unchanged at 8 mM, and decreased at 16 mM. Esterification was stimulated at 3.2 mM lactate. b) Addition of glutamine (0.1 mM) instead of lactate stimulated incomplete and complete oxidation of palmitate (1 mM), whereas high medium glutamine (10 mM) inhibited palmitate (1 mM) utilization, esterification, and oxidation to CO(2) but increased its incomplete oxidation. The low rate of exogenous palmitate oxidation observed in this study and the finding that exogenous palmitate oxidation is only partially inhibited at very high concentrations of exogenous lactate or glutamine are consistent with the view that these exogenous substrates contribute little to the oxidative metabolism of rat renal cortex in vitro, which probably depends on the supply of substrates endogenous to the tissue.

Animals↗
PubMed1989

Glycoprotein Ib and glycoprotein IX in human platelets are acylated with palmitic acid through thioester linkages.

The glycoprotein (GP) Ib-IX complex is a major component of the platelet membrane which mediates adhesion of platelets to exposed subendothelium. GP Ib is a heterodimer with a large alpha chain (Mr = 135,000-145,000) and small beta chain (Mr = 22,000-27,000) linked by a disulfide bond(s). GP Ib is bound in a noncovalent 1:1 complex with GP IX (Mr = 17,000-22,000). We labeled isolated human platelets with [3H] palmitate or surface-labeled platelet membrane glycoproteins with sodium periodate-[3H]sodium borohydride and immunoprecipitated the GP Ib-IX complex from radiolabeled platelet lysates using a mouse monoclonal antibody (SZ.1) which recognizes the intact complex. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography of immunoprecipitates from [3H]palmitate-labeled platelets revealed two radiolabeled bands under reducing conditions at 24 and 19 kDa and two bands under nonreducing conditions at 170 and 19 kDa. As demonstrated by the parallel analysis of immunoprecipitates from periodate-[3H]sodium borohydride-labeled platelets, the [3H]palmitate-labeled bands obtained under reducing conditions corresponded to GP Ib beta and GP IX and the ones obtained under nonreducing conditions to intact GP Ib and GP IX, respectively. Using alkaline methanolysis followed by high pressure liquid chromatography analysis of the methanolysis products, we demonstrated that the radioactivity associated with the GP Ib-IX complex from [3H]palmitate-labeled platelets was, in fact, covalently bound [3H]palmitate in ester linkage to protein. The protein-fatty acid linkage was also disrupted by hydroxylamine at neutral pH. Thus, this study demonstrates that GP Ib beta and GP IX in human platelets are both fatty acid-acylated with palmitate through thioester linkages.

Acylation↗
PubMed1984

In vitro acylation of rat gastric mucus glycoprotein with [3H]palmitic acid.

The incorporation of fatty acids into gastric mucus glycoproteins was studied by incubating rat gastric mucosal cell suspensions with [9,10-3H]palmitic acid and [3H]proline. The mucus glycoprotein polymer, secreted into the growth medium (extracellular) and that contained within the cells (intracellular), was purified from the other components of the secretion, thoroughly delipidated, and then analyzed for the radiolabeled tracers. Both pools of mucus glycoprotein, incubated in the presence of [3H]palmitic acid, contained radioactive label which could not be removed by gel filtration, CsCl density gradient centrifugation, sodium dodecyl sulfate-gel electrophoresis, or lipid extraction. Treatment of the purified mucus glycoprotein with 1 M hydroxylamine or 0.3 M methanolic KOH released the radioactivity, thus indicating that [3H]palmitic acid was covalently bound by ester linkage to the glycoprotein. The released radioactivity was associated mainly (87%) with palmitic acid. The incorporation ratio of [3H]proline to [3H]palmitic acid was 0.12:1.0 in the extracellular glycoprotein and 1.38:1.0 in the intracellular glycoprotein, which suggested that acylation of mucus glycoprotein occurs in the intracellular compartment after completion of its polypeptide core. The fact that incorporation of [3H]palmitic acid was greater in the glycoprotein subunits than in the glycoprotein polymer indicates that acylation takes place near the end of subunit processing but before their assembly into the high molecular weight mucus glycoprotein polymer.

Acylation↗
PubMed1982

Increased incorporation of 14C-palmitate into tissue lipids by isolated heart myocytes in endotoxic shock.

The incorporation of 14C-palmitate into various classes of tissue lipids by isolated adult dog heart myocytes was studied in an attempt to understand the pathophysiology of myocardial dysfunction during endotoxic shock. The results showed that the incorporation of 14C-palmitate into phospholipids was increased by 85.3% and 108.8% at 0.5 hours and two hours, respectively, following endotoxin (0.5 mg Escherichia coli lipopolysaccharide B per kg body weight) administration. Incorporation of radioactive palmitate into triglycerides was increased by 50.9% and 107.2% at 0.5 and two hours, respectively, postendotoxin. Incorporation of 14C-palmitate into diglycerides was stimulated by 51.9% and 64.5% at 0.5 and two hours, respectively, after endotoxin injection. The incorporation of 14C-palmitate into tissue-free fatty acids and unaltered at 0.5 hours but it was increased by 211.7% at two hours postendotoxin. These data demonstrated that myocardial membrane lipid profile was greatly altered by increased incorporation of 14C-palmitate into phospholipids and neutral lipids after endotoxin administration. An alteration in myocardial lipid profile, as reported in this study, may contribute to the development of myocardial dysfunction during shock.

Acyl Coenzyme A↗
PubMed1980

External assessment of myocardial metabolism with C-11 palmitate in vivo.

The externally detected rate of clearance of C-11 palmitate ([11C]palmitic acid) from isolated hearts varies directly with CO2 production from neutral lipids and with physiological indexes of myocardial oxygen consumption. The present study was performed to determine whether myocardial metabolism could be quantified noninvasively in vivo in a fashion analogous to that in the isolated heart. Opened chest, male rabbits were injected with C-11 palmitate (100-200 muCi) and coincidence counts were detected externally with two NaI(TI) crystals so placed that their colinear field of view encompassed the heart. The monoexponential rate of clearance of tracer--obtained from the portion of the residue-detection curve reflecting metabolism of fatty acid incorporated into neutral lipids--correlated directly with induced changes in tension-time index after injections into the left atrium (r = 0.96, n = 12), right atrium (r = 0.86, n = 14), and ear vein (r = 0.93, n = 14). Clearance of labeled palmitate from the vascular pool within the field of detection (determined with both C-14 palmitate and red blood cells labeled with C15O-hemoglobin) was rapid and did not significantly affect measurements of palmitate clearance from the heart itself.

Animals↗
PubMed1995

Incorporation of [1-carbon-11]palmitate in monkey brain using PET.

UNLABELLED: We determined regional incorporation coefficients (k*) of plasma [1-11C]palmitate into stable brain lipids of anesthetized monkeys with PET. METHODS: Carbon-11-palmitate was injected intravenously in untreated animals and in animals pretreated with methyl palmoxirate (MEP), an inhibitor of beta-oxidation of palmitate in the brain and periphery. Plasma radioactivity was followed, and brain radioactivity was determined at various times using PET. A least-squares method was used to fit the data to an operational equation to obtain regional values of k* and of cerebral blood volume (Vb) in individual experiments. RESULTS: MEP significantly decreased the integral of plasma [11C]CO2 following 11C-palmitate infusion. Mean values of k* in monkeys not given MEP were 4.9, 4.2, 4.9, 4.0 and 2.9 x 10(-5) ml/sec.g for the temporal, frontal, parietal and occipital cortices and white matter, respectively. With the exception of k* in white matter, which was increased by MEP, k* in the other brain regions was not significantly changed by MEP. The Vb ranged from 0.035 ml/g to 0.048 ml/g in gray matter regions and equaled 0.022 ml/g in white matter. CONCLUSION: PET can be used to determine regional incorporation coefficients of 11C-palmitate into the primate brain in vivo. Combined with MEP, 11C-palmitate could be used with PET to examine regional brain phospholipid metabolism in humans in normal and pathological conditions.

Animals↗
PubMed1977

Kinetics of bilirubin binding to bovine serum albumin and the effects of palmitate.

The binding of bilirubin to bovine serum albumin has been determined to be a second order process, first order in each reactant. Formation of the bilirubin-albumin complex was observed as an increase in absorbance at 480 nm by stopped flow spectrophotometry. The effect of long chain fatty acid on the binding of bilirubin was investigated at palmitic acid levels of 0 to 7 mol/mol of albumin at 37 degrees and pH 7.4. The second order rate constant is 1.5 X 10(6) M-1 S-1 when the palmitate/albumin ratio is less than 5 and drops to 0.5 X 10(6) M-1 S-1 when the palmitate/albumin ratio reaches 6. The equilibrium association constant for the bilirubin-albumin complex is 5.5 X 10(6) M-1 when the palmitate/albumin ratio is less than 1, 18 X 10(6) M-1 when the palmitate/albumin ratio is between 1 and 5, and 3 X 10(6) M-1 when the palmitate/albumin ratio is greater than 5. The mechanism of the effect of palmitate varies with the total palmitate level. At low molar ratios, addition of palmitate has no effect on the association rate but decreases the dissociation rate. At high molar ratios, addition of palmitate decreases the association rate and increases the dissociation rate. It is suggested that palmitate affects the ability of the protein to undergo the conformational changes needed to accommodate bilirubin.

Bilirubin↗
PubMed2002

Ectoprotein kinase-mediated phosphorylation of FAT/CD36 regulates palmitate uptake by human platelets.

Glycoprotein IV (FAT/CD36) has been shown to be phosphorylated by a cAMP-dependent, platelet membrane-bound ectokinase. In this study, we demonstrate that ectophosphorylation of FAT/CD36 regulates initial palmitate uptake. This is the first time that short-term regulation of the activity of a long-chain fatty acid carrier could be shown. Phosphorylation of FAT/CD36 was paralleled by a significant decrease in initial palmitate uptake by morphologically and functionally intact platelets. Maximum inhibition of palmitate uptake was achieved at 0.5 nM extracellular ATP, being significantly decreased to 72% compared to the control. Inhibition of palmitate uptake was abolished by co-incubation with the specific protein kinase A inhibitor peptide PKI or with beta,gamma-methylene-ATP, and was reversible upon addition of alkaline phosphatase. An extracellular ATP concentration above 5 microM completely prevented the ectophosphorylation-mediated inhibition of palmitate uptake. We conclude that FAT/CD36-mediated palmitate uptake by human platelets is short-term regulated via cAMP-dependent ectophosphorylation of FAT/CD36.

Blood Platelets↗
PubMed2006

Glucose, palmitate and pro-inflammatory cytokines modulate production and activity of a phagocyte-like NADPH oxidase in rat pancreatic islets and a clonal beta cell line.

AIMS/HYPOTHESIS: Acute or chronic exposure of beta cells to glucose, palmitic acid or pro-inflammatory cytokines will result in increased production of the p47(phox) component of the NADPH oxidase and subsequent production of reactive oxygen species (ROS). METHODS: Rat pancreatic islets or clonal rat BRIN BD11 beta cells were incubated in the presence of glucose, palmitic acid or pro-inflammatory cytokines for periods between 1 and 24 h. p47(phox) production was determined by western blotting. ROS production was determined by spectrophotometric nitroblue tetrazolium or fluorescence-based hydroethidine assays. RESULTS: Incubation for 24 h in 0.1 mmol/l palmitic acid or a pro-inflammatory cytokine cocktail increased p47(phox) protein production by 1.5-fold or by 1.75-fold, respectively, in the BRIN BD11 beta cell line. In the presence of 16.7 mmol/l glucose protein production of p47(phox) was increased by 1.7-fold in isolated rat islets after 1 h, while in the presence of 0.1 mmol/l palmitic acid or 5 ng/ml IL-1beta it was increased by 1.4-fold or 1.8-fold, respectively. However, palmitic acid or IL-1beta-dependent production was reduced after 24 h. Islet ROS production was significantly increased after incubation in elevated glucose for 1 h and was completely abolished by addition of diphenylene iodonium, an inhibitor of NADPH oxidase or by the oligonucleotide anti-p47(phox). Addition of 0.1 mmol/l palmitic acid or 5 ng/ml IL-1beta plus 5.6 mmol/l glucose also resulted in a significant increase in islet ROS production after 1 h, which was partially attenuated by diphenylene iodonium or the protein kinase C inhibitor GF109203X. However, ROS production was reduced after 24 h incubation. CONCLUSIONS/INTERPRETATION: NADPH oxidase may play a key role in normal beta cell physiology, but under specific conditions may also contribute to beta cell demise.

Animals↗
PubMed2005

Lipid characterization of seed oils from high-palmitic, low-palmitoleic, and very high-stearic acid sunflower lines.

Information obtained in recent years regarding the enzymes involved in FA synthesis can now be applied to develop novel sunflower lines by incorporating enzymes with specific characteristics into lines with a defined background. We have generated three highly saturated mutant lines in this way and characterized their FA content. The new high-palmitic, low-palmitoleic lines CAS-18 and CAS-25, the latter on a high-oleic background, have been selected from the high-stearic mutant CAS-3 by introducing a deficient stearic acid desaturase in a high-palmitic background from the previously developed mutant lines CAS-5 and CAS-12, respectively. As such, the desaturation of palmitic acid and the synthesis of palmitoleic acid and its derivatives (asclepic and palmitolinoleic acids) were reduced in these high-palmitic lines, increasing the stearic acid content. Likewise, introducing a FA thioesterase from a high-palmitic line (e.g., CAS-5) into the high-stearic CAS-3 increased the stearic acid content from 27 to 32% in the new high-stearic line CAS-31. As previously described in high-palmitic lines, high growth temperatures did not reduce the linoleic acid content of the oil. Furthermore, the FA composition of TAG, DAG, and phospholipids was modified in these lines. Besides a high degree of saturation, the TAG from these new vegetable oils have a low content of saturated FA in the sn-2 position. The alpha asymmetric coefficient obtained also indicates that the saturated FA are asymmetrically distributed within the TAG molecules. Indeed, the disaturated TAG content rose from 31.8 to 48.2%. These values of disaturated TAG are the highest to date in a temperate oilseed.

Fatty Acids, Monounsaturated↗
PubMed1975

Palmitic acid activation of peroxidase and its possible significance in mango ripening.

Palmitic acid stimulated the activity of mango peroxidase and reversed the inhibition due to the peroxidase inhibitor present in the preclimacteric fruit. The palmitic acid effect appeared to saturate in the range of 45 to 60 muM palmitic acid. Crude fatty acid extract of the mango exerted similar effect. The percentage stimulation was pH-dependent. Palmitic acid stimulated the enzyme by 18 percent at its optimum pH (5) but the stimulation was in excess of 63 percent at pH 2.5. At pH 2.5 the enzyme concentration versus velocity plot was non-linear and the activation by palmitic acid appeared to saturate between 32 and 48 muM concentration of the effector. The inhibition of the enzyme at and above 0.86 muM concentration of substrate (H202) was not found in the presence of palmitic acid. The effector also changed the heat inactivation kinetics of the enzyme and activated only two out of the four peroxidase isoenzymes present in the climacteric fruit extracts. The results presented indicate the regulatory nature of the enzyme and support its significance in fruit ripening.

Carbon Dioxide↗
PubMed1977

Determination of amniotic fluid palmitic acid concentration for the estimation of fetal lung maturity.

Palmitic acid concentrations in amniotic fluid (AF) were determined in 135 patients with normal and pathological pregnancies between the 27th and 42nd week of gestation. There was a sharp rise in the mean palmitic acid concentration after the 34th weeks of gestation from 2.7 mug/ml to 9.9 mug/ml at term. This increase is almost identical with the rise of AF-lecithin. It was found that between 70% and 100% of AF-palmitic acid originates from lecithin. 65 patients were delivered within 24 h after amniotic fluid sampling. 7 infants of these patients developed a respiratory distress syndrome (RDS). In all cases with RDS AF-palmitic acid concentration was far below 5 mug/ml. Assuming an AF-palmitic acid concentration greater than 5 mug/ml for characterising fetal lung maturity (=no RDS), there were no false negative results, but 16% false positive results. However, the determination of AF-palmitic acid concentration seems to be a most reliable method for the assessment of fetal lung maturity.

Amniotic Fluid↗
PubMed1980

Gas chromatographic determination with flash methylation of palmitic acid in amniotic fluid in prediction of fetal lung maturity.

A new method for determination of palmitic acid in amniotic fluid was developed. The dipalmitoyl lecithin was hydrolysed, and after extraction the palmitic acid was flash methylated in the injector of the gas chromatograph. The between batch coefficient of variation was 6.0% at 40 and 70 mumol/l of palmitic acid concentrations in 500 microliters amniotic fluid. The accuracy of the method was demonstrated by linearity, recovery and correlation studies. The correlation coefficient was 0.98 between the new and bortrifluoride methylating method. The concentrations of lecithin and palmitic acid in amniotic fluid showed a correlation coefficient of 0.97. If the concentration of palmitic acid falls below 80 mumol/l respiration distress syndrome is likely. The new method was simple and easy to carry out and could be adjusted for haemoglobin contamination of the amniotic fluid. It was concluded that the determination of palmitic acid in amniotic fluid was a reliable method for the assessment of fetal lung maturity that could replace the determination of lecithin concentration.

Amniotic Fluid↗
PubMed2006

Palmitate activates AMP-activated protein kinase and regulates insulin secretion from beta cells.

AMP-activated protein kinase (AMPK) is an energy sensor that regulates cellular metabolism. Changes in AMPK activity contribute to the regulation of insulin secretion. Epidemiological evidence links the ingestion of saturated fatty acid with hyperinsulinemia. The aim of the present study was to examine the effects of palmitate on beta cell AMPK activity and insulin secretion. Isolated rat islets and MIN6 beta cells were treated acutely (5-60 min) or chronically (24 h) with palmitate. Insulin secretion, AMPK and acetyl CoA carboxylase phosphorylation were assessed. The acute effects of palmitate included AMPK activation and augmentation in insulin secretion. Activation of AMPK by 24h pretreatment with palmitate suppressed glucose-stimulated insulin secretion, but not the response of insulin secretion to combined stimuli of glucose and palmitate. This study demonstrated that palmitate availability affected beta cell AMPK activity. In beta cells, an increase in AMPK activity may be required for fatty acid-induced fatty acid oxidation and prevention of lipotoxicity.

AMP-Activated Protein Kinases↗
PubMed2006

Sequential activation of caspases and synergistic beta-cell cytotoxicity by palmitate and anti-Fas antibodies.

To assess the mechanism of beta-cell lipotoxicity in comparison with Fas-mediated cell death, we used a mouse beta-cell clone stably transfected with human Fas. Palmitate induced beta-cell death in correlation with medium glucose levels between 5 and 20 mmol/l, while Fas-mediated cytotoxicity was observed irrespective of glucose concentration. At the glucose level of 10 mmol/l, palmitate induced caspase-6 activity within 3 h, and caspase-3 activity after a lag period of 6 h. The activities of caspases were correlated with glucose concentration. A caspase-6 inhibitor attenuated caspase-3 activation and cell death induced by palmitate. Oxfenicine, an inhibitor of carnitine palmitoyltransferase-1, attenuated both palmitate-induced cytotoxicity and activation of caspases. Finally, beta-cell cytotoxicity caused by the combination of anti-Fas and palmitate at 25 mmol/l of glucose was greater than the sum of those induced by each. These observations suggest that palmitate induces sequential activation of caspase-6 and caspase-3 through a mitochondrial signal(s), and caspase-6 plays a primary role in the mechanism. Fas-mediated beta-cell death and lipotoxicity may share common mechanisms involving caspase activation, and thereby synergistically inducing beta-cell death, although upstream signaling pathways are distinct.

Animals↗
PubMed1997

Palmitate incorporation into lipids pools of contracting red and white muscles.

We compared the incorporation of the blood-borne [14C]-palmitate into selected lipid and phospholipid pools in rat muscles (soleus, red and white gastrocnemius), at rest and during contractions (15 and 60 tetani/min) in one leg (5 min) while the contralateral leg served as a control. [1-(14)C]-palmitate (20 microCi/rat) was administered into the carotid artery (t = 1 min). [14C]-palmitate deposition was greatest in soleus (100%) and lower in red (82%) and white gastrocnemius muscles (63%), respectively (p < 0.05). [14C] was deposited primarily into the tri-acylglycerol (approximately 50%) and phospholipid pools (approximately 30%) of soleus and red gastrocnemius muscles, and into the di-acylglycerol (approximately 30%), tri-acylglycerol (approximately 30%) and phospholipid pools (approximately 30%) in white gastrocnemius muscle. During contraction the concentrations of tri-acylglycerol were not changed. But, contraction increased [14C]-palmitate incorporation into soleus and red gastrocnemius muscles (600-700%) and into white gastrocnemius muscles (200%). Slightly more [14C] was directed from the phospholipids into the tri-acylglycerol pool during contraction. [14C]-palmitate deposition was also increased in the subclasses of phospholipids during contraction in red and white gastrocnemius. In conclusion, the deposition of [14C]palmitate into different lipid and phospholipid pools is quite rapid, and is dependent on contraction and the muscle fiber type.

Animals↗
PubMed2002

Palmitic is the main fatty acid carried by lipids of detergent-resistant membrane fractions from neural and non-neural cells.

Lipids extracted from detergent-resistant membrane fractions, thought to derive from membrane domains, were analyzed for fatty acid composition. The proportion of palmitic acid in fractions isolated from neurons (cerebellar granule cells) and from neural-like cell lines (neuroblastomaglioma NG108-15) nearly doubled (reaching about 54% of total fatty acids) with respect to cell WCL, indicating their enrichment in palmitic acid-carrying lipids. The proportion of palmitic acid in detergent-resistant fractions obtained from caveolin-transfected NG108-15 cells was comparable with that obtained from caveolin-negative cells, ruling out a specific role of this protein in recruiting palmitoylated lipid species. The enrichment in palmitic acid was remarked also in membrane fractions isolated from non-neuronal cell lines (A431) using either detergents or detergent-free techniques. Lipid fractionation and mass spectrometry experiments show that palmitic acid-rich phosphatidylcholine species are responsible of the peculiar fatty acid composition of these fractions. All together these results suggest that the enrichment in palmitic acid-rich phosphatidylcholine species is a common feature of neural and non-neural cell lines and may play a major role in the biogenesis of membrane domains.

Animals↗
PubMed1969

The effect of starvation on the incorporation of palmitate into glycerides and phospholipids of rat liver homogenates.

1. Glyceride biosynthesis from glycerol phosphate and [1-(14)C]palmitate was studied in liver homogenates of rats that were fed ad libitum or starved for 36-40hr. The changes in enzyme activity were related to total DNA content or total liver homogenate as these were found to be equivalent and to be the most meaningful parameters. 2. In liver homogenates from fed rats, labelled palmitate was incorporated mainly into phosphatidate (58% of the total incorporation into lipids), diglycerides (25%) and triglycerides (16%), whereas monoglycerides, cholesterol esters and phospholipids other than phosphatidate were labelled only to a small extent. Addition of particle-free supernatant to full homogenates increased the total incorporation of palmitate by 45% and the pattern of incorporation altered to 53% incorporated into triglycerides, 24% into diglycerides and 17% into phosphatidate. This result suggested that, in liver homogenates, phosphatidate phosphohydrolase (EC 3.1.3.4) may be rate-limiting in the biosynthesis of glycerides via the glycerol phosphate pathway. 3. Upon starvation, the amount of palmitate incorporated per liver into total phospholipids plus glycerides was decreased to between 68% and 75% of that observed with fed animals. In homogenates from fed animals 41-44% of the labelled phospholipids plus glycerides was in glycerides; this value increased to between 63% and 75% with starved rats. Of the palmitate incorporated into total phospholipids, between 85% and 86% was found in phosphatidate, independent of the nutritional state of the animal. The ratio of palmitate incorporated into triglycerides/diglycerides rose from 0.7, obtained with fed rats, to 1.0 with starved animals. 4. These results indicate that starvation caused a decrease in the activity (per total liver) of acyl-CoA-glycerol phosphate acyltransferase(s) (EC 2.3.1.15) and an increase in the activity of acyl-CoA-diglyceride acyltransferase (EC 2.3.1.20). The largest change, however, seemed to be related to the increased activity of the phosphatidate phosphohydrolase in the particle-free supernatant. 5. The latter enzyme was assayed in the particle-free supernatant with membrane-bound phosphatidate as substrate. In starvation, the activity per total liver was increased to between 130% and 190% and the specific activity to between 180% and 320% of the values for fed rats.

Acyltransferases↗