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PubMed1995

Palmitate-induced beta-cell insensitivity to glucose is coupled to decreased pyruvate dehydrogenase activity and enhanced kinase activity in rat pancreatic islets.

We previously found that long-term exposure to fatty acids impairs glucose-induced insulin release. In the present study, we investigated whether impairment is related to decreased pyruvate dehydrogenase (PDH) and increased PDH kinase activity. Rat pancreatic islets were cultured for 48 h in RPMI-1640 medium with or without 0.125 mmol/l palmitate. Potentiation of insulin responses to succinic acid monomethylester (SAM) by 10 mmol/l acetate and pyruvate were subsequently compared in order to assess whether generation of acetyl-coenzyme A (CoA) from pyruvate was deficient in the intact beta-cell. Potentiation by acetate was similar in control and palmitate-preexposed islets. In contrast, pyruvate potentiated SAM-induced response by 122% in control but by only 39% in palmitate-exposed islets (P < 0.001). In extracts of palmitate-exposed islets, the active (unphosphorylated) form of PDH was decreased by 50% and total PDH activity (assessed after phosphatase treatment) by 25%. The proportion of active form to total PDH activity was also reduced (42.7 +/- 2.6% after palmitate vs. 66.6 +/- 4.3% in control islets, P < 0.01). In the same preparations, PDH kinase activity was enhanced 1.7-fold by palmitate in terms of the rate constant of ATP-dependent inactivation of PDH (P < 0.05). To test for a role of free (not PDH-bound) kinase, a PDH-free mitochondrial fraction was prepared, and its kinase activity was tested against a pig heart PDH preparation. Free kinase activity was increased 1.9-fold in palmitate-treated islets (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed2002

The fate of [U-(13)C]palmitate extracted by skeletal muscle in subjects with type 2 diabetes and control subjects.

The current study investigated the fate of a [U-(13)C]palmitate tracer extracted by forearm muscle in type 2 diabetic and control subjects. We studied seven healthy lean male subjects and seven obese male subjects with type 2 diabetes using the forearm muscle balance technique with continuous intravenous infusion of the stable isotope tracer [U-(13)C]palmitate under baseline conditions and during intravenous infusion of the nonselective beta-agonist isoprenaline (ISO; 20 ng *kg(-1) lean body mass* min(-1)). In skeletal muscle of control subjects, there was a significant release of (13)C-labeled oxidation products in the form of (13)CO(2) (15% of (13)C uptake from labeled palmitate) and a significant release of (13)C-labeled glutamine (release of (13)C-labeled atoms from glutamine was 6% of (13)C uptake from labeled palmitate), whereas in type 2 diabetic subjects there was no detectable release of (13)CO(2) and (13)C-glutamine, despite a significant uptake of [U-(13)C]palmitate (60% of control value). There was net uptake of arterial (13)C-labeled glutamate by forearm muscle in both groups. Also, the ISO-induced increase in arterial glutamine enrichment and arterial concentration of (13)C-glutamine was more pronounced in the diabetic group relative to control subjects. In view of the diminished ISO-induced release of (13)C-glutamine from type 2 diabetic muscle, the latter data indicate that more [U-(13)C]palmitate entered the liver in the diabetic group and was incorporated into newly synthesized glutamine and glutamate molecules. Thus, the lack of release of (13)C-labeled oxidation products by type 2 diabetic muscle during beta-adrenergic stimulation, despite significant [U-(13)C]palmitate uptake, indicates differences in the handling of fatty acids between type 2 diabetic subjects and healthy control subjects.

Adrenergic beta-Agonists↗
PubMed2003

Monounsaturated fatty acids prevent the deleterious effects of palmitate and high glucose on human pancreatic beta-cell turnover and function.

Glucotoxicity and lipotoxicity contribute to the impaired beta-cell function observed in type 2 diabetes. Here we examine the effect of saturated and monounsaturated fatty acids at different glucose concentrations on human beta-cell turnover and secretory function. Exposure of cultured human islets to saturated fatty acid and/or to an elevated glucose concentration for 4 days increased beta-cell DNA fragmentation and decreased beta-cell proliferation. In contrast, the monounsaturated palmitoleic acid or oleic acid did not affect DNA fragmentation and induced beta-cell proliferation. Moreover, each monounsaturated fatty acid prevented the deleterious effects of both palmitic acid and high glucose concentration. The cell-permeable ceramide analogue C(2)-ceramide mimicked both the palmitic acid-induced beta-cell apoptosis and decrease in proliferation. Furthermore, the ceramide synthetase inhibitor fumonisin B1 blocked the deleterious effects of palmitic acid on beta-cell turnover. In addition, palmitic acid decreased Bcl-2 expression and induced release of cytochrome c from the mitochondria into the cytosol, which was prevented by fumonisin B1 and by oleic acid. Finally, each monounsaturated fatty acid improved beta-cell secretory function that was reduced by palmitic acid and by high glucose. Thus, in human islets, the saturated palmitic acid and elevated glucose concentration induce beta-cell apoptosis, decrease beta-cell proliferation, and impair beta-cell function, which can be prevented by monounsaturated fatty acids. The deleterious effect of palmitic acid is mediated via formation of ceramide and activation of the apoptotic mitochondrial pathway, whereas Bcl-2 may contribute to the protective effect of monounsaturated fatty acids.

Adult↗
PubMed1991

In vivo incorporation of [9,10(-3)H]-palmitate into a rat metastatic brain-tumor model.

Lipid metabolism of an intracerebrally implanted brain tumor and normal brain was investigated in awake Fischer 344 rats using intravenously injected [9,10(-3)H]-palmitate as a probe. A suspension of Walker 256 carcinosarcoma cells (250 cells in 5 microliters medium), with or without 1% low-melting-point agar, was implanted into the caudate nucleus of rats 8 to 9 weeks old. Control animals received an intracerebral injection without tumor cells. Seven days after implantation, awake rats were infused intravenously for 5 minutes with [9,10(-3)H]-palmitate (6.4 mCi/kg). The rats were killed 20 minutes after initiation of the infusion and coronal brain slices were obtained for quantitative autoradiography and light histological study. Tumor cell masses were histologically well demarcated from the surrounding brain tissue. Tumor tissue incorporation of [9,10(-3)H]-palmitate was heterogeneous, ranging on average from 3.1- to 6.1-fold greater than in the corresponding contralateral brain. In addition, incorporation corresponded to regional tumor cell density. The incorporation rate constant of [9,10(-3)H]-palmitate in tumor was significantly increased compared to control brain and was independent of tumor size. Necrotic areas within tumors showed no incorporation of radiolabeled palmitate. Brain surrounding the tumors and control injection sites showed reactive gliosis, and possessed 30% greater incorporation of [9,10(-3)H]-palmitate than contralateral normal brain. These results suggest that [9,10(-3)H]-palmitate can be used to image brain tumors in vivo, measuring turnover and/or synthesis of tumor and brain lipid.

Animals↗
PubMed1978

Oxidation of [U-14C] palmitic acid by cock spermatozoa.

When washed cock spermatozoa were incubated with [U-14 C] palmitic acid at 37 C for 2 hr under aerobic conditions, radioactivity was recovered as carbon dioxide indicating the fatty acid was oxidized. Little if any radioactivity was recovered as carbon dioxide when spermatozoa were killed by boiling, indicating the necessity for viable spermatozoa for the successful incorporation and oxidation of palmitic acid. To determine whether the oxidation of palmitic acid could serve as a source of energy for cock spermatozoa, ATP concentrations of spermatozoa were compared immediately following ejaculation and after 1,2, and 3 hr of incubation (37 C) with and without the addition of palmitic acid. At 1,2, and 3 hr of incubation, spermatozoa with palmitic acid as a substrate produced significantly (P less than or equal to .03) more ATP (2.62, 2.24, and 1.26 micrograms ATP/10(9) cells, respectively) than did spermatozoa without palmitic acid (1.62, 1.11, and .79 micrograms ATP/10(9) cells, respectively). These findings indicate that palmitic acid, one of the most abundant long-chain saturated fatty acids in cock spermatozoa, can be utilized as a source of energy.

Adenosine Triphosphate↗
PubMed1999

Effects of diets enriched in lauric, palmitic or oleic acids on blood coagulation and fibrinolysis.

In this study we compared the effects of specific saturated fatty acids (lauric acid and palmitic acid) with those of a monounsaturated fatty acid (oleic acid) on coagulation and fibrinolytic parameters in healthy women and men. Eighteen women and fourteen men consumed, in random order, three experimental diets, each for six weeks. The diets consisted of solid foods and approximately 70% [28 percent of energy (En%)] of the fat calories was supplied. As determined from duplicate portions, in the lauric acid diet 7.3 En% and in the palmitic acid diet 6.1 En% of oleic acid were exchanged for lauric or palmitic acid, respectively. The lauric acid diet also contained some (average 1.8 En%) more myristic acid. Compared with the oleic acid diet, factor VIIam in the female subjects was 9% higher with the lauric acid diet (P = 0.0036; 95% CI, 3 to 14%) and 10% higher with the palmitic acid diet (P = 0.0011; 95% CI, 5 to 16%). Changes in men were not significant. Plasminogen Activator Inhibitor (PAI-1) activity was higher on the palmitic acid compared with the oleic acid diet (difference between diets of 2.3 U/ml; P = 0.0098; 95% CI, 0.4 to 4.3 U/ml) and the lauric acid diet (difference between diets of 2.2 U/ml; P = 0.0123; 95% CI, 0.2 to 4.1 U/ml). No significant differences between diets were observed for antithrombin III activity, fibrinogen concentrations, fragment 1+2 concentrations, plasminogen or alpha2-antiplasmin activity. From this study, we conclude that diets rich in lauric or palmitic acid, compared with a diet rich in oleic acid, unfavourably influence factor VIIam activity, in a gender specific manner. In addition, the plasminogen activator inhibiting capacity of the plasma is impaired with a palmitic acid rich diet compared with an oleic or lauric acid rich diet.

Adult↗
PubMed2000

Oleate activates phosphatidylinositol 3-kinase and promotes proliferation and reduces apoptosis of MDA-MB-231 breast cancer cells, whereas palmitate has opposite effects.

Epidemiological studies and experiments using animal models and cultured breast cancer cells have suggested that a high intake of dietary fat could increase breast cancer risk. Little is known about the biochemical pathways by which various free fatty acids (FFAs) influence breast cancer cell proliferation and apoptosis. The present study was designed to investigate the effects of the two most abundant circulating FFAs, oleate and palmitate, on established human breast cancer cell lines after a short period of serum starvation. The unsaturated FFA oleate (C:18:1) stimulated cell proliferation, whereas the saturated FFA palmitate (C:16) dose dependently inhibited it. The half maximal effective concentrations of oleate and palmitate in the presence of albumin were 5 and 25 microM, respectively. The growth-inhibitory effect of palmitate in MDA-MB-231 cells was related to the induction of apoptosis as indicated by morphological and biochemical criteria. Moreover, oleate protected cells against the proapoptotic action of palmitate. Oleate and palmitate increased and decreased phophatidylinositol 3-kinase (PI3-K) activity, respectively, and the actions of the two FFAs on the enzyme were antagonistic. The PI3-K inhibitors wortmannin and LY294002 completely blocked the proliferative action of oleate. 2-Bromopalmitate, a nonmetabolizable analogue, did not affect MDA-MB-231 cell proliferation, suggesting that palmitate must be metabolized to exert its effect. Thus, various types of fatty acids are not equivalent with respect to their actions on breast cancer cell proliferation and apoptosis. The results support the concept that PI3-K is implicated in the control of breast cancer cell growth by FFAs and that PI3-K may provide a link between fat and cancer. The data are also consistent with the view that the type of FFA and their ratios in the diet in addition to the total amount of fat influence mammary carcinogenesis.

Apoptosis↗
PubMed1967

Rates of tissue uptake of palmitic acid-1-14C complexed with albumin by two different procedures.

The effect was investigated of two different methods of preparing an albumin-palmitic acid complex on the tissue uptake of the palmitic acid, both in vivo and in vitro. Complex A was prepared by exposing monomolecular layers of palmitic acid-1-(14)C deposited on a solid surface to albumin dissolved in buffer. Complex B was prepared by the interaction of albumin with a micellar solution of palmitate-1-(14)C. The radioactivities and chemical compositions of the two complexes were almost identical. Rat epididymal fat pads took up, during a 1 hr incubation, about 2.5 times as much palmitic acid from complex A as from complex B; the extent of esterification of the incorporated label was equal for the two complexes. The fractional turnover rate of palmitic acid of complex A, administered intravenously to dogs, was about twice that of palmitic acid from complex B. The label of the two complexes recirculated in the esterified fatty acid fraction of plasma to an equal extent. It is proposed that differences in the orientation of the fatty acid molecules may affect their interaction with the binding sites of albumin and that the metabolic differences of the resulting complexes are related to differences in the ease of transfer of the fatty acid from the complex to receptor sites of tissues.

Adipose Tissue↗
PubMed1977

[Calcium palmitate and cholesterol gallstones].

Ca-palmitate is an abundant secondary constituent of cholesterol gallstones, especially of "multiple facet" and "barrel" stones. 60% of the 146 stones obtained by operation or autopsy contained crystalline Ca-palmitate. From these 70% were multiple and 11% solitary stones. The average percentage of Ca-palmitate calculated from 30 quantitative analyses amount to 1,75% with regard to the dry weight of stones. The occurrence of Ca-palmitate in gallbladder stones mainly depends on concrements which undergo structural alterations (formation of fissures for example) during their stay in the gallbladder and which are impregnated by bile. Ca-palmitate crystallizes within the fissures of these stones after concentration of included bile. There is no important hint that Ca-palmitate plays a role in stone nucleation. The occurence of Ca-palmitate in bile may be favoured by decreased micellar solubilization of palmitinic acid and by increased concentration of Ca as a result of inflammation.

Calcium↗
PubMed2004

Depot pipotiazine palmitate and undecylenate for schizophrenia.

BACKGROUND: Antipsychotic drugs are usually given orally but compliance may be problematic. The development of depot injections in the 1960s gave rise to their extensive use as a means of long-term maintenance treatment. Pipotiazine palmitate is a depot from the phenothiazine family of antipsychotic drugs. OBJECTIVES: To assess the clinical, social and economic effects of depot pipotiazine palmitate and undecylenate compared with placebo, oral antipsychotics and other depot antipsychotic preparations for people with schizophrenia. SEARCH STRATEGY: For this update we searched the Cochrane Schizophrenia Group's Register (June 2003). We also inspected references of all identified trials for more studies and contacted relevant industries. SELECTION CRITERIA: We included all randomised clinical trials comparing depot pipotiazine palmitate and undecylenate to oral antipsychotics or other depot preparations for people with schizophrenia. DATA COLLECTION AND ANALYSIS: We reliably selected, quality rated and independently extracted data from relevant studies. We calculated the random effects relative risk (RR), the 95% confidence intervals (CI) and, where possible the number needed to treat (NNT) on an intention-to-treat basis. For continuous data, we calculated weighted mean differences (WMD). We only presented scale data for those tools that had attained pre-specified levels of quality. MAIN RESULTS: When pipotiazine palmitate was compared with 'standard' oral antipsychotic no differences were found for outcomes of global impression (n=53, 1 RCT, RR 2.57, CI 0.8 to 8.6), relapse (n=124, 1 RCT, RR 1.55 CI 0.76 to 3.2), study attrition (n=219, 3 RCTs, RR 1.37 CI 0.8 to 2.4) and behaviour (n=124, 1 RCT, WMD 4.65, CI -1.1 to 10.4). There was also no reported difference in adverse effects such as tardive dyskinesia or the need for anticholinergic drugs. Sixteen studies compared pipotiazine palmitate with other depot preparations (n=1123). Pipotiazine palmitate was consistently equivalent to other depots in terms of a range of outcomes, including global impression (n=217, 4 RCTs, RR not improved 0.99 CI 0.91 to 1.07), relapse (n=239, 5 RCTs, RR relapse by 1 year 0.98 CI 0.55 to 1.75), and adverse effects (n=337, 5 RCTs, RR needing anticholinergic medication 0.98 CI 0.84 to 1.15). REVIEWERS' CONCLUSIONS: Although well-conducted and reported randomised trials are still needed to fully inform practice (no trial data exists reporting hospital and services outcomes, satisfaction with care and economics) pipotiazine palmitate is a viable choice for both clinician and recipient of care.

Administration, Oral↗
PubMed1980

2H- and 31P-NMR studies of cholesteryl palmitate in sphingomyelin dispersions.

Dispersions (50 wt% in water) of sphingomyelin/cholesteryl palmitate (95 : 5 mol%) have been studied by 2H- and 31P-NMR spectroscopy between 25 and 60 degrees C. The deuterated esters, cholesteryl palmitate-d31 and cholesteryl palmitate-16, 16, 16-d3, were used for 2H-NMR studies. Of the 5 mol% cholesteryl palmitate added, 1.5 mol% was found to incorporate in the sphingomyelin and this amount remained constant throughout the temperature range studied. The remainder of the cholesteryl palmitate was present as regions of solid. At temperatures above the gel-to-liquid crystalline phase transition of sphingomyelin the NMR spectra indicate that a fraction of the cholesteryl palmitate and sphingomyelin is undergoing rapid isotropic motions. This fraction, which increases with increasing temperature above the phase transition, is probably composed of small bilayer structures. When 50 mol% cholesterol (relative to sphingomyelin) was added to the sphingomyelin/cholesteryl palmitate dispersion, the isotropic component in the NMR spectral was no longer present, the gel-to-liquid crystalline phase transition was removed, and the incorporation of ester in the membrane decreased by more than an order of magnitude.

Animals↗
PubMed1998

Retinyl palmitate reduces hepatic fibrosis in rats induced by dimethylnitrosamine or pig serum.

BACKGROUND/AIMS: Lipid peroxidation has been found to be associated with Ito cell activation. Ito cells are the principal collagen-producing cells and the main storage sites of retinoids. However, the relationship between retinoids and hepatic fibrosis is complex. The aim of this study was to elucidate the role of retinoids as a fibrosuppressant: the effects of retinoids on hepatic fibrosis induced in rats by dimethylnitrosamine or pig serum, as well as on rat Ito cells in primary culture, were examined in order to assess the antioxidant activity of retinoids. METHODS: Male Wistar rats were given a single injection of 40 mg/kg dimethylnitrosamine or 0.5 ml PS twice weekly for 10 weeks. In each model, rats were treated with retinyl palmitate for 2 weeks before hepatotoxin treatments or for the last 2 weeks of the treatments. The cumulative amount of retinyl palmitate administered in each experiment was 2, 10, or 20x10(4) IU/rat. RESULTS: Retinyl palmitate treatment before or after administration of dimethylnitrosamine or pig serum suppressed the induction of hepatic fibrosis, restored hepatic retinyl palmitate levels, prevented increases in hepatic levels of collagen and malondialdehyde, a product of lipid peroxidation, and prevented increases in deposition of type III collagen and the number of alpha-smooth muscle actin (alpha-SMA) positive-Ito cells in the liver. Retinyl palmitate supplementation resulted in a dose-dependent reduction of alpha-SMA expression and an oxidative burst in cultured Ito cells. In addition, retinyl palmitate inhibited Fe2+/adenosine 5'-diphosphate-induced lipid peroxidation in rat liver mitochondria and showed radical scavenging activity. CONCLUSIONS: These findings suggest that retinyl palmitate may suppress the induction of hepatic fibrosis, at least in part, by the inhibition of Ito cell activation through its antioxidant activity.

Animals↗
PubMed1992

A study of the chylomicron metabolism in WHHL rabbits after fat loading. Discrepancy between results based on measurement of apoprotein B-48 or retinyl palmitate.

We studied the metabolism of chylomicrons in homozygous Watanabe heritable hyperlipidaemic (WHHL) rabbits and in cholesterol-fed or normally fed New Zealand White (NZW) rabbits by measuring the concentrations of apoprotein B-48 and of retinyl palmitate in their serum after feeding fat plus this vitamin according to two different protocols. Compared with NZW controls, retinyl palmitate accumulated in both hyperlipidaemic groups under study, not only in the d less than 1.019 fraction but also in the low-density lipoprotein (LDL) fraction. A strong correlation was found between the retinyl palmitate concentration in either the d less than 1.019 fraction or the LDL fraction of the WHHL rabbits and the concentrations of cholesterol and triacylglycerols in these fractions. This suggests that retinyl palmitate is exchanged rapidly between exogenous and endogenous lipoproteins. This is supported by the lack of a correlation between the retinyl palmitate concentrations and the intensity of the apoprotein B-48 band in the respective d less than 1.019 fractions or LDL fractions; in most fractions, in which large amounts of retinyl palmitate were present, the intensity of the apoprotein B-48 band was not increased compared with the fasting concentrations. Assuming that retinyl palmitate is a marker for the transfer of exogenous lipids, the results of our experiments indicate that the removal of exogenous lipids is delayed by complexing to endogenously synthesized lipoproteins. However, the clearance of apoprotein B-48 is normal and thus independent of the LDL-receptor activity.

Animals↗
PubMed2003

Uptake of vitamin A in buccal mucosal cells after topical application of retinyl palmitate: a randomised, placebo-controlled and double-blind trial.

Retinoids have been reported to produce regressions in metaplastic changes of the mucosal epithelium. In order to define the role of these micronutrients in the prevention of squamous metaplasia of the oral cavity, it is necessary to measure their uptake in target tissues such as the buccal mucosal epithelium. We demonstrated in a trial that retinyl palmitate applied topically via a toothpaste is taken up by buccal mucosal cells in young healthy volunteers. In the randomised, parallel-designed, placebo-controlled and double-blind trial, forty volunteers divided in two groups cleaned their teeth either with a placebo toothpaste or a retinyl palmitate-containing toothpaste (1 mg/g) for 56 d. Buccal mucosal cells samples were taken from the healthy volunteers during the retinyl palmitate application and the following wash-out phase to determine the concentration of retinyl palmitate and retinol by HPLC. Supplementary blood samples were taken from the volunteers on days 0 and 56 to investigate changes in plasma retinyl palmitate and retinol concentrations. Results from only thirty participants (sixteen placebo and fourteen treated subjects) were used in the statistical evaluation as the remaining sample results were spoiled by a technical defect during the HPLC analysis. A significant (P<0.05) uptake of retinyl palmitate in buccal mucosal cells after 7 d and a significant (P<0.05) increase of plasma retinol after 17 d was demonstrated in our present study. The uptake of retinyl palmitate and the following hydrolysis to retinol led to an enrichment of vitamin A in buccal mucosal cells.

Absorption↗
PubMed1973

Streptococcal pharyngitis therapy: comparison of clindamycin palmitate and potassium phenoxymethyl penicillin.

Clindamycin palmitate and potassium phenoxymethyl penicillin were evaluated in 103 children with upper respiratory illnesses and pharyngeal group A streptococci, from November 1970 to July 1971. The children were assigned randomly by weight to one of the antibiotic regimens given orally for 10 days. Clindamycin palmitate and potassium phenoxymethyl penicillin dosages were 75 and 125 mg, respectively, in 5 ml tid for children weighing less than 25 kg, and 150 and 250 mg, respectively, in 10 ml bid for children weighing 25 kg or more. Recurrences of the original streptococcal group A, M, and T types within 3 weeks after the end of treatment were classified as failures. The failure rates were: clindamycin palmitate, 10% (5 of 52), and potassium phenoxymethyl penicillin, 18% (9 of 51). Possible drug-related rashes were observed in 8 of 52 clindamycin palmitate-treated patients. The geometric mean minimal inhibitory concentrations of clindamycin and penicillin against 103 isolates of group A streptococci were 0.033 and 0.007 mug/ml, respectively. The serum concentrations about 70 min after ingesting 150 mg of clindamycin palmitate averaged 3.8 mug/ml and after 250 mg of potassium phenoxymethyl penicillin averaged 0.9 mug/ml. Clindamycin palmitate was as effective as potassium phenoxymethyl penicillin in eradicating group A streptococci from the pharynx in tid and bid regimens. Nevertheless, because of its rash-producing tendency in some patients and higher cost, clindamycin palmitate should not be preferred to penicillin for treatment of streptococcal sore throat in the non-penicillin-allergic patient.

Child↗
PubMed1984

Perinatal rat lung retinol (vitamin A) and retinyl palmitate.

The potential role for retinol (vitamin A alcohol) in the differentiation of the developing lung prompted this study in the perinatal rat. High performance liquid chromatography was used to separate, detect, and quantitate retinol and retinyl palmitate in lipid extracts of tissue and serum. Fetal and maternal blood showed the presence of retinol, whereas no retinyl palmitate was detected. On the other hand, fetal and postnatal lungs contained retinyl palmitate as well as retinol. Considerable changes in the content of lung retinyl palmitate were found during lung development. Fetal lungs (17-21 days of gestation) contained 2.3 +/- 0.36 micrograms/g wet weight (mean +/- SD) of retinyl palmitate and 0.14 +/- 0.05 micrograms/g of retinol. Lungs of pups (1-10 days old) contained much less retinyl palmitate, 0.63 +/- 0.20 micrograms/g, whereas the amount of retinol was the same as in fetal lungs. The surprisingly high content of retinyl palmitate in fetal lung and its depletion after birth may be functionally related to retinol action in the developing lung.

Animals↗
PubMed1998

Detection of retinyl palmitate and retinol in the liver of mice injected with excessive amounts of retinyl acetate.

The transport of subcutaneously injected retinyl acetate (RA, 100,000 IU/mouse, 105,470 nM) was investigated in male ICR mice (10-week-old) at 0, 3, 6, 12, 18, 24 and 72 hr after a single injection. The retinol and retinyl palmitate levels of liver homogenates, bile in the gallbladder and serum from peripheral blood were measured by high performance liquid chromatography (HPLC) method. Retinyl palmitate in the lipid droplets of hepatocytes and Ito cells was localized by a modified gold chloride staining method. Accumulation of retinyl palmitate peaked at 12 hr post-injection and decreased thereafter until 24 hr post-injection. Fluorescence microscopy revealed many fluorescent vitamin A-containing lipid droplets in hepatocytes around central veins at 12 hr post-injection, but such droplets were not observed in the vehicle control mice or at in the RA-injected mice after 18 hr of injection. Electron microscopic observation also indicated that many retinyl esters-containing lipid droplets were observed in hepatocytes around the central veins at 12 hr post-injection, but no droplets were seen in the controls or 18 hr post-injection. The retinyl palmitate levels in liver homogenates assessed by HPLC decreased from 12 to 24 hr post-injection and increased significantly in bile, while retinol in liver homogenates and serum markedly increased. One of the morphological alterations was intense vacuolization in hepatocyte cell cords from the portal toward the central vein observed at 24 hr post-injection. Transitional lipid droplets between vacuoles and lipid droplets were identified in those hepatocytes. These results of HPLC analysis of retinol and retinyl palmitate in liver homogenates, serum, and bile, together with the results of gold chloride staining suggested that subcutaneously injected RA was first incorporated in hepatocytes at 12 hr and then partially metabolized through vacuoles, transferred into the blood and secreted into the bile over a 24 hr period. Many retinyl esters-containing lipid droplets were visualized in Ito cells at 72 hr post-injection. Most of vitamin A in the liver homogenates measured by HPLC was retinyl palmitate. Therefore, the contents in those lipid droplets might be retinyl palmitate.

Animals↗
PubMed2000

Improved method of determining retinol and retinyl palmitate in rat liver and serum by high-performance liquid chromatography.

In this study, we examined the effect of certain analytical procedures to determine the best method of recovering the ingested retinoids, specifically retinol and retinyl palmitate, from rat liver and serum. In this experiment, the best extraction solvent for retinol was n-hexane and that for retinyl palmitate was ethyl acetate. The best results were obtained using a mobile phase (n-hexane-diethyl ether, 76:24, v/v) as the sample solvent in the assay for liver retinol, similarly, chloroform as the sample solvent in the assay for serum retinol, and for liver retinyl palmitate, the best sample solvent was methanol-toluene (5: 5, v/v). The assayed values of retinol and retinyl palmitate measured in ethanol (0.125% BHT added) and extraction solvent (0.025% BHT added) were significantly higher than those when no BHT was added to the ethanol and extraction solvent. The determination methods for extracting retinol and retinyl palmitate from the liver varied according to the conditions layed out above. Simultaneous determination of retinol and retinyl palmitate has been illustrated in previous papers by various authors: however, we found that the individual determination of retinol and retinyl palmitate was necessary to accurately assay each retinoid.

Animals↗