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PubMed2005

Saturated free fatty acids and apoptosis in microvascular mesangial cells: palmitate activates pro-apoptotic signaling involving caspase 9 and mitochondrial release of endonuclease G.

BACKGROUND: In type 2 diabetes, free fatty acids (FFA) accumulate in microvascular cells, but the phenotypic consequences of FFA accumulation in the microvasculature are incompletely understood. Here we investigated whether saturated FFA induce apoptosis in human microvascular mesangial cells and analyzed the signaling pathways involved. METHODS: Saturated and unsaturated FFA-albumin complexes were added to cultured human mesangial cells, after which the number of apoptotic cells were quantified and the signal transduction pathways involved were delineated. RESULTS: The saturated FFA palmitate and stearate were apoptotic unlike equivalent concentrations of the unsaturated FFA oleate and linoleate. Palmitate-induced apoptosis was potentiated by etomoxir, an inhibitor of mitochondrial beta-oxidation, but was prevented by an activator of AMP-kinase, which increases fatty acid beta-oxidation. Palmitate stimulated an intrinsic pathway of pro-apoptotic signaling as evidenced by increased mitochondrial release of cytochrome-c and activation of caspase 9. A caspase 9-selective inhibitor blocked caspase 3 activation but incompletely blocked apoptosis in response to palmitate, suggesting an additional caspase 9-independent pathway. Palmitate stimulated mitochondrial release of endonuclease G by a caspase 9-independent mechanism, thereby implicating endonuclease G in caspase 9-independent regulation of apoptosis by saturated FFA. We also observed that the unsaturated FFA oleate and linoleate prevented palmitate-induced mitochondrial release of both cytochrome-c and endonuclease G, which resulted in complete protection from palmitate-induced apoptosis. CONCLUSIONS: Taken together, these results demonstrate that palmitate stimulates apoptosis by evoking an intrinsic pathway of proapoptotic signaling and identify mitochondrial release of endonuclease G as a key step in proapoptotic signaling by saturated FFA and in the anti-apoptotic actions of unsaturated FFA.

Apoptosis↗
PubMed1997

Stimulation of islet protein kinase C translocation by palmitate requires metabolism of the fatty acid.

The secretory, metabolic, and signaling aspects of glucose/palmitate interaction on beta-cell function have been studied on rat islets. Palmitate potentiated the glucose-induced insulin response of perifused islets at suprathreshold (>3 mmol/l) sugar concentrations. This potentiating effect could be suppressed by 8-bromo-cGMP, which also blocks palmitate metabolism. Palmitate did not modify glucose utilization, but it slightly reduced glucose oxidation and concomitantly increased lactate production. The very low rate of palmitate oxidation (80-fold lower than that of 20 mmol/l glucose) might explain its lack of effect on glycolysis and hence that the glucose/fatty acid cycle is inoperative in islet cells. However, glucose determines the metabolic fate of exogenous palmitate, which is mainly diverted toward lipid synthesis at high sugar concentrations and might then generate lipid messengers for cell signaling. Palmitate did not increase glucose-induced production of inositol-1,4,5-trisphosphate, but it stimulated the translocation of protein kinase C activity from a cytosolic to a particulate fraction at 20 but not at 3 mmol/l glucose. This increased translocation was partially or completely blocked by hydroxycitrate or 8-bromo-cGMP, respectively, which are agents interfering with palmitate metabolism (inhibiting lipid synthesis). The metabolic interaction between glucose and palmitate might generate lipid messengers (diacylglycerol, phosphatidylserine) necessary for the activation of islet protein kinase C, which would in turn result in a potentiation of glucose-induced insulin secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2004

Palmitate stimulation of glucagon secretion in mouse pancreatic alpha-cells results from activation of L-type calcium channels and elevation of cytoplasmic calcium.

We have investigated the short-term effects of the saturated free fatty acid (FFA) palmitate on pancreatic alpha-cells. Palmitate (0.5 or 1 mmol/l bound to fatty acid-free albumin) stimulated glucagon secretion from intact mouse islets 1.5- to 2-fold when added in the presence of 1-15 mmol/l glucose. Palmitate remained stimulatory in islets depolarized with 30 mmol/l extracellular K(+) or exposed to forskolin, but it did not remain stimulatory after treatment with isradipine or triacsin C. The stimulatory action of palmitate on secretion correlated with a 3.5-fold elevation of intracellular free Ca(2+) when applied in the presence of 15 mmol/l glucose, a 40% stimulation of exocytosis (measured as increases in cell capacitance), and a 25% increase in whole-cell Ca(2+) current. The latter effect was abolished by isradipine, suggesting that palmitate selectively modulates l-type Ca(2+) channels. The effect of palmitate on exocytosis was not mediated by palmitoyl-CoA, and intracellular application of this FFA metabolite decreased rather than enhanced Ca(2+)-induced exocytosis. The stimulatory effects of palmitate on glucagon secretion were paralleled by a approximately 50% inhibition of somatostatin release. We conclude that palmitate increases alpha-cell exocytosis principally by enhanced Ca(2+) entry via l-type Ca(2+) channels and, possibly, relief from paracrine inhibition by somatostatin released by neighboring delta-cells.

Animals↗
PubMed2005

Palmitate-induced apoptosis in cultured bovine retinal pericytes: roles of NAD(P)H oxidase, oxidant stress, and ceramide.

Apoptosis of pericytes (PCs) is an early event in diabetic retinopathy. It is generally thought to be a consequence of sustained hyperglycemia. In keeping with this, long-term (>7 days) incubation of cultured PCs in a high-glucose media has been shown to increase apoptosis. We examine here whether the saturated free fatty acid palmitate, the concentration of which is often elevated in diabetes, has similar effects on cultured PCs. Incubation with 0.4 mmol/l palmitate for 24 h induced both oxidant stress and apoptosis, as evidenced by a sixfold increase in DCF fluorescence and a twofold increase in caspase-3 activation, respectively. NAD(P)H oxidase appeared to be involved in these responses, since overexpression of dominant-negative subunits of NAD(P)H oxidase, such as phox47(DN), diminished oxidant stress, and phox67(DN) and N-17 RAC1(DN) prevented the increase in caspase-3 activity. Likewise, overexpression of vRAC, a constitutively active RAC1, increased caspase-3 activity to the same extent as palmitate alone. The effects of vRAC and palmitate were not additive. In parallel with the increases in oxidative stress, the redox-sensitive transcription factor nuclear factor-kappaB (NF-kappaB) was activated in cells incubated with 0.4 mmol/l palmitate. Furthermore, inhibition of NF-kappaB activation by various means inhibited caspase-3 activation. Finally, incubation with palmitate increased the cellular content of ceramide, a molecule linked to apoptosis and increases in oxidative stress and NF-kappaB activation in other cells. In keeping with such a role, in PCs both coincubation with fumonisin B1 (a ceramide synthase inhibitor) and overexpression of ceramidase I reversed the proapoptotic effect of palmitate. On the other hand, they increased rather than decreased DCF fluorescence. In conclusion, the results suggest that palmitate-induced apoptosis in PCs is associated with activation of NAD(P)H oxidase and NF-kappaB and an increase in ceramide. The precise interactions between these molecules in causing apoptosis and the importance of oxidant stress as a contributory factor remain to be determined.

Animals↗
PubMed2004

Dietary palmitic acid influences LDL-mediated lymphocyte proliferation differently to other mono- and polyunsaturated fatty acids in rats.

Recent studies suggest that the biological effects of saturated fatty acids depend on the length of their chain. We compared the effect of diets containing different fatty acids on plasma lipids and lymphocyte proliferation in the presence of lovastatin and with increasing amounts of LDL. Lymphocytes from rats fed with a diet rich in palmitic acid had a greater lymphocyte proliferation capacity than those from rats fed with diets rich in oleic acid, linoleic acid, or fish oil. This effect was maintained when small amounts of polyunsaturatwed fatty acids (PUFA; sunflower oil) were added to the palmitic acid diet. LDL receptor activity, measured by the capacity of lovastatin to revert the inhibition of lymphocyte proliferation with increasing amounts of LDL in the medium, was greater in the rats fed with palmitic acid, and was similar to the other groups when small amounts of PUFA were added. All the groups had similar levels of plasma cholesterol, but the LDL levels were significantly lower in the group fed with palmitic acid plus PUFA. The highest HDL-cholesterol (HDLc) levels were found in the palmitic acid group and the lowest LDL-cholesterol (LDLc)/HDLc ratio in the palmitic acid plus PUFA group. These results suggest that diets rich in palmitic acid do not raise total cholesterol, but reduce LDLc or keep it normal, and raise HDLc levels. This effect may be partly due to an increase in LDL receptor activity. The inclusion of small amounts of PUFA in the diet rich in palmitic acid substantially modified the LDL receptor response in the lymphocytes, suggesting that the proportion of different families of dietary fatty acids may be more important than the individual amount of each in absolute terms to explain their effects on plasma lipids and lipoproteins.

Analysis of Variance↗
PubMed1981

Investigation of [14C] linoleic acid conversion into [14C] arachidonic acid and placental transfer of linoleic and palmitic acids across the perfused human placenta.

In five separate experiments in which single placental lobes were perfused, [14C] antipyrine, [3H] dextran and a fatty acid mixture containing [14C] linoleic and [3H] palmitic acids were added to the maternal circuit. Samples of fetal and maternal perfusate, taken at intervals, were analysed for radioactivity and fatty acid content. The relative placental transport rates of antipyrine, linoleic and palmitic acids and the changes in maternal and fetal circuit content of linoleic, palmitic and arachidonic acids were measured. Mean transfer rates of 150, 0.023 and 0.034 mumol min-1 were obtained for [14C] antipyrine, [3H] palmitic and [14C] linoleic acids, respectively. The transfer of [3H] dextran was negligible. The transfer rates of linoleic and palmitic acids did not differ significantly from one another. The maternal circuit content of palmitic and arachidonic acids increased, whereas linoleic acid content decreased. The fetal content of all three acid increased but in the case of arachidonic and palmitic acids the increase was not as great as that seen in the maternal circuit. In no experiment was radioactivity detected in maternal or fetal perfusate arachidonic acid. It is concluded that linoleic and palmitic acids cross the placenta from the maternal to the fetal side. This transfer appears to be non-selective. The large amounts of arachidonic acid that are released into the perfusate probably originate from placental lipids other than free linoleic acid.

Antipyrine↗
PubMed1977

Fetal lung maturity, as assessed by gas-liquid chromatographic determination of phospholipid palmitic acid in amniotic fluid.

We describe a new and specific method for measurement of lecithin palmitic acid in amniotic fluid. Dipalmitoyl lecithin, the major alveolar surfactant, has previously been estimated by measuring the lecithin-sphingomyelin ratio, total lecithin, total phospholipid phosphorus, and (or) total palmitic acid. Our method is more specific for estimation of dipalmitoyl lecithin, because nonphospholipid sources of palmitic acid are removed by solvent extraction. Using a hexane/2-propanol/sulfuric acid system, we obviated the major interferences from triglycerides and free fatty acids. The palmitic acid derived from the phospholipid fraction is measured by gas-liquid chromatography of its methyl ester. No contribution appears to be made by sphingomyelin palmitic acid--probably owing to the mild hydrolysis conditions. The measured palmitic acid therefore appears to be derived from lecithins, principally dipalmitoyl lecithin. The value for palmitic acid determined by this method correlates well with the lecithin-sphingomyelin ratio and total phospholipid phosphorus. Infants are unlikely to develop respiratory distress syndrome when the measured palmitic acid in amniotic fluid exceeds 8.0 mg/liter, which corresponds to an lecithin-sphingomyelin ratio of 2.0.

Amniotic Fluid↗
PubMed2000

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

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

Journal Article↗
PubMed1999

Palmitate induces apoptosis via a direct effect on mitochondria.

The fatty acid palmitate can induce apoptosis. Here we show that the palmitate-induced dissipation of the mitochondrial transmembrane potential (Delta Psi m), which precedes nuclear apoptosis, is not prevented by inhibitors of mRNA synthesis, protein synthesis, caspases, or pro-apoptotic ceramide signaling. However, the mitochondrial and nuclear effects of palmitate are inhibited by overexpression of anti-apoptotic proto-oncogene product Bcl-2 and exacerbated by 2-bromo-palmitate as well as by carnitine. The cytoprotective actions of Bcl-2, respectively, is not antagonized by etomoxir, an inhibitor of carnitine palmitoyl transferase 1 (CPT1), suggesting that the recently described physical interaction between CPT1 and Bcl-2 is irrelevant to Bcl-2-mediated inhibition of palmitate-induce apoptosis. When added to purified mitochondria, palmitate causes the release of soluble factors capable of stimulating the apoptosis of isolated nuclei in a cell-free system. Mitochondria purified from Bcl-2 over-expressing cells are protected against the palmitate-stimulated release of such factors. These data suggest that palmitate causes apoptosis via a direct effect on mitochondria.

Journal Article↗
PubMed1995

Effect of dietary retinyl palmitate on the promotion of altered hepatic foci by 3,3',4,4'-tetrachlorobiphenyl and 2,2',4,4',5,5'-hexachlorobiphenyl in rats initiated with diethylnitrosamine.

The purpose of this study was to determine the effects of dietary vitamin A on the tumor promoting effect of 3,3',4,4'-TCB and 2,2',4,4',5,5'-HCB in a two-stage rat hepatocarcinogenesis model with diethylnitrosamine (DEN, 150 mg/kg) as the initiator. Two weeks after DEN injection rats were fed a purified diet containing either 2000 or 100,000 IU of vitamin A in the form of retinyl palmitate. Rats received four biweekly injections of 3,3',4,4'-TCB, 2,2',4,4',5,5'-HCB (300 mumol/kg), or both (150 mumol/kg each) in corn oil (10 ml/kg) for 8 weeks. Control animals received vehicle only. Six rats in each group that received no DEN treatment were used as additional control animals. Ten days after the last injection the rats were killed. In rats fed the low retinyl palmitate diet, treatment with 3,3',4,4'-TCB, 2,2',4,4',5,5'-HCB or both compounds lowered hepatic retinyl palmitate content. This effect was prevented by high dietary retinyl palmitate supplementation in rats treated with 2,2',4,4',5,5'-HCB, but not 3,3',4,4'-TCB or both compounds together. Histopathological examination of the liver showed that high dietary retinyl palmitate lessened the severity of hepatocellular necrosis and fatty changes induced by 3,3',4,4'-TCB alone or in combination with 2,2',4,4',5,5'-HCB. The latter did not cause significant pathological lesions to the liver. However, high dietary retinyl palmitate was not able to prevent thymic involution caused by 3,3',4,4'-TCB. The number and volume of altered hepatic foci were increased by 2,2',4,4',5,5'-HCB and particularly 3,3',4,4'-TCB; no synergistic effect was seen. Supplementation with high dietary retinyl palmitate diminished the number and volume of foci. These results show that supplementation with high dietary retinyl palmitate protects against hepatocellular necrosis, fatty changes, and preneoplastic changes induced by 3,3',4,4'-TCB as well as against preneoplastic changes induced by 2,2',4,4',5,5'-HCB. In addition, these two agents did not synergistically induce preneoplastic changes in DEN-induced rats.

Animals↗
PubMed1993

Pharmacological properties of beta-amyrin palmitate, a novel centrally acting compound, isolated from Lobelia inflata leaves.

Effects of beta-amyrin palmitate isolated from the leaves of Lobelia inflata were studied on the central nervous system of mice and were compared with those of antidepressant drugs, mianserin and imipramine. In the forced swimming test, beta-amyrin palmitate, like mianserin and imipramine, reduced the duration of immobility of mice significantly in a dose-dependent manner (5, 10 and 20 mg kg-1). beta-Amyrin palmitate (5, 10 and 20 mg kg-1) or mianserin (5, 10 and 20 mg kg-1) elicited a dose-related reduction in locomotor activity of mice and antagonized locomotor stimulation induced by methamphetamine. In contrast, imipramine (5, 10 and 20 mg kg-1) increased locomotor activity and potentiated methamphetamine-induced hyperactivity. beta-Amyrin palmitate showed no effect on reserpine-induced hypothermia, whilst mianserin (10 mg kg-1) and imipramine (10 and 20 mg kg-1) antagonized the reserpine-induced effect. Unlike imipramine, beta-amyrin palmitate and mianserin did not affect haloperidol-induced catalepsy, tetrabenazine-induced ptosis and apomorphine-induced stereotypy. beta-Amyrin palmitate and imipramine had no effects on the head-twitch response induced by 5-hydroxytryptophan, whereas mianserin (5, 10 and 20 mg kg-1) decreased it in a dose-dependent manner. A potentiating effect of beta-amyrin palmitate (5, 10 and 20 mg kg-1) on narcosis induced by sodium pentobarbitone was stronger than that of imipramine (10, 20 and 40 mg kg-1) but weaker than that of mianserin (2.5, 5 and 10 mg kg-1). These results suggest that beta-amyrin palmitate has similar properties in some respects to mianserin and might possess a sedative action.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Inheritance and Interaction of Low Palmitic and Low Linolenic Soybean.

Decreasing the palmitic and linolenic acid content of soybean [Glycine max (L.) Merrill] oil would help improve its nutritional quality and oxidative stability. The altered fatty acid profile in soybean germplasm lines with decreased levels of palmitic and linolenic acid have been developed at the University of Guelph, Canada, by combining different mutant alleles through hybridization. The objectives of this study were to determine the inheritance and interaction of palmitic and linolenic acid levels in RG3 and RG1, and the effects of these altered fatty acid levels on other fatty acids. RG3 and RG1 (low palmitic approximately 45 g kg(-1) and linolenic approximately 40 g kg(-1)) were crossed reciprocally to several soybean lines with altered or normal fatty acid profiles. Analysis of the reciprocal F(2) generations indicated no maternal or cytoplasmic effects for palmitic or linolenic acid content. Chi-square analyses of the F(2) generation demonstrated that RG3 and RG1 contained two alleles, fap1 and fapx, that controlled palmitic acid content. In addition, RG1 had a third allele, fan, which reduced its linolenic acid content. Calculation of gene substitution values indicated additive gene action at the fap1 and fan loci, whereas the fapx locus involved partial dominance. Correlation coefficients indicated no association between palmitic and linolenic acid. Decreases in palmitic and linolenic acid content were associated primarily with increases in linoleic acid content. Since fap1, fapx, and fan were inherited independently of each other and appeared to behave in an additive manner, RG3 and RG1 can be used in breeding programs as additional valuable sources of germplasm with altered fatty acid profiles.

Journal Article↗
PubMed1989

Protective effects of retinyl palmitate on streptozotocin- and alloxan-induced beta cell toxicity and diabetes in the rat.

The cellular effects of retinoids may be relevant to protection against chemical-induced diabetes mellitus. To determine whether retinyl palmitate protects the beta cell from streptozotocin- and alloxan-induced diabetes, we injected streptozotocin, 60 mg/kg, or alloxan, 100 mg/kg, with or without varying doses of retinyl palmitate intraperitoneally or by tail vein. Plasma glucose was measured for over 4 weeks. To determine if the protective effects of retinyl palmitate were mediated through effects on superoxide dismutase, a scavenger of tissue free radicals, we determined whether retinyl palmitate affected islet superoxide dismutase activity. Retinyl palmitate, given intraperitoneally or by tail vein, protected against both streptozotocin- and alloxan-induced diabetes. The effect was dependent on the route of administration. When given intraperitoneally, the protective effect was greater than when given intravenously. When given by tail vein, the protective effect was dose dependent. Retinyl palmitate in vitro did not affect insulin secretion or islet superoxide dismutase. We conclude that retinyl palmitate treatment protects against streptozotocin- and alloxan-induced diabetes. Further studies are needed to determine whether retinyl palmitate protects against the development of diabetes in other animal models and whether this effect is relevant to diabetes in man.

Alloxan↗
PubMed1987

Labeled oxidation products from [1-14C], [U-14C] and [16-14C]-palmitate in hepatocytes and mitochondria.

When [1-14C], [U-14C], and [16-14C]palmitate were oxidized by isolated rat hepatocytes, there was a differential distribution of label as a percent of total oxidized products, such that 14CO2 from [1-14C] greater than [U-14C] greater than [16-14C]palmitate and acid-soluble radioactivity from [16-14C] greater than [U-14C] greater than [1-14C]palmitate. The oxidation of [2,3-14C]succinate to 14CO2 by isolated hepatocytes was only 9.1% of that from [1,4-14C]succinate, demonstrating that the differences in distribution of labeled products are in part due to less 14CO2 production from label in the even carbon positions entering the citric acid cycle. Apparent total ketone body production from [16-14C]palmitate was markedly higher than [1-14C] and [U-14C]palmitate. In addition, the 14C-acetone:14CO2 ratio derived from decarboxylation of labeled acetoacetate from [1-14C]palmitate was less than 1 and positively correlated to the rate of fatty acid oxidation in hepatocytes. These findings indicate that the known preferential incorporation of the omega-C2 unit of fatty acids into 14C-ketone bodies also contributed to the differential distribution of labeled products and that this contribution was greatest at the lower rates of fatty acid oxidation. In isolated mitochondria, the distribution of label to 14CO2 and acid-soluble radioactivity from [1-14C], [U-14C] and [16-14C]palmitate was qualitatively similar to that seen with hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗
PubMed1992

Palmitic acid enhances cholesterol gallstone incidence in Sasco hamsters fed cholesterol enriched diets.

In an established hamster model of cholesterol cholelithiasis, a semipurified lithogenic diet containing 4% butterfat and 0.3% cholesterol leads to the production of cholesterol gallstones in only 50-60% of animals after a 6-wk feeding period. The purpose of this study was to investigate whether gallstone incidence could be increased while feeding a nutritionally adequate diet of moderate cholesterol content. The semipurified lithogenic diet was modified as follows: (i) substitution of 1.2% palmitic acid for 4% butterfat, and (ii) varying the amount of dietary cholesterol from 0.0 to 0.3% with either butterfat or palmitic acid as the lipid component of the diet. Substitution of palmitic acid for butterfat produced a significantly higher incidence of cholesterol gallstones (94% vs. 53%). Palmitic acid also raised the incidence of gallstones when added to the 0.1% and 0.2% cholesterol diets as compared to butterfat: 0% vs. 44% and 50% vs. 81%, respectively. Gallstone incidence increased from 0% to nearly 100% when the cholesterol content of the palmitic acid diets was raised from 0.0% to 0.3%, indicating a dose response effect with respect to dietary cholesterol. Hamsters fed cholesterol-free diets did not form gallstones. Increased dietary cholesterol led to increased liver weight associated with a significant increase in liver cholesterol concentration. However, the palmitic acid groups had significantly lower liver cholesterol values than the corresponding butterfat groups. Serum and biliary cholesterol concentrations increased with increasing dietary cholesterol intake, but there were no differences between the butterfat and palmitic acid groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

The action of vasopressin and calcium on palmitate metabolism in hepatocytes and isolated mitochondria from rat liver.

Vasopressin inhibits fatty acid oxidation and stimulates fatty acid esterification, glycogenolysis, and lactate production in hepatocytes from fed rats. In cells from fasted rats, the effect of the hormone on palmitate oxidation was absent, while gluconeogenesis was stimulated. The inhibitory action of vasopressin on palmitate oxidation was not due to the increased lactate production. Neither was it correlated to glycogen content or stimulation of glycogenolysis, which were restored earlier than the vasopressin effect on palmitate oxidation when previously fasted rats were refed a carbohydrate diet. The level of malonyl-CoA was moderately increased by vasopressin. Isolated mitochondria from rat liver were incubated in the presence of [U-14C]palmitate, ATP, CoA carnitine, glycerophosphate, ethylene glycol bis(beta-aminoethyl ether) N,N'-tetraacetic acid, and varying amounts of calcium. The oxidation of palmitate was inhibited when the concentration of free calcium was increased from about 0.1 to 10 microM. Simultaneously, palmitate esterification was stimulated. This effect of calcium was observed also with mitochondria from fasted rats and with octanoate as well as palmitate as the substrate. Carnitine acylation was not affected by calcium. The possibility that the observed effects of calcium on mitochondrial fatty acid utilization is part of the mechanism of action of vasopressin on hepatocyte fatty acid metabolism is discussed.

Animals↗
PubMed1982

Palmitate oxidation by intact preparations of skeletal muscle.

1. The palmitate oxidation by intact preparations of rat hemidaphragm, m.soleus and m.flexor digitorum brevis and by teased fibers of human m.pectoralis was studied. 2. The structural and metabolic viability of the in vitro preparations was shown by a low leakage of soluble creatine kinase, a constant rate of palmitate oxidation and only a small stimulatory effect of L-carnitine. 3. With hemidaphragm the palmitate oxidation rate increases with both the palmitate concentration (0-3 mM) and the palmitate/albumin molar ratio (0.5-5.0). 4. The apparent Km for palmitate oxidation was about 1.5 mM at 0.1 and 0.2 mM albumin and about 2.7 mM at 0.4 and 0.6 mM albumin, which correlates with the higher affinity of albumin for palmitate at lower palmitate/albumin molar ratios. 5. After prolonged starvation the apparent Km at 0.4 mM albumin is markedly lower. In whole homogenates of diaphragm the apparent Km at 0.4 mM albumin is only about 370 microM. 6. The calculated maximal oxidation rate was not significantly different for all albumin concentrations examined (23-32 nmol/min per g), did not change after starvation and appears to be of the same order of magnitude as the rate of endogenous fatty acid consumption (30-40 nmol/min per g). 7. Results suggest that substrate availability is a main factor for the oxidation rate of exogenous palmitate by hemidiaphragm in vitro and that the magnitude of the apparent Km is largely dependent upon the degree of label dilution with fatty acids of endogenous origin.

Animals↗
PubMed1983

Palmitate incorporation into different brain regions in the awake rat.

A quantitative method is presented to examine palmitate flux into a stable metabolic compartment in individual brain regions of awake rats. Following the i.v. injection of [14C]palmitate, brain radioactivity rose and then fell until, at 4 h, a stable concentration was reached that was maintained for up to 24 h. The flux of plasma palmitate into this 4 h compartment was calculated by dividing regional brain radioactivity at 4 h, as determined by quantitative autoradiography, by the integral of the plasma palmitate specific activity. Palmitate flux varied from 2.0 x 10(-5) mumol/g.s into the internal capsule to 9.3 x 10(-5) mumol/g.s into the arcuate nucleus, and generally was proportional to the regional cerebral metabolic rate for glucose, as measured with 2-deoxy-D-[1-14C]glucose. The results demonstrate that it is possible to determine unidirectional palmitate flux into a stable metabolic compartment in individual brain regions of awake rats, that flux into gray matter regions generally exceeds flux into white matter, and that palmitate flux is proportional to published values for regional brain oxidative metabolism.

Absorption↗