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PubMed1974

The amounts and rates of export of polysaccharides found within the membrane system of maize root cells.

1. Maize seedling roots were incubated in vivo with d-[U-(14)C]glucose for 2, 5, 10, 15, 30 and 45min. The total incorporation of radioactivity into polysaccharide components in isolated fractions was investigated, and the pattern of incorporation into different polysaccharide components within the rough endoplasmic reticulum, Golgi apparatus and exported material was analysed. 2. The membrane compartments reached a saturation value of radioactivity in polysaccharide components by 30min incubation. Radioactivity in exported polysaccharide continued to increase after that time. The latter was formed and maintained by a steady-state turnover of polysaccharide synthesis and transport from the membrane system. 3. If the only access of the slime polysaccharide to the cell surface is via dictyosome-derived vesicles, the amount of slime components in the Golgi apparatus would have to be displaced every 0.3min in order to maintain the observed rates of increase in slime. This is in contrast with a displacement time of about 2.5min that is necessary for polysaccharide components in the Golgi apparatus to produce the observed increase in cell-wall material. The activity of the membrane system in the production of maize root slime is 8 times as great as that of the membrane system involved in cell-wall synthesis. 4. If the amount of polysaccharide material in the Golgi apparatus is maintained only by inflow of polymeric material from the rough endoplasmic reticulum the total amount of slime components in the rough endoplasmic reticulum would have to be displaced every 7min to maintain a constant amount in the Golgi apparatus. If the endoplasmic reticulum contributed directly to the cell surface in the synthesis of cell-wall material, displacement times necessary to maintain the observed rate of polymer production would be very slow.

Arabinose↗

PubMed2000

Myocardial blood flow, function, and metabolism in repetitive stunning.

UNLABELLED: Myocardial hibernation refers to a state of persistent left ventricular dysfunction resulting from a chronically reduced blood flow, which is improved or reversed with revascularization. Increased glucose uptake in areas with reduced blood flow at rest on PET has been used successfully to diagnose hibernating myocardium. However, hibernation may represent persistent myocardial stunning resulting from repeated episodes of ischemia and reperfusion rather than from chronic underperfusion. We sought to determine the inter-relationship between blood flow, metabolism, and function in a canine model of repetitive myocardial stunning. METHODS: Ten dogs underwent 4 sequential 5-min intervals of balloon occlusion of the anterior descending or circumflex arteries, each separated by 5 min of reperfusion. Regional blood flow, metabolism, and function were evaluated 3-4 h after reperfusion in all dogs and 24 h and 1 wk after reperfusion in 5 dogs. Regional wall motion was evaluated with echocardiography. Regional blood flow was assessed with radioactive microspheres and by [(13)N]ammonia and PET. Measurements of oxidative metabolism and glucose uptake (during hyperinsulinemic-euglycemic clamping) were derived with [(11)C]-acetate, FDG, and PET. RESULTS: Regional wall motion was severely decreased after the 4 cycles of ischemia, remained impaired 24 h after reperfusion, and normalized after 1 wk. During reflow, blood flow in stunned regions was restored to near-normal levels (0.89 +/- 0.07 versus 0.95 +/- 0.07 mL/g/min, P = 0.023). However, glucose uptake in stunned regions was significantly decreased at 4 h (73% +/- 5% of remote, P < 0.001), remained depressed after 24 h of reflow (83% +/- 4% of remote, P = 0.013), and fully recovered at 1 wk (101% +/- 10% of remote, P = 0.88). Similarly, oxidative metabolism in stunned regions was significantly decreased at 4 h (84% +/- 2% of remote, P < 0.001) and at 24 h (90% +/- 2% of remote, P = 0.005) and recovered to near-normal levels after 1 wk of reperfusion (97% +/- 1% of remote, P = 0.024). The time course of change in postischemic dysfunction correlated with the recovery of oxidative metabolism (r=0.57; P=0.009). CONCLUSION: Myocardium subjected to repetitive stunning showed a prolonged yet reversible reduction in systolic function that was associated with a significant downregulation of glucose and oxidative metabolism despite restoration of normal myocardial blood flow. These findings suggest a unique metabolic adaptation in repetitive stunning that is different from that typically seen in clinical and experimental models of hibernation.

Animals↗

PubMed1989

In vivo administration of glucose oxidase conjugated with monoclonal antibodies to angiotensin-converting enzyme. The tissue distribution, blood clearance, and targeting into rat lungs.

A conjugate between glucose oxidase (GO) and monoclonal antibody to human angiotensin-converting enzyme (ACE) cross-reacting with rat ACE (MoAb9b9) has been prepared by oxidation of the cardohydrate moiety of the enzyme with sodium periodate. The conjugate (GO-MoAb9b9) thus obtained retained both antigen-binding capacity and enzymatic activity. The fate of the conjugate in vivo after intravenous injection was studied using conjugates containing radiolabeled enzyme. GO-MoAb9b9 was specifically accumulated in rat lungs upon in vivo administration, as compared with free enzyme and nonimmune IgG-conjugated glucose oxidase. The specificity of the conjugate accumulation expressed as the localization ratio (the ratio between radioactivity of gram tissue to that of blood) (Loc. Ratio) reached a value up to 50 on the second day after injection, in contrast to native enzyme and to IgG-conjugated enzyme (Loc. Ratio was less than 0.5 for both preparations). The Loc. Ratio of GO-MoAb9b9 was even higher than that of the original antibody MoAb9b9 and was equal to 20, which is probably explained by an extremely rapid blood clearance of the conjugate from the circulation. The administration of excess free MoAb9b9 dramatically inhibited the conjugate targeting in the lung without any effect on liver uptake. At doses ranging from 10 to 1,000 micrograms/rat, the conjugate was accumulated in the lung without saturation of the antigen determinants of the target. At minimal doses, the efficiency of targeting achieved 5 to 7% of the conjugate injected. With elevation of the dose, the efficiency of targeting decreased to 2.5% of the injected dose (1 mg of GO-MoAb9b9 per rat). A sixfold greater accumulation of unmodified radiolabeled MoAb9b9 compared with the GO-MoAb9b9 conjugate in rat lung has been observed, though the kinetics of desorption from the target organ was similar for both the antibody and the conjugate. In the bloodstream, the conjugate persisted for at least 5 days without binding to blood cells; all circulating radioactivity was associated with proteins. A considerable part of the conjugate (to 50%) circulated as a tight antibody-enzyme complex for several days. The conjugate retained its antigen-binding capacity for at least 24 h; during this period, its enzymatic activity decreased by less than 40%. The results obtained provide the experimental ground for further attempts to apply glucose oxidase conjugates for local modulation of inflammation and elimination of the target cells.

Animals↗

PubMed1988

The effect of ethanol on phospholipid metabolism in rat pancreas.

The phospholipid effect involves agonist-induced breakdown of phosphatidyl inositol (or polyinositides) generating second messengers followed by increased incorporation of 32P during the resynthetic phase of the cycle. Ethanol, an aetiological factor in pancreatitis, has been shown to have various effects on pancreatic secretion. In this study ethanol decreased the incorporation of 32P into phosphatidyl inositol but had no effect on the stimulated breakdown of prelabelled phosphatidyl inositol. However, in addition to recycling of phosphatidyl inositol stimulation of pancreatic tissue results in increased incorporation of precursors into other phospholipids. Cholecystokinin increased the incorporation of both [U-14C] glucose and 32P into phosphatidyl ethanolamine 3-fold but had no effect on 32P incorporation into phosphatidyl choline. As well as increased incorporation of 32P into phosphatidyl inositol (8-fold) cholecystokinin also increased the incorporation of [U-14C] glucose into phosphatidyl inositol (4-5-fold) implying significant de novo synthesis of 1,2 diacyl glycerol in addition to the currently accepted recycling of the 1,2 diacyl glycerol back to phosphatidyl inositol. Ethanol caused an inhibition of 32P incorporation into total phospholipid of rat pancreas during basal and stimulated conditions. When individual phospholipids were separated ethanol was found to decrease the incorporation of 32P into phosphatidyl choline under basal conditions and into all phospholipids during cholecystokinin stimulation. With [U-14C] glucose as the precursor, ethanol inhibited its incorporation into phosphatidyl choline only. Ethanol did not alter the total 32P radioactivity in the aqueous phase of the pancreatic extract nor the percent incorporated into nucleotides. This excluded decreased uptake of 32P and incorporation into nucleotides as a mechanism for the differential inhibition of 32P versus [U-14C] glucose incorporation into phospholipids other than phosphatidyl choline under stimulated conditions.

Animals↗

PubMed1990

Re-examination of the presence of alpha-lactalbumin in the epididymis of the rat.

Using an assay for alpha-lactalbumin in which galactosyltransferase activity was stabilized and a tissue phosphatase inhibitor was present, no evidence was found for alpha-lactalbumin-like activity in rat epididymal tissue, epididymal fluids or medium from cultured epididymal epithelial cells with either glucose or N-acetylglucosamine as acceptor. However, when assay conditions were suboptimal, apparent transfer of radioactivity to both acceptors could be demonstrated in the epididymis and other tissues. In these assays the amount of alpha-lactalbumin registered was linearly correlated to the extent of stimulation of alpha-lactalbumin added exogenously to tissue extracts as internal standards. When rete testis fluid from rats was used as source of galactosyltransferase under suboptimal conditions, no transfer to glucose was demonstrable in epididymal fluid and an apparent decreased transfer to N-acetylglucosamine could be explained by increases in (pyro)phosphatase activity. Putative alpha-lactalbumin activity in the epididymis may be an artefact of unoptimized assays.

Acetylglucosamine↗

PubMed2004

Glucose accumulation can account for the initial water flux triggered by Na+/glucose cotransport.

Over the last decade, several cotransport studies have led to the proposal of secondary active transport of water, challenging the dogma that all water transport is passive. The major observation leading to this interpretation was that a Na+ influx failed to reproduce the large and rapid cell swelling induced by Na+/solute cotransport. We have investigated this phenomenon by comparing a Na+/glucose (hSGLT1) induced water flux to water fluxes triggered either by a cationic inward current (using ROMK2 K+ channels) or by a glucose influx (using GLUT2, a passive glucose transporter). These proteins were overexpressed in Xenopus oocytes and assayed through volumetric measurements combined with double-electrode electrophysiology or radioactive uptake measurements. The osmotic gradients driving the observed water fluxes were estimated by comparison with the swelling induced by osmotic shocks of known amplitude. We found that, for equivalent cation or glucose uptakes, the combination of substrate accumulations observed with ROMK2 and GLUT2 are sufficient to provide the osmotic gradient necessary to account for a passive water flux through SGLT1. Despite the fact that the Na+/glucose stoichiometry of SGLT1 is 2:1, glucose accumulation accounts for two-thirds of the osmotic gradient responsible for the water flux observed at t = 30 s. It is concluded that the different accumulation processes for neutral versus charged solutes can quantitatively account for the fast water flux associated with Na+/glucose cotransport activation without having to propose the presence of secondary active water transport.

Animals↗

PubMed1989

Energy balance and diabetes. The effects of cold exposure, exercise training, and diet composition on glucose tolerance and glucose metabolism in rat peripheral tissues.

The effects of cold exposure, exercise training, and diet (high fat versus high carbohydrate) on glucose tolerance and glucose metabolism in rat peripheral tissues will be briefly reviewed. Stimulation of energy expenditure by cold exposure (4 degrees C) or exercise training generally leads to decreased plasma insulin levels and to an improvement in glucose tolerance, suggesting that insulin action on peripheral tissues is increased when energy expenditure is stimulated. On the contrary, feeding high-fat diets to sedentary rats living in the warm (25 degrees C) induces hyperinsulinemia and insulin resistance resulting in a marked deterioration of glucose tolerance. Nevertheless, cold exposure reverses the diabetogenic effects of high-fat feeding, demonstrating that nutrition-induced insulin resistance is amplified in sedentary animals living at temperatures close to thermoneutrality. Radioactive tracer studies of 2-deoxyglucose uptake in peripheral tissues revealed that cold exposure synergistically potentiates the effects of insulin on glucose uptake in skeletal muscles as well as in white and brown adipose tissues. However, more recent data showed that cold exposure improves glucose tolerance and stimulates glucose uptake in starved animals (ie., in the virtual absence of circulating insulin) nearly by the same order of magnitude as in fed animals. It is therefore concluded that cold exposure, and possibly also exercise, improve glucose tolerance and stimulate glucose uptake in peripheral tissues primarily by enhancing glucose oxidation via insulin-independent pathways, and secondarily by increasing the responsiveness of peripheral tissues to insulin.

Acclimatization↗

PubMed1989

Decrease in insulin binding to aortic endothelial cells cultured with high glucose concentration.

We studied the effects of glucose on specific insulin binding to cultured endothelial cells from the bovine aorta. We cultured the cells in Dulbecco's modified Eagle's medium, containing 100 or 300 mg/dl glucose or 100 mg/dl glucose plus 200 mg/dl mannitol. We added 125I-insulin to monolayers of these cells and counted the radioactivity resulting. Specific insulin binding increased with time and dosage. Maximal binding resulted from 0.17 nM 125I-insulin being incubated for 30 min at 37 degrees C, and amounted to 0.35% per 10(5) cells being bound in cultures of 100 mg/dl glucose. The higher concentration of glucose led to significantly less binding (P less than 0.05) (0.24 +/- 0.03% vs. 0.38 +/- 0.02%, n = 6). The addition of mannitol, on the other hand, did not affect binding. All three incubation conditions produced curvilinear competition curves. Scatchard analysis showed that insulin bound significantly less (P less than 0.05) to endothelial cells in 300 mg/dl glucose than to those in 100 mg/dl glucose (4.0 +/- 1.2 nmol/l vs. 12.8 +/- 3.1, n = 6, mean +/- SEM). Insulin binding capacity, however, did not change. We conclude that glucose can reduce insulin binding to endothelial cells and that it may reduce receptor-related insulin transport into and out of the cells.

Animals↗

PubMed1994

Effect of different sepsis-related cytokines on lipid synthesis by isolated hepatocytes.

Cytokines seem to play an important role in the metabolic disturbances that are commonly associated with sepsis. In this study, we analyzed the effect of tumor necrosis factor, interleukin-1 and interleukin-6, as well as that of tumor necrosis factor in combination with interleukin-1 or interleukin-6, both on free fatty acids and on phospholipid synthesis by isolated rat hepatocytes. All three cytokines and combinations caused inhibited D-[U-14C]glucose incorporation into phosphatidylcholine (tumor necrosis factor = 6.39 +/- 1.13 pmol/microgram protein vs. control = 12.90 +/- 0.98 pmol/microgram protein, n = 7; p < 0.001). However, when [U-14C]palmitate was used as radioactive precursor, tumor necrosis factor, either alone or in the presence of the other cytokines, stimulated phosphatidylcholine synthesis. D-[U-14C]glucose incorporation into free fatty acids and triacylglycerol was also significantly stimulated, whereas phosphatidylinositol labeling was found inhibited by the assayed cytokines. Our results demonstrate an effect of sepsis-related cytokines, more evident for tumor necrosis factor, on hepatocyte lipid synthesis either from glucose or palmitate. Also, the findings support the hypothesis that cytokine-induced changes in hepatocyte lipid synthesis can contribute to the impairment in lipidic metabolism seen in patients with sepsis.

Animals↗

PubMed2000

Enhancing effect of saccharides on the mutagenicity of 2-chloro-4-methylthiobutanoic acid.

The mutagenicity of 2-chloro-4-methylthiobutanoic acid (CMBA), a nitrite-treated Sanma fish mutagen, in Salmonella typhimurium TA100 was enhanced by addition of D-glucose during the CMBA-treatment. Several other monosaccharides also enhanced the mutagenicity of CMBA, and the order of the enhancing potency was found to be D-mannose, D-glucose>D-fructose, D-ribose, D-galactose. A disaccharide, maltose, showed only little enhancement. No enhancement was found with L-glucose. We investigated whether saccharides affect uptake of [methyl-14C]CMBA into S. typhimurium TA100. Saccharides which enhanced CMBA-induced mutagenesis increased the uptake. L-Glucose did not enhance the uptake. There was good correlation between the enhanced mutagenesis and increased radioactivity in Salmonella, suggesting that the enhancing effect of monosaccharide on the CMBA-induced mutagenesis results from the enhanced uptake of the mutagen into bacteria.

Butyrates↗

PubMed1990

Hepatic and extrahepatic responses to insulin in NIDDM and nondiabetic humans. Assessment in absence of artifact introduced by tritiated nonglucose contaminants.

It is well established that patients with non-insulin-dependent diabetes mellitus (NIDDM) are resistant to insulin. However, the contribution of hepatic and extrahepatic tissues to insulin resistance remains controversial. The uncertainty may be at least in part due to errors introduced by the unknowing use in previous studies of impure isotopes to measure glucose turnover. To determine hepatic and extrahepatic responses to insulin in the absence of these errors, steady-state glucose turnover was measured simultaneously with [6-3H]- and [6-14C]glucose during sequential 5- and 4-h infusions of insulin at rates of 0.4 and 10 mU.kg-1.min-1 in diabetic and nondiabetic subjects. At low insulin concentrations, [6-3H]- and [6-14C]glucose gave similar estimates of glucose turnover. Hepatic glucose release was equal to but not below zero in the nondiabetic subjects, but persistent glucose release (P less than 0.001) and decreased glucose uptake (P less than 0.001) was observed in the diabetic patients. At high insulin concentrations, both isotopes underestimated glucose turnover during the 1st h after initiation of the high-dose insulin infusion. More time (P less than 0.05) was required to reachieve steady state in NIDDM than nondiabetic subjects. At steady state, [6-3H]- but not [6-14C]glucose systematically underestimated (P less than 0.05) glucose turnover in both groups due to the presence of a tritiated nonglucose contaminant. The percentage of radioactivity in plasma due to tritiated contaminants was linearly related to turnover.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Regional glucose metabolic rates in the human brain: a PET study.

With the purpose of determining the regional cerebral glucose metabolic rates (rCMRglu) in the normal human brain in resting state, we measured with PET and FOG, as the tracer, the distribution of regional radioactivity levels in the brains of seven young healthy volunteers. The individual brain images were stereotactically standardised with the help of a computerised brain atlas. In the next steps, the global cerebral glucose metabolic rate (gCMRglu) in the individual subjects was normalised to 34 mumol/ 100 g/min, followed by the averaging of the stereotactically standardised and metabolically normalised brain images across the subject population. In the final step, on the basis of high precision anatomical information, three-dimensional (3-D) volumes-of-interest (VOI's), covering over thirty anatomical structures in the brain, were created and the rCMRglu values inside the VOI's were determined in the averaged image. The present measurements of the rCMRglu values are in outstanding agreement with those determined in earlier quantitative PET-FDG studies, demonstrating that stereotactically standardised and metabolically normalised images of regional radioactivity distributions in the brain can be used for quantitative determination of rCMRglu values.

Adult↗

PubMed1985

Cerebral metabolism in fetal lamb after maternal infusion of ethanol.

Cerebral uptake of glucose and O2 (VCO2) was measured in 10 chronically catheterized fetal lambs during a control period, after a 1-h maternal infusion of ethanol (1.0 g X kg-1 X h-1) and 1-h postethanol infusion, to determine if alterations in cerebral metabolism might occur. Brachiocephalic artery and sagittal vein blood samples were analyzed for glucose, O2 content, blood gases, pH, and ethanol. Cerebral blood flow (Qc) was measured with a radioactive microsphere technique. VCO2 decreased significantly, from 140 +/- 13 mumol X 100 g-1 X min-1 during the control period to 91 +/- 8 (P less than 0.05) with the ethanol infusion, with a related fall in Qc, 177 +/- 12 to 104 +/- 9 ml X 100 g-1 X min-1 (P less than 0.001), the cerebral arteriovenous O2 difference being little changed. Cerebral glucose uptake, although decreased, was not significantly changed with the ethanol infusion, because the cerebral arteriovenous difference for glucose increased with the related fall in Qc. We conclude that maternal infusion of ethanol results in a decreased fetal VCO2 with a related fall in Qc. If prolonged, this decrease in cerebral oxidative metabolism might well affect cerebral development and provide a mechanism whereby chronic alcohol intake contributes to central nervous system growth anomalies and dysfunction of infants exposed to alcohol in utero.

Animals↗

PubMed1993

Monitoring in vivo oxidation of 14C-labelled substrates to 14CO2 by brain microdialysis.

Cultured brain cells oxidize glucose and numerous alternate substrates to CO2 for energy production, however, the importance of these observations to the intact brain have not been established. We have adapted in vivo brain microdialysis procedures to measure the rate of 14CO2 formation from 14C-glutamate, 14C-glutamine, and 14C-glucose in the hippocampus of awake unanesthetized free-moving rats. Two, 9 and 16 days after surgery (to implant guide cannulae) microdialysis probes were inserted into the guide cannulae and perfused with artificial CSF containing either 14C-glutamate, 14C-glutamine or 14C-glucose. Dialysate fractions were collected during 20 min intervals for determination of 14CO2. The amount of labelled 14CO2 increased for 40 to 60 min and then plateaued and remained relatively constant for at least 6 hours. When the probe was removed from the hippocampus and inserted into a vial containing non-radioactive CSF, 14CO2 production dropped rapidly. The quantity of 14CO2 recovered from glutamate was greater than from glucose or glutamine reflecting pool sizes, uptake characteristics and point of entry into oxidative pathways. The microdialysis system was verified by using model systems with cultured astrocytes suspended in media to simulate the brain. The present results indicate brain microdialysis may be used to study the role of alternate substrates in specific brain regions under varying physiological states.

Amino Acids↗

PubMed1980

Effect of substrate on release of myocardial norepinephrine and ventricular arrhythmias following reperfusion of the ischemic isolated working rat heart.

Isolated rat hearts were prelabeled with 3H-norepinephrine (NE), submitted to coronary artery ligation, and perfused through the left atrium with a modified Krebs-Henseleit solution containing 3 mM potassium and four different substrates: 5.5 mM glucose, 5.5 mM glucose plus 0.15 or 0.5 mM palmitate bound to albumin in a molar ratio of 6:1, and 11 mM glucose. The coronary artery ligature was removed after 30 min of perfusion of the ischemic working heart. With all substrates the release of radioactivity in the coronary effluent remained relatively constant during the ischemic period. Reperfusion was associated with a sudden release of radioactivity and of 3H-NE, but the intensity of the efflux was influenced by the nature of the perfusion substrate. The highest release was observed with 5.5 mM glucose and the lowest release in the presence of 0.15 mM palmitate. Intermediate and similar releases were seen with the two other substrates. On reperfusion of the ischemic heart, ventricular arrhythmias (tachycardia and fibrillation) were very marked with 5.5 mM glucose and in the presence of 0.5 mM palmitate. They were significantly delayed in the presence of 0.15 mM palmitate and almost absent with 11 mM glucose. These results do not show a relationship between the amount of NE liberated during the post-ischemic period and the extent of ventricular reperfusion arrhythmias. We conclude that either myocardial NE is not implicated in the genesis of reperfusion arrhythmias or that cardiac vulnerability to the arrhythmogenic effect of NE is influenced by the metabolic state of the myocardium, which is dependent on the nature of the perfusion substrate.

Animals↗

PubMed1975

In vivo measurement of brain glucose transport and metabolism employing glucose- -11C.

The radiopharmaceutical glucose--11C was used in vivo measurement of brain-glucose transport kinetics and metabolism in the rhesus monkey. Radiotracer was injected intravenously as a bolus. Radioactivity was continuously recorded from the head and from the arterial blood via an indwelling peripheral artery catheter for a collectionperiod of 2-3 min. To correct the reading obtained from the head for radioactivitycontained in blood, a second intravenous injection of the vascular tracer -15O-labeled carboxyhemoglobin was used. The method was tested in nine phencyclidine-anesthetized monkeys in which cerebral glucose metabolism (CMRGlc) was simultaneously measured by our method and by a standard method emplying the Fick principle. A highlysignificant correlation was found between the two methods of measuring CMRGlc (r =0.929). In addition, our model predicted a ratio of forward-to-reverse glucose flux across the blood-brain barrier (BBR) (1.37 plus or minus 0.23 SD), the brain-to-bloodglucose concentration ratio across the BBB (0.633 plus or minus 0.14), the relative tissue free-glucose space (17 plus or minus 7%), the brain free-glucose concentration (13.6plus or minus 8.5 mg/100 g of tissue), and the brain free-glucose turnover time (2.96 plus or minus 1.98 min). author

Animals↗

PubMed1976

Formation of glutamate and GABA in epileptogenic tissue from human hippocampus in vitro.

The levels of some amino acids and the incorporation rates of 14C from glucose and acetate were estimated in control human brain tissue and epileptogenic foci from human hippocampus incubated in glucose-saline medium. In the epileptogenic tissue the level of glutamine and the incorporation of radioactivity from both substrates into glutamine were lowered, mainly from acetate. These results suggest damaged glial metabolism. The relative increase of glutamate and decrease of glutamate formation in epileptogenic tissue were similar to the changes caused in rat brain slices by increased concentration of potassium in the incubation medium.

Acetates↗

PubMed1991

Substrate utilization for phosphatidylcholine synthesis by type II pneumocytes of neonatal rats.

Type II pneumocytes isolated from neonatal rat lungs, using an isolation procedure developed for adult rats, were found to be phenotypically stable and metabolically active in culture. The cells, purified by metrizamide gradient centrifugation and differential adherence, were capable of synthesizing phospholipids from 14C-labeled choline, palmitate, glucose, and acetoacetate. Regardless of the 14C-labeled substrates used, greater than two thirds of the radioactivity incorporated into phosphatidylcholine was recovered in disaturated phosphatidylcholine, the major component of surfactant phospholipids. The incorporation of palmitate into phosphatidylcholine and other phospholipids (i.e. phosphatidyl-ethanolamine, -glycerol, -serine, and -inositol) indicates that the neonatal type II cells have the capacity to produce surfactant lipids. The neonatal cells preferentially utilized acetoacetate over glucose as a precursor of phospholipids. In the adult type II cells, glucose was incorporated into phospholipids more rapidly than acetoacetate. The rate of glucose incorporation in the neonatal cells was enhanced by exogenous insulin. The preferential utilization of acetoacetate by the neonatal type II cells is consistent with the stimulated acetoacetyl CoA synthetase pathway in the lung. The depressed glucose incorporation into phospholipid, on the other hand, may be attributed to insulin insufficiency in the neonate.

Acetoacetates↗