scholarly journals Competition among oxidizable substrates in brains of young and adult rats. Whole homogenates

1984 ◽  
Vol 219 (1) ◽  
pp. 125-130 ◽  
Author(s):  
L M Roeder ◽  
J T Tildon ◽  
J H Stevenson
Keyword(s):  
Brain Tissue ◽  
Ketone Bodies ◽  
Adult Brain ◽  
Adult Rats ◽  
Young Rats ◽  
Age Dependent ◽  
14Co2 Production ◽  
Presence And Absence

The rates of conversion into 14CO2 of D-(-)-3-hydroxy[3-14C]butyrate, [3-14C]acetoacetate, [6-14C]glucose and [U-14C]glutamine were measured in the presence and absence of unlabelled alternative oxidizable substrates in whole homogenates from the brains of young and adult rats. The addition of unlabelled glutamine resulted in decreased 14CO2 production from [6-14C]glucose in brain homogenates from both young and adult rats. In contrast, glucose had no effect on [U-14C]glutamine oxidation. In suckling animals, both 3-hydroxybutyrate and acetoacetate decreased the rate of oxidation of [6-14C]glucose, but in adults only 3-hydroxybutyrate had an effect, and to a lesser degree. The addition of unlabelled glucose markedly enhanced the rates of oxidation of both ketone bodies in adult brain tissue and had little or no effect in the young. The rate of production of 14CO2 from [U-14C]glutamine was increased by the addition of unlabelled ketone bodies in brain homogenates from young, but not from adult rats. In the converse situation, unlabelled glutamine added to 14C-labelled ketone bodies diminished 14CO2 production in young rats, but had no effect in adult animals. These results revealed a complex age-dependent pattern of interaction in which certain substrates apparently competed with each other, whereas an enhanced rate of 14CO2 production was found with others.

scholarly journals Competition among oxidizable substrates in brains of young and adult rats. Dissociated cells

1984 ◽  
Vol 219 (1) ◽  
pp. 131-135 ◽  
Author(s):  
L M Roeder ◽  
J T Tildon ◽  
D C Holman
Keyword(s):  
Plasma Membranes ◽  
Ketone Bodies ◽  
Age Groups ◽  
Cell Types ◽  
Adult Brain ◽  
Brain Cells ◽  
Adult Rats ◽  
Young Rats ◽  
Dissociated Cells ◽  
14Co2 Production

The rates of conversion of D-(-)-3-hydroxy[3-14C]butyrate, [3-14C]acetoacetate, [6-14C]glucose and [U-14C]glutamine into 14CO2 were measured in the presence and absence of alternative oxidizable substrates in intact dissociated cells from the brains of young and adult rats. When unlabelled glutamine was added to [6-14C]glucose or unlabelled glucose was added to [U-14C]glutamine, the rate of 14CO2 production was decreased in both young and adult rats. The rate of oxidation of 3-hydroxy[3-14C]butyrate was also decreased by the addition of unlabelled glutamine in both age groups, but in the reverse situation, i.e. unlabelled 3-hydroxybutyrate added to [U-14C]glutamine, only the brain cells from young rats were affected. No significant effects were seen when glutamine and acetoacetate were combined. The addition of either of the two ketone bodies to [6-14C]glucose markedly lowered the rate of 14CO2 production in young rats, but in the adult only 3-hydroxybutyrate was effective and the magnitude of decrease in the rate of [6-14C]glucose oxidation was much lower than in young animals. Unlabelled glucose decreased the rate of [3-14C]acetoacetate oxidation to a minor extent in brain cells from both age groups; when added to 3-hydroxy[3-14C]butyrate, glucose had no effect in young rats and greatly enhanced 14CO2 production in adult brain cells. Many of these patterns of substrate interaction in dissociated brain cells differ from those in whole homogenates; they may be a function of the plasma membranes and the role of a carrier-mediated transport system or a reflection of a difference in the population of cell types or subcellular organelles in these two preparations.

scholarly journals Subcellular localization of γ-aminobutyrate transaminase and glutamate dehydrogenase in adult rat brain. Evidence for at least two small glutamate compartments in brain

1975 ◽  
Vol 152 (3) ◽  
pp. 469-475 ◽  
Author(s):  
G L Reijnierse ◽  
H Veldstra ◽  
C J Van den Berg
Keyword(s):  
Monoamine Oxidase ◽  
Glutamate Dehydrogenase ◽  
Brain Tissue ◽  
Isocitrate Dehydrogenase ◽  
Brain Mitochondria ◽  
Adult Brain ◽  
Adult Rats ◽  
Adult Rat ◽  
Mitochondrial Fractions

The subcellular localizations of γ-aminobutyrate transaminase (EC 2.6.1.19) and glutamate dehydrogenase (EC 1.4.1.2) in brain tissue of adult rats were compared with each other and with those of NAD+-isocitrate dehydrogenase (EC 1.1.41) and monoamine oxidase (EC 1.4.3.4; kynuramine as substrate). Crude mitochondrial fractions from brain tissue were centrifuged in continuous sucrose density gradients. γ-Aminobutyrate transaminase and glutamate dehydrogenase were always found at a higher density than NAD+-isocitrate dehydrogenase and monoamine oxidase. When centrifuged for 1 h at 53 000gav., there was a slight difference between the distribution profiles of glutamate dehydrogenase and γ-aminobutyrate transaminase. This difference was larger when the centrifugation time was only 15 min. It is concluded that there are subpopulations of brain mitochondria with differing proportions of γ-aminobutyrate transaminase and glutamate dehydrogenase. The results are discussed in relation to evidence obtained with labelled precursors in vivo that there are at least two small glutamate compartments in adult brain.

Fish oil and treadmill exercise have age-dependent effects on episodic memory and oxidative state of the hippocampus

2017 ◽  
Vol 42 (5) ◽  
pp. 503-510 ◽  
Author(s):  
Patrícia Fortes Cavalcanti de Macêdo ◽  
Janatar Stella Vasconcelos de Melo ◽  
Laís Alves Ribeiro Costa ◽  
Glauber Rudá F. Braz ◽  
Shirley M. de Sousa ◽  
...  
Keyword(s):  
Episodic Memory ◽  
Fish Oil ◽  
Treadmill Exercise ◽  
Antioxidant Defenses ◽  
Dependent Manner ◽  
Sod Activity ◽  
Adult Rats ◽  
Young Rats ◽  
Age Dependent ◽  
Oxidative State

There is a growing interest to better understand how lifestyle choices can improve memory functions. Treadmill exercise and long-chain n-3 polyunsaturated fatty acids found in fish oil are able to stimulate hippocampal antioxidant defenses and improve memory. The aim was to test whether fish oil and exercise can improve rat’s performance on memory tasks and optimize hippocampal antioxidant state in an age-dependent manner. Therefore, young and adult rats were exercised and received fish oil during 4 weeks. The exercise was performed for 30 min/day, with the speed gradually increasing from the first to the last week. Afterwards, episodic memory was measured by the recognition of object identity and spatial location. Hippocampal oxidative state was investigated with the levels of malondialdehyde (MDA), carbonyls content, antioxidant enzymatic activity (superoxide dismutase (SOD), catalase (CAT)), and antioxidant nonenzymatic activity (reduced glutathione, sulfhydryl content). The adult rats treated with fish oil and exercise (FO&EX) were able to recognize object’s shape and placement; however, FO&EX young rats had impaired spatial recognition (p < 0.05). The FO&EX young rats did not have reduced MDA or carbonyl content, though either fish oil or exercise reduced MDA (p < 0.05) and carbonyl levels (p < 0.01). Exercise increased SOD (p < 0.001) and CAT activities (p < 0.05), and fish oil enhanced SOD activity (p < 0.05) in young rats. At adulthood, exercise increased MDA levels (p < 0.05), and FO&EX reduced MDA (p < 0.001). Finally, exercise and fish oil improved nonenzymatic antioxidant defense (p < 0.05) only in adult rats. Results support age-dependent effects of fish oil and exercise on memory and oxidative state of the hippocampus during either neurodevelopment or adulthood.

Age-Dependent Regional Mechanical Properties of the Rat Hippocampus and Cortex

2009 ◽  
Vol 132 (1) ◽  
Author(s):  
Benjamin S. Elkin ◽  
Ashok Ilankovan ◽  
Barclay Morrison
Keyword(s):  
Mechanical Properties ◽  
Elastic Modulus ◽  
Brain Injury ◽  
Brain Tissue ◽  
Compression Tests ◽  
Unconfined Compression ◽  
Tissue Stiffness ◽  
Adult Rats ◽  
Age Dependent ◽  
Indentation Strain

Age-dependent outcomes following traumatic brain injury motivate the study of brain injury biomechanics in experimental animal models at different stages of development. Finite element models of the rat brain are used to better understand the mechanical mechanisms behind these age-dependent outcomes; however, age- and region-specific rat brain tissue mechanical properties are required for biofidelity in modeling. Here, we have used the atomic force microscope (AFM) to measure region-dependent mechanical properties for subregions of the cortex and hippocampus in P10, P17, and adult rats. Apparent elastic modulus increased nonlinearly with indentation strain, and a nonlinear Ogden hyperelastic model was used to fit the force-deflection data. Subregional heterogeneous distributions of mechanical properties changed significantly with age. Apparent elastic modulus was also found to increase overall with age, increasing by >100% between P10 and adult rats. Unconfined compression tests (ε=−0.3) were performed on whole slices of the hippocampus and cortex of P10, P17, and adult rats to verify the mechanical properties measured with the AFM. Mean apparent elastic modulus at an indentation strain of 30% from AFM measurements for each region and age correlated well with the long-term elastic modulus measured from 30% unconfined compression tests (slope not significantly different from 1, p>0.05). Protein, lipid, and sulfated glycosaminoglycan content of the brain increased with age and were positively correlated with tissue stiffness, whereas water content decreased with age and was negatively correlated with tissue stiffness. These correlations can be used to hypothesize mechanistic models for describing the mechanical behavior of brain tissue as well as to predict relative differences between brain tissue mechanical properties of other species, at different ages, and for different regions based on differences in tissue composition.

scholarly journals Transfer of rhodamine-123 into the brain and cerebrospinal fluid of fetal, neonatal and adult rats

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Liam M. Koehn ◽  
Katarzyna M. Dziegielewska ◽  
Mark D. Habgood ◽  
Yifan Huang ◽  
Norman R. Saunders
Keyword(s):  
Cerebrospinal Fluid ◽  
Fetal Brain ◽  
Maternal Blood ◽  
Adult Brain ◽  
Rhodamine 123 ◽  
Patient Specific ◽  
Adult Rats ◽  
Blood Brain ◽  
The Brain ◽  
Brain Barriers

Abstract Background Adenosine triphosphate binding cassette transporters such as P-glycoprotein (PGP) play an important role in drug pharmacokinetics by actively effluxing their substrates at barrier interfaces, including the blood-brain, blood-cerebrospinal fluid (CSF) and placental barriers. For a molecule to access the brain during fetal stages it must bypass efflux transporters at both the placental barrier and brain barriers themselves. Following birth, placental protection is no longer present and brain barriers remain the major line of defense. Understanding developmental differences that exist in the transfer of PGP substrates into the brain is important for ensuring that medication regimes are safe and appropriate for all patients. Methods In the present study PGP substrate rhodamine-123 (R123) was injected intraperitoneally into E19 dams, postnatal (P4, P14) and adult rats. Naturally fluorescent properties of R123 were utilized to measure its concentration in blood-plasma, CSF and brain by spectrofluorimetry (Clariostar). Statistical differences in R123 transfer (concentration ratios between tissue and plasma ratios) were determined using Kruskal-Wallis tests with Dunn’s corrections. Results Following maternal injection the transfer of R123 across the E19 placenta from maternal blood to fetal blood was around 20 %. Of the R123 that reached fetal circulation 43 % transferred into brain and 38 % into CSF. The transfer of R123 from blood to brain and CSF was lower in postnatal pups and decreased with age (brain: 43 % at P4, 22 % at P14 and 9 % in adults; CSF: 8 % at P4, 8 % at P14 and 1 % in adults). Transfer from maternal blood across placental and brain barriers into fetal brain was approximately 9 %, similar to the transfer across adult blood-brain barriers (also 9 %). Following birth when placental protection was no longer present, transfer of R123 from blood into the newborn brain was significantly higher than into adult brain (3 fold, p < 0.05). Conclusions Administration of a PGP substrate to infant rats resulted in a higher transfer into the brain than equivalent doses at later stages of life or equivalent maternal doses during gestation. Toxicological testing of PGP substrate drugs should consider the possibility of these patient specific differences in safety analysis.

Developmental study of benzodiazepine effects on monosynaptic GABAA-mediated IPSPs of rat hippocampal neurons

1993 ◽  
Vol 70 (3) ◽  
pp. 1076-1085 ◽  
Author(s):  
C. Rovira ◽  
Y. Ben-Ari
Keyword(s):  
Hippocampal Neurons ◽  
Receptor Agonist ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Developmental Study ◽  
Type I ◽  
Gamma Aminobutyric Acid ◽  
Adult Rats ◽  
Young Rats ◽  
In Cells

1. The effects of type I (BZ1) and type II (BZ2) benzodiazepine receptor ligands on monosynaptic gamma-aminobutyric acid (GABA)A-mediated inhibitory postsynaptic potentials (IPSPs) and on responses to exogenously applied GABA were studied using intracellular recordings from CA3 pyramidal cells of rat hippocampal slices taken at different postnatal stages [postnatal day 4 (P4)-P35)]. 2. The effects of midazolam, a BZ1 and BZ2 receptor agonist, were tested on the monosynaptic IPSPs at different stages. Monosynaptic, bicuculline-sensitive IPSPs were evoked by hilar stimulation in presence of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) antagonists [6-cyano-7-nitroquinoxaline-2,3-dione (10 microM) and D(-)2-amino-5-phosphonopentanoic acid (50 microM)]. Midazolam at 300 nM maximally increased the duration and amplitude of monosynaptic GABAA-mediated IPSPs in neurons from pups (P4-P6, n = 6) and young (P7-P12, n = 8) and adult (P25-P35, n = 9) rats. All the effects of midazolam on IPSPs were reversed by the antagonist Ro 15-1788 (10 microM). 3. The effect of midazolam was also tested on the response to exogenously applied GABA (5 mM) in the presence of tetrodotoxine [TTX (1 microM)]. In neurons from young rats (n = 9), midazolam (1 nM-1 microM) did not change the responses to exogenously applied GABA, whereas in adult rats (n = 8) midazolam maximally increased GABA currents at 30 nM. 4. The effect of zolpidem, a BZ1 receptor agonist, was tested on monosynaptic IPSPs and GABA currents at different stages. Zolpidem (10 nM-1 microM) was inactive in cells from young rats (n = 12). In neurons from adult rats, zolpidem maximally increased the duration and amplitude of the monosynaptic IPSPs at 300 nM (n = 5) and the amplitude of GABA current at 30-100 nM (n = 5). 5. Methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) (300 nM), an inverse agonist of BZ1 and BZ2 receptors, decreased the amplitude and duration of monosynaptic IPSPs in neurons from pups (n = 3) and young (n = 4) and adult (n = 5) rats. In all cases, full recovery was obtained after exposure to R0 15-1788 (10 microM). DMCM (300 nM-10 microM) failed to reduce GABA responses in cells from young (n = 3) or adult (n = 7) rats. 6. Results indicate that the regulation by benzodiazepine of GABAA-mediated IPSPs varies with the developmental stage.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Age- and location-dependent differences in store depletion-induced h-channel plasticity in hippocampal pyramidal neurons

2014 ◽  
Vol 111 (6) ◽  
pp. 1369-1382 ◽  
Author(s):  
Ann M. Clemens ◽  
Daniel Johnston
Keyword(s):  
Pyramidal Neurons ◽  
Cyclopiazonic Acid ◽  
Neural Basis ◽  
Adult Rats ◽  
Hippocampal Pyramidal Neurons ◽  
Store Depletion ◽  
Whole Cell Patch Clamp ◽  
Age Dependent ◽  
Adaptive Processes ◽  
Cellular Dysfunction

Disruptions of endoplasmic reticulum (ER) Ca2+ homeostasis are heavily linked to neuronal pathology. Depletion of ER Ca2+ stores can result in cellular dysfunction and potentially cell death, although adaptive processes exist to aid in survival. We examined the age and region dependence of one postulated, adaptive response to ER store-depletion (SD), hyperpolarization-activated cation-nonspecific ( h)-channel plasticity in neurons of the dorsal and ventral hippocampus (DHC and VHC, respectively) from adolescent and adult rats. With the use of whole-cell patch-clamp recordings from the soma and dendrites of CA1 pyramidal neurons, we observed a change in h-sensitive measurements in response to SD, induced by treatment with cyclopiazonic acid, a sarcoplasmic reticulum/ER Ca2+-ATPase blocker. We found that whereas DHC and VHC neurons in adolescent animals respond to SD with a perisomatic expression of SD h plasticity, adult animals express SD h plasticity with a dendritic and somatodendritic locus of plasticity in DHC and VHC neurons, respectively. Furthermore, SD h plasticity in adults was dependent on membrane potential and on the activation of L-type voltage-gated Ca2+ channels. These results suggest that cellular responses to the impairment of ER function, or ER stress, are dependent on brain region and age and that the differential expression of SD h plasticity could provide a neural basis for region- and age-dependent disease vulnerabilities.

Age-dependent activation of PKC isoforms by angiotensin II in the proximal nephron

2001 ◽  
Vol 281 (3) ◽  
pp. R861-R867 ◽  
Author(s):  
Dianne M. Boesch ◽  
Jeffrey L. Garvin
Keyword(s):  
Specific Binding ◽  
Age Groups ◽  
Proximal Tubules ◽  
Ang Ii ◽  
Fluid Absorption ◽  
Adult Rats ◽  
Young Rats ◽  
Age Related ◽  
Pkc Isoforms ◽  
Pkc Β

ANG II increases fluid absorption in proximal tubules from young rats more than those from adult rats. ANG II increases fluid absorption in the proximal nephron, in part, via activation of protein kinase C (PKC). However, it is unclear how age-related changes in ANG II-induced stimulation of the PKC cascade differ as an animal matures. We hypothesized that the response of the proximal nephron to ANG II decreases as rats mature due to a reduction in the amount and activation of PKC rather than a decrease in the number or affinity of ANG II receptors. Because PKC translocates from the cytosol to the membrane when activated, we first measured PKC activity in the soluble and particulate fractions of proximal tubule homogenates exposed to vehicle or 10−10 M ANG II from young (26 ± 1 days old) and adult rats (54 ± 1 days old). ANG II increased PKC activity to the same extent in homogenates from young rats (from 0.119 ± 0.017 to 0.146 ± 0.015 U/mg protein) ( P < 0.01) and adult rats (from 0.123 ± 0.020 to 0.156 ± 0.023 U/mg protein) ( P < 0.01). Total PKC activity did not differ between groups (0.166 ± 0.018 vs. 0.181 ± 0.023). We next investigated whether activation of the α-, β-, and γ-PKC isoforms differed by Western blot. In homogenates from young rats, ANG II significantly increased activated PKC-α from 40.2 ± 6.5 to 60.2 ± 9.5 arbitrary units (AU) ( P < 0.01) but had no effect in adult rats (46.1 ± 5.1 vs. 48.5 ± 8.2 AU). Similarly, ANG II increased activated PKC-γ in proximal tubules from young rats from 47.9 ± 13.2 to 65.6 ± 16.7 AU ( P < 0.01) but caused no change in adult rats. Activated PKC-β, however, increased significantly in homogenates from both age groups. Specifically, activated PKC-β increased from 8.6 ± 1.4 to 12.2 ± 2.1 AU ( P < 0.01) in homogenates from nine young rats and from 19.0 ± 5.5 to 25.1 ± 7.1 AU ( P < 0.01) in homogenates from 12 adult rats. ANG II did not alter the amount of soluble PKC-α, -β, and -γ significantly. The total amount of PKC-α and -γ did not differ between homogenates from young and adult rats, whereas the total amount of PKC-β was 59.7 ± 10.7 and 144.9 ± 41.8 AU taken from young and adult rats, respectively ( P < 0.05). Maximum specific binding and affinity of ANG II receptors were not significantly different between young and adult rats. We concluded that the primary PKC isoform activated by ANG II changes during maturation.

scholarly journals Competition of glycerol with other oxidizable substrates in rat brain

1986 ◽  
Vol 237 (1) ◽  
pp. 47-51 ◽  
Author(s):  
M C McKenna ◽  
L I Bezold ◽  
S J Kimatian ◽  
J T Tildon
Keyword(s):  
Rat Brain ◽  
Glutamine Metabolism ◽  
Glycerol Oxidation ◽  
Adult Rats ◽  
Adult Rat ◽  
Rat Pups ◽  
Age Related ◽  
Adult Rat Brain ◽  
14Co2 Production ◽  
Age Related Changes

The rate of conversion of [1,3-14C]glycerol into 14CO2 was measured in the presence and absence of unlabelled alternative substrates in whole homogenates from the brains of young (4-6 and 18-20 days old) and adult rats. Unlabelled glucose decreased 14CO2 production from [1,3-14C]glycerol by about 40% at all ages studied. Unlabelled 3-hydroxybutyrate significantly decreased the 14CO2 production from both low (0.2 mM) and high (2.0 mM) concentrations of glycerol in 4-6- and 18-20-day-old rat pups. However, the addition of 3-hydroxybutyrate had no effect on the rate of 14CO2 production from 2.0 mM-glycerol in adult rats, suggesting that the interaction of 3-hydroxybutyrate with glycerol in adult rat brain is complex and may be related to the biphasic kinetics previously reported for glycerol oxidation. Unlabelled glutamine decreased the production of 14CO2 by brain homogenates from 18-20-day-old and adult rats, but not in 4-6-day-old rat pups. In the converse situation, the addition of unlabelled glycerol to whole brain homogenates had little effect on the rate of 14CO2 production from [6-14C]glucose, 3-hydroxy[3-14C]butyrate and [U-14C]glutamine, although some significant differences were noted. Collectively these results suggest that glycerol and these other substrates may be metabolized in separate subcellular compartments in brain such that the products of glucose, 3-hydroxybutyrate and glutamine metabolism can dilute the oxidation of glycerol, but the converse cannot occur. The data also demonstrate that there are complex age-related changes in the interaction of glycerol with 3-hydroxybutyrate and glutamine. The fact that glycerol oxidation was only partially suppressed by the addition of 1-5 mM-glucose, -3-hydroxybutyrate or -glutamine could also suggest that glycerol may be selectively utilized as an energy substrate in some discrete brain region.

scholarly journals Long-term modulation of type L pyruvate kinase activity in young and mature rats

1982 ◽  
Vol 204 (1) ◽  
pp. 329-338 ◽  
Author(s):  
Milinda E. James ◽  
James B. Blair
Keyword(s):  
Protein Synthesis ◽  
Pyruvate Kinase ◽  
Total Protein ◽  
Time Course ◽  
Enzyme Level ◽  
Enzyme Synthesis ◽  
Synthesis Rate ◽  
Adult Rats ◽  
Young Rats ◽  
Sucrose Diet

The regulation of type L pyruvate kinase concentrations in liver of young (35–45 days old) and adult (60–85 days old) rats starved and re-fed a 71% sucrose diet was investigated. Re-feeding is accompanied by an increase in the enzyme level in liver determined kinetically and immunologically. A constant ratio of kinetic activity to immunological activity was observed under all conditions examined, indicating that activity changes are the result of a regulation of synthesis or degradation and not an interconversion between kinetically active and inactive forms of the enzyme. Synthesis of pyruvate kinase was directly examined by using hepatocytes isolated from starved and re-fed rats. A stimulation of pyruvate kinase synthesis is observed on re-feeding. This increase in synthesis of pyruvate kinase is retained by the isolated hepatocyte for up to 7h in the absence of hormonal stimuli. Administration of glucagon (1μm) to the isolated hepatocytes had no influence on synthesis of pyruvate kinase and no evidence for a glucagon-directed degradation of the enzyme was found. Re-feeding the rat was followed by a transient increase in the synthesis of pyruvate kinase. The peak rate of synthesis was observed before a detectable increase in the enzyme concentration. After a rapid synthesis period, a new steady-state level of the enzyme was achieved and synthesis rates declined. The time course and magnitude for the response to the sucrose diet was dependent on the age of the rat. In young rats, an increase in pyruvate kinase synthesis is observed within 6h and peak synthesis occurs at 11h after re-feeding sucrose. The peak synthesis rate for pyruvate kinase for young rats represents approx. 1% of total protein synthesis. With adult rats, increased pyruvate kinase synthesis is not observed for 11h, with peak synthesis occurring at 24h after re-feeding. In the older rats, peak pyruvate kinase synthesis constitutes greater than 4% of total protein synthesis. Continued re-feeding of the adult rat beyond 24h is accompanied by a decline of pyruvate kinase synthesis to approx. 1.5% of total protein synthesis. The concentration of the enzyme, however, does not decline during this period, suggesting that control of pyruvate kinase degradation as well as synthesis occurs.

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