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PubMed1991

Hepatocyte heterogeneity in uptake and metabolism of malate and related dicarboxylates in perfused rat liver.

1. In isolated perfused rat liver a near-maximal net malate uptake of about 120 nmol g-1 min-1 was observed at influent malate concentrations above 100 mumol l-1 and a half-maximal uptake at about 50 mumol l-1 in influent. 14CO2 production from added [U-14C]malate paralleled hepatic net malate uptake, however, 14CO2 production exceeded net malate uptake by 20-25%. This was observed in antegrade as well as in retrograde perfusions and regardless of whether NH4Cl was added to the influent perfusate. Stimulation of glutamine synthesis by NH4Cl only slightly affected net malate uptake and 14CO2 production, but resulted in a marked stimulation of [14C]glutamine release from the liver. 2. Because [U-14C]malate uptake by the liver (reflecting the influent/effluent concentration difference of labeled malate) could at least in part involve a malate/malate exchange mechanism, net malate uptake (as determined from the influent/effluent concentration difference of enzymatically assayable malate) may underestimate hepatic [U-14C]malate uptake. On the other hand, during metabolic steady states 14CO2 production from added [U-14C]malate can be considered as an upper limit estimate of [U-14C]malate uptake by the liver. Assuming that 14CO2 production equals [U-14C]malate uptake by the liver, extrapolation studies suggest that during maximal rates of NH4Cl-stimulated glutamine synthesis 80-110% of the [U-14]malate taken up by the liver was used for glutamine synthesis. This was true for retrograde and antegrade perfusions. Similar data, i.e. a 100-130% incorporation regardless of the direction of perfusion, were obtained when [U-14C]malate uptake was assumed to equal net malate uptake by the liver. 3. Substitution of Na+ in the perfusion fluid by choline abolished net malate uptake by the liver and inhibited 14CO2 production from [U-14C]malate by more than 90%. 4. 2-Oxoglutarate inhibited [14C]malate uptake and [1-14C]oxoglutarate uptake by the liver was inhibited by malate, fumarate, succinate and oxaloacetate, but not by aspartate and glutamate. Inhibition of [1-14C]oxoglutarate uptake and of 14CO2 production from added labeled 2-oxoglutarate by malate and fumarate seemed largely competitive. Malate, fumarate and succinate not only inhibited [1-14C]oxoglutarate uptake, but also stimulated the release of unlabeled 2-oxoglutarate from the liver. 5. The data are consistent with a predominant uptake of vascular malate by perivenous glutamine synthetase containing hepatocytes when glutamine synthesis is stimulated to Vmax values by NH4Cl. Malate and other citric acid cycle dicarboxylates, but not aspartate and glutamate, may compete with 2-oxoglutarate for uptake into perivenous glutamine synthesizing hepatocytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Cytoplasmic malate levels in maize root tips during K+ ion uptake determined by 13C-NMR spectroscopy.

13C-NMR spectroscopy was used to determine the level of cytoplasmic malate in maize root tips that exhibited different rates of malate synthesis. Intracellular malate was 13C-labeled at carbons 1 and 4 by perfusing root tips with 5 nM H13CO3-. This labeling reflects the activities of phosphoenolpyruvate carboxylase and malate dehydrogenase (production of [4-13C]malate), and fumarase (scrambling of 13C-label between C1 and C4 of malate). In vivo 13C-NMR spectra contained a clearly resolved resonance from cytoplasmic [4-13C]malate, while the resonance from cytoplasmic [1-13C]malate overlapped with others. After 90 min of H13CO3- treatment, 13C-labeling of organic acid pools had reached steady-state. Thereafter, the ratios [13C]malate/[12C + 13C]malate and [1-13C]malate/[4-13C]malate in tissue extracts remained constant; evidence is presented that these ratios were the same for both cytoplasmic and total cellular malate. Hence, the intensity of the cytoplasmic [4-13C]malate signal was proportional to the amount of cytoplasmic malate in root tips. Potassium sulfate stimulate malate synthesis in maize root tips, relative to root tips perfused with HCO3- alone; total cellular malate doubled after approx. 1 h of 5 mM K2SO4-treatment. Cytoplasmic malate increased from approx. 3.5 mM to approx. 7.5 mM within 45 min of the onset of K2SO4-treatment, declining slightly thereafter. The possible effects of these changing cytoplasmic malate concentration on the enzymes involved in malate metabolism are discussed.

Cytoplasm↗
PubMed1999

Effects of DL-malate on ruminal metabolism and performance of cattle fed a high-concentrate diet.

To determine the effects of DL-malate on ruminal metabolism, four steers equipped with ruminal cannulas were fed an 80% rolled grain (75% corn:25% wheat) diet twice daily with a DMI equal to 2.0% of BW (485+/-24.8 kg). DL-Malate was infused into the rumen on two consecutive days in 500 mL of phosphate buffer to provide 0, 27, 54, or 80 g of DL-malate/d. Ruminal pH linearly increased (P < .01) with DL-malate concentration and was greater (P < .01) for DL-malate than for the control steers (6.07 vs 5.77). DL-Malate treatment linearly decreased (P < .10) total VFA and tended to linearly increase (P = .10) acetate concentration. Propionate, butyrate, and L-lactate concentrations and acetate:propionate ratio were not affected (P > .10) by DL-malate. Three finishing studies were conducted to determine the effects of feeding DL-malate on growth rate and feed efficiency. In a 98-d experiment, 33 crossbred steers were randomly allotted in a Calan gate feeding system to three DL-malate levels (0, 40, and 80 g/d). Steers (initial weight = 367+/-4.5 kg) were fed a rolled corn-based diet twice daily. After 84 d on feed, gain efficiency (gain:feed) tended to improve with more DL-malate (linear, P < .10) and was 8.1% greater (P < .05) for DL-malate than for the control. The ADG linearly increased (P < .05) with more DL-malate and was 8.6% greater (P = .10) for DL-malate than for the control. After 98-d on feed, ADG was linearly increased (P = .09) by DL--malate, and the greatest increase occurred with 80 g of DL-malate. In the second performance study, 27 Angus steers were randomly allotted in a Calan gate feeding system to three DL-malate concentrations (0, 60, and 120 g/d). Steers (initial weight = 432+/-4.6 kg) were fed diets used in the first finishing study twice daily, but DL-malate was included during the 10-d step-up period. During the 10-d step-up period, feed efficiency and ADG linearly increased (P = .01) with more DL-malate. DL-Malate had little effect on steer and heifer performance or plasma constituents in a 113-d finishing study. Collectively, these results suggest that feeding DL-malate to cattle consuming high-grain diets alleviates subclinical acidosis, and it improved animal performance in two finishing studies.

Animal Feed↗
PubMed1990

The metabolism of malate by cultured rat brain astrocytes.

Since malate is known to play an important role in a variety of functions in the brain including energy metabolism, the transfer of reducing equivalents and possibly metabolic trafficking between different cell types; a series of biochemical determinations were initiated to evaluate the rate of 14CO2 production from L-[U-14C]malate in primary cultures of rat brain astrocytes. The 14CO2 production from labeled malate was almost totally suppressed by the metabolic inhibitors rotenone and antimycin A suggesting that most of malate metabolism was coupled to the electron transport system. A double reciprocal plot of the 14CO2 production from the metabolism of labeled malate revealed biphasic kinetics with two apparent Km and Vmax values suggesting the presence of more than one mechanism of malate metabolism in these cells. Subsequent experiments were carried out using 0.01 mM and 0.5 mM malate to determine whether the addition of effectors would differentially alter the metabolism of high and low concentrations of malate. Effectors studied included compounds which could be endogenous regulators of malate metabolism and metabolic inhibitors which would provide information regarding the mechanisms regulating malate metabolism. Both lactate and aspartate decreased 14CO2 production from 0.01 mM and 0.5 mM malate equally. However, a number of effectors were identified which selectively altered the metabolism of 0.01 mM malate including aminooxyacetate, furosemide, N-acetylaspartate, oxaloacetate, pyruvate and glucose, but had little or no effect on the metabolism of 0.5 mM malate. In addition, alpha-ketoglutarate and succinate decreased 14CO2 production from 0.01 mM malate much more than from 0.5 mM malate. In contrast, a number of effectors altered the metabolism of 0.5 mM malate more than 0.01 mM. These included methionine sulfoximine, glutamate, malonate, alpha-cyano-4-hydroxycinnamate and ouabain. Both the biphasic kinetics and the differential action of many of the effectors on the 14CO2 production from 0.01 mM and 0.5 mM malate provide evidence for the presence of more than one pool of malate metabolism in cultured rat brain astrocytes.

Animals↗