Protein Synthesis Rates in Rats with Portacaval Shunts

Dunlop, David S.; Kaufman, H.; Zanchin, Giorgio; Lajtha, Ábel

doi:10.1111/j.1471-4159.1984.tb05413.x

Cited by 10 publications

(14 citation statements)

References 8 publications

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“…These findings are consistent with studies in isolated, intact hippocampus from adult mice showing that extracellular glutamate was oxidized in greater amounts with increasing concentration, and glutamate reduced oxidation of glucose (Dunlop et al, 1984). Recently, the glutamate transporter was shown to form multi-enzyme complexes with glycolytic enzymes and mitochondria that facilitate oxidation of very low levels (8 μmol/L) of glutamate as it is transported into the astrocytes (Genda et al, 2011; Bauer et al, 2012).…”

Section: Glutamate Is An Important Astrocytic Energy Sourcesupporting

confidence: 90%

“…Because astrocytes have much greater glutamate oxidative rates than GABAergic neurons and the corresponding rates in glutamatergic neurons were negligible, glutamate degradation is predominantly astrocytic (Hertz et al, 1988; Waagepetersen et al, 2002). The conclusion that glutamate is an important energy substrate for astrocytes is strongly supported by (i) the glucose-sparing actions of extracellular glutamate in cultured astrocytes (Swanson et al, 1990; Yu et al, 1992; Peng et al, 2001; Qu et al, 2001) and in isolated, intact hippocampus from adult mice (Dunlop et al, 1984), (ii) robust stimulation of astrocytic respiration by glutamate (Eriksson et al, 1995), and (iii) similar rates of astrocytic oxygen consumption with either glucose or glutamate as sole substrate (Hertz and Hertz, 2003). Under steady state conditions, oxidation of glutamate and GABA approximates the anaplerotic rate, which is ~15% of the total pyruvate oxidation rate (Hertz, 2011; Rothman et al, 2011), and glutamate synthesis and degradation in astrocytes produces nearly as much ATP as direct oxidation of glucose (Hertz et al, 1999; Hertz et al, 2007).…”

Section: Glutamate Is An Important Astrocytic Energy Sourcementioning

confidence: 99%

“…However, more laboratories have reported that glutamate treatment caused either no change or reduced glucose consumption (Dunlop et al, 1984; Swanson et al, 1990; Hertz et al, 1998; Peng et al, 2001; Qu et al, 2001; Liao and Chen, 2003; Dienel and Cruz, 2004) and no change or diminished lactate release (Dunlop et al, 1984; Gramsbergen et al, 2003; Liao and Chen, 2003; Dienel and Cruz, 2004). The basis for these phenotypic differences has never been established, but it probably lies within the culturing procedures (Hertz et al, 1998).…”

Section: Astrocytic Energetics Glycolysis and Lactate Shuttlingmentioning

confidence: 99%

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Astrocytic energetics during excitatory neurotransmission: What are contributions of glutamate oxidation and glycolysis?

Dienel

2013

Neurochemistry International

104

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Astrocytic energetics of excitatory neurotransmission is controversial due to discrepant findings in different experimental systems in vitro and in vivo. The energy requirements of glutamate uptake are believed by some researchers to be satisfied by glycolysis coupled with shuttling of lactate to neurons for oxidation. However, astrocytes increase glycogenolysis and oxidative metabolism during sensory stimulation in vivo, indicating that other sources of energy are used by astrocytes during brain activation. Furthermore, glutamate uptake into cultured astrocytes stimulates glutamate oxidation and oxygen consumption, and glutamate maintains respiration as well as glucose. The neurotransmitter pool of glutamate is associated with the faster component of total glutamate turnover in vivo, and use of neurotransmitter glutamate to fuel its own uptake by oxidation-competent perisynaptic processes has two advantages, substrate is supplied concomitant with demand, and glutamate spares glucose for use by neurons and astrocytes. Some, but not all, perisynaptic processes of astrocytes in adult rodent brain contain mitochondria, and oxidation of only a small fraction of the neurotransmitter glutamate taken up into these structures would be sufficient to supply the ATP required for sodium extrusion and conversion of glutamate to glutamine. Glycolysis would, however, be required in perisynaptic processes lacking oxidative capacity. Three lines of evidence indicate that critical cornerstones of the astrocyte-to-neuron lactate shuttle model are not established and normal brain does not need lactate as supplemental fuel: (i) rapid onset of hemodynamic responses to activation delivers oxygen and glucose in excess of demand, (ii) total glucose utilization greatly exceeds glucose oxidation in awake rodents during activation, indicating that the lactate generated is released, not locally oxidized, and (iii) glutamate-induced glycolysis is not a robust phenotype of all astrocyte cultures. Various metabolic pathways, including glutamate oxidation and glycolysis with lactate release, contribute to cellular energy demands of excitatory neurotransmission.

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Section: Glutamate Is An Important Astrocytic Energy Sourcesupporting

confidence: 90%

Section: Glutamate Is An Important Astrocytic Energy Sourcementioning

confidence: 99%

Section: Astrocytic Energetics Glycolysis and Lactate Shuttlingmentioning

confidence: 99%

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Astrocytic energetics during excitatory neurotransmission: What are contributions of glutamate oxidation and glycolysis?

Dienel

2013

Neurochemistry International

104

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“…Construction of a portacaval anastomosis alone induces, besides portasystemic shunting of gut derived blood, a relative and absolute reduction of liver mass. 15-17 37 Urea synthesis capacity is limited in portacaval shunted rats, probably related to the reduced liver mass. '5"6 To these effects of portacaval anastomosis alone, the effects of chronic bile duct ligation were added.…”

Section: Discussionmentioning

confidence: 99%

Intestinal glutamine and ammonia metabolism during chronic hyperammonaemia induced by liver insufficiency.

Dejong

Deutz

Soeters

1993

Gut

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During liver insufficiency, besides portasystemic shunting, high arterial glutamine concentrations could enhance intestinal glutamine consumption and ammonia generation, thereby aggravating hyperammonaemia. To investigate this hypothesis, portal drained viscera (intestines) fluxes and jejunal tissue concentrations of ammonia and glutamine were measured in portacaval shunted rats with a ligated bile duct, portacaval shunted, and sham operated rats, seven and 14 days after surgery, and in normal unoperated controls. Effects of differences in food intake were minimised by pair feeding portacaval shunted and sham operated with portacaval shunted rats with biliary obstruction. At both time points, arterial ammonia was increased in the groups with liver insufficiency. Also, arterial glutamine concentration was raised in ali operated groups compared with normal unoperated controls. At both time points, ammonia production by portal drained viscera was reduced in portacaval shunted rats with biliary obstruction, portacaval shunted, and sham operated rats compared with normal unoperated controls, and no major differences were found between these operated groups. At day 7 in ali operated groups glutamine uptake by portal drained viscera was lower than in normal unoperated controls, but no major differences were found at day 14. These experiments show that ammonia generation by portal drained viscera remains unchanged in rats with chronic liver insufficiency despite alterations in arterial glutamine concentrations and intestinal glutamine uptake. The hyperammonaemia seems to be mainly determined by the portasystemic shunting. (Gut 1993; 34: 24 November 1992 Ammonia is still considered to be of crucial importance in the pathogenesis of hepatic encephalopathy.' The gut and kidney are generally considered to be the most important sites of ammonia production.2'-In the gut, the main sources of ammonia production are the bacterial breakdown of urea2 367 and the mucosal utilisation of glutamine as an energy substrate.2 37I In the physiological situation virtually all ammonia generated in the gut is immediately cleared by hepatic urea synthesis, and thus hepatic venous ammonia concentrations are lower than arterial concentrations. Therefore, in healthy subjects, systemic ammonia concentrations are probably mainly set by the interaction between renal ammonia production and ammonia consumption by other organs. During liver cirrhosis induced by chronic liver disease this situation changes drastically, because ammonia generated in the intestines bypasses hepatic clearance by intra or extrahepatic portasystemic shunts.910 Also, the diminished urea synthesis and glutamine synthetase capacity9' may reduce ammonia detoxification in the liver. These combined factors probably cause the systemic hyperammonaemia found during liver insufficiency.It has been suggested that systemic hyperammonaemia during chronic liver failure leads to enhanced ammonia detoxification via alternative pathways.'2 It is generally believed that the ener...

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“…129 In contrast, another study in PCA rats showed no difference in the rate of protein synthesis in different organs. 130 An increased skeletal muscle proteolysis mediated by the ubiquitin proteasome pathway has been described in the bile duct ligated rat. 131 However, the bile duct ligated rat as a model of cirrhosis differs from human cirrhosis because secondary biliary cirrhosis in humans is extremely rare and steatorrhea and malabsorption that accompany this procedure affect the muscle mass independent of cirrhosis.…”

Section: Pathogenesis and Mechanisms Of Sarcopenia In Cirrhosismentioning

confidence: 99%

Malnutrition in Cirrhosis: Contribution and Consequences of Sarcopenia on Metabolic and Clinical Responses

Periyalwar¹,

Dasarathy²

2012

Clinics in Liver Disease

215

232

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Protein Synthesis Rates in Rats with Portacaval Shunts

Cited by 10 publications

References 8 publications

Astrocytic energetics during excitatory neurotransmission: What are contributions of glutamate oxidation and glycolysis?

Astrocytic energetics during excitatory neurotransmission: What are contributions of glutamate oxidation and glycolysis?

Intestinal glutamine and ammonia metabolism during chronic hyperammonaemia induced by liver insufficiency.

Malnutrition in Cirrhosis: Contribution and Consequences of Sarcopenia on Metabolic and Clinical Responses

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