Some effects of glucose concentration and anoxia on glycolysis and metabolite concentrations in the perfused liver of fetal guinea pig

Faulkner, Anne; Jones, C. T.

doi:10.1016/0304-4165(78)90255-6

Cited by 7 publications

(3 citation statements)

References 44 publications

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“…Complete medium contains 25 mM glucose, whereas supplementation of the starvation medium with as little as 5 µM prevents formation of starvation-induced filopodia (Table S3). This concentration is much lower than necessary for glycolysis (Faulkner and Jones, 1978); therefore, we propose that the prevention of Myo19-mitochondria localization to starvation-induced filopodia is mediated by glucose signaling events rather than metabolic homeostasis. In support of this, glucose starvation results in activation of a unique signature of phosphotyrosine signaling associated with focal adhesions, actin remodeling and F-actin stabilization (Arber et al, 1998;Miki et al, 1998;Graham et al, 2012).…”

Section: Discussionmentioning

confidence: 81%

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

Shneyer

Ušaj

Henn

2016

Journal of Cell Science

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Mitochondria respond to environmental cues and stress conditions. Additionally, the disruption of the mitochondrial network dynamics and its distribution is implicated in a variety of neurodegenerative diseases. Here, we reveal a new function for Myo19 in mitochondrial dynamics and localization during the cellular response to glucose starvation. Ectopically expressed Myo19 localized with mitochondria to the tips of starvation-induced filopodia. Corollary to this, RNA interference (RNAi)-mediated knockdown of Myo19 diminished filopodia formation without evident effects on the mitochondrial network. We analyzed the Myo19-mitochondria interaction, and demonstrated that Myo19 is uniquely anchored to the outer mitochondrial membrane (OMM) through a 30-45-residue motif, indicating that Myo19 is a stably attached OMM molecular motor. Our work reveals a new function for Myo19 in mitochondrial positioning under stress.

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Section: Discussionmentioning

confidence: 81%

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

Shneyer

Ušaj

Henn

2016

Journal of Cell Science

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“…They also confirm the stimulation of glycolysis by anoxia and show, in addition, that incubation of hepatocytes from fed rats particularly in the presence of high glucose concentrations greatly diminishes the wellknown effect of anoxia on liver adenine nucleotides (Hems & Brosnan, 1970;Faupel et al, 1972;Sharma et al, 1980;Vincent et al, 1982 Uyeda et al, 1981) and the stimulation of glycolysis by glucose is best explained by the accumulation of this effector. Stimulation of glycolysis by anoxia, often referred to as the Pasteur effect, also involves the regulation of phosphofructokinase 1 (for reviews, see Krebs, 1972;Newsholme & Start, 1973;Ramaiah, 1974;Sols, 1976 Pi (Hems & Brosnan, 1970;Faupel et al, 1972;Faulkner & Jones, 1978;Sharma et al, 1980;Vincent et al, 1982; the present paper). IMP, hypoxanthine and uric acid, degradative products of the adenine nucleotides that accumulate during anoxia or ischaemia (Weber et al, 1977;Sharma, 1981;Vincent et al, 1982) From results reported here and previously (Van Schaftingen et al, 1980b;Hue et al, 198 la,b, 1982) (Hue et al, 1982).…”

Section: Stimulation Ofglycolysis By Glucose and Anoxiamentioning

confidence: 88%

Role of fructose 2,6-bisphosphate in the stimulation of glycolysis by anoxia in isolated hepatocytes

Hue¹

1982

Biochemical Journal

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1. Incubation of hepatocytes from fed or starved rats with increasing glucose concentrations caused a stimulation of lactate production, which was further increased under anaerobic conditions. 2. When glycolysis was stimulated by anoxia, [fructose 2,6-bis-phosphate] was decreased, indicating that this ester could not be responsible for the onset of anaerobic glycolysis. In addition, the effect of glucose in increasing [fructose 2,6-bisphosphate] under aerobic conditions was greatly impaired in anoxic hepatocytes. [Fructose 2,6-bisphosphate] was also diminished in ischaemic liver, skeletal muscle and heart. 3. The following changes in metabolite concentration were observed in anaerobic hepatocytes: AMP, ADP, lactate and L-glycerol 3-phosphate were increased; ATP, citrate and pyruvate were decreased: phosphoenolpyruvate and hexose 6-phosphates were little affected. Concentrations of adenine nucleotides were, however, little changed by anoxia when hepatocytes from fed rats were incubated with 50 mM-glucose. 4. The activity of ATP:fructose 6-phosphate 2-phosphotransferase was not affected by anoxia but decreased by cyclic AMP. 5. The role of fructose 2,6-bisphosphate in the regulation of glycolysis is discussed.

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“…4) is essentially as that found in dog intestines by Chiu et al (1970) and in bullfrog gastric mucosa by Spenney and Bhown (1977) and intestinal mucosa (Chiu et al, 1970). It is well-known that during hypoxia the cellular content of ATP rapidly declines (Chiu et al, 1970;Faulkner and Jones, 1978). It is also well-known that reduced cellular content of ATP parallels the degree of injury to gastric (Spenney and Bhown, 1977) and intestinal mucosa (Chiu et al, 1970).…”

Section: Discussionmentioning

confidence: 99%

Hypothermic Perfusion of Isolated Cat Small Intestine Metabolic Changes Related to Mucosal Lesions

Daehlin¹,

Romslo²,

Nilsen³

et al. 1979

Eur Surg Res

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Cat small intestines were perfused for 48 h under hypothermia (4–8 °C) with a buffered salt-albumin solution. Mucosal lesions developed with subepithelial edema and villous desquamation and corresponding cellular dysfunction. The morphological changes correlated to a decrease in the content of adenosine triphosphate of the intestine and a release of intracellular enzymes to the perfusate and the intestinal secretions. The change in enzymatic activity was most pronounced for alkaline phosphatase. Determination of adenosine triphosphate of the intestine together with cellular enzymes of the perfusate and the intestinal secretions should be considered a rapid and reliable method to assess the degree of cellular damage during hypothermic perfusion.

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Some effects of glucose concentration and anoxia on glycolysis and metabolite concentrations in the perfused liver of fetal guinea pig

Cited by 7 publications

References 44 publications

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

Role of fructose 2,6-bisphosphate in the stimulation of glycolysis by anoxia in isolated hepatocytes

Hypothermic Perfusion of Isolated Cat Small Intestine Metabolic Changes Related to Mucosal Lesions

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