INFLUENCES OF THYROXINE AND INSULIN ON THE TURNOVER AND FATE OF HIGH-ENERGY PHOSPHATE

1964 ◽  
Vol 42 (6) ◽  
pp. 777-786 ◽  
Author(s):  
Dorothy S. Dow
Keyword(s):  
Skeletal Muscle ◽  
Energy Transfer ◽  
Adenosine Triphosphate ◽  
Cell Structure ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Nucleoside Phosphorylase ◽  
Mitochondrial Permeability ◽  
Energy Acceptor

Ingestion by the weanling rat of thyroxine in an amount greatly in excess of physiological requirements resulted in significant increases in the rates of turnover of the high-energy compounds phosphocreatine (PC), adenosine diphosphate (ADP), and adenosine triphosphate (ATP) and in significant decreases in their concentrations in skeletal muscle. Nucleoside phosphorylase and myokinase activities and rates of pyrophosphate splitting of ATP and of utilization of ATP for nuclear syntheses were unaltered in thyrotoxic muscle. The findings suggest that increased extramitochondrial utilization of ATP for glycolysis may be the factor responsible for the increased phosphorylating capacity of the thyrotoxic animal. An effect of thyroxine on mitochondrial permeability as well as on rate of formation of the high-energy intermediate would appear to explain the observed results.A further enhancement of the already markedly elevated thyrotoxic rate of phosphorylation was effected by the superimposition of insulin. Insulin also effected increases in the concentrations of the high-energy compounds. It is apparent that insulin acts by reducing the utilization of ATP for phosphorylation of glucose and thus increases the mitochondrial availability of high-energy acceptor. This increased mitochondrial affinity for high-energy compounds results in an enhancement of mitochondrial energy transfer processes.The findings appear to involve both thyroxine and insulin in the control of cell structure.

High Energy Phosphates During Hibernation and Arousal in the Ground Squirrel

1958 ◽  
Vol 195 (1) ◽  
pp. 233-236 ◽  
Author(s):  
Marilyn L. Zimny ◽  
Roy Gregory
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Adenosine Triphosphate ◽  
Ground Squirrel ◽  
Inorganic Phosphate ◽  
Liver Glycogen ◽  
High Energy ◽  
Ground Squirrels ◽  
High Energy Phosphates ◽  
High Energy Phosphate

Biochemical levels of inorganic phosphate, adenosine triphosphate, phosphocreatine and glycogen were determined on cardiac muscle, skeletal muscle and liver samples from hibernated 13-striped ground squirrels and those allowed to awaken for intervals of 7.5, 15 and 30 minutes. Cardiac muscle glycogen increases during hibernation apparently at the expense of skeletal muscle and liver glycogen. Glycolysis occurs in these tissues during early arousal, followed later by glycogenesis. Adenosine triphosphate is maintained in both cardiac and skeletal muscle during hibernation and is used as an energy source during arousal. It appears that glycolysis is important in resynthesizing phosphocreatine. From this study of periods of relatively low and high metabolic demands we conclude that phosphocreatine is a ‘transport’ form of high-energy phosphate forming adenosine triphosphate from the phosphate pool when and where needed in the cycle of intermediary metabolism.

Differential energetic response of brain vs. skeletal muscle upon glycemic variations in healthy humans

2008 ◽  
Vol 294 (1) ◽  
pp. R12-R16 ◽  
Author(s):  
Kerstin M. Oltmanns ◽  
Uwe H. Melchert ◽  
Harald G. Scholand-Engler ◽  
Maria C. Howitz ◽  
Bernd Schultes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Underlying Mechanism ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
High Energy Phosphate ◽  
Available Energy ◽  
Healthy Humans ◽  
High Energy Phosphate Metabolism ◽  
The Brain

The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using 31P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by 31P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain ( P = 0.013), while there was a similar trend in the hypopglycemic condition ( P = 0.055). Skeletal muscle content remained constant in both conditions ( P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to −4%) revealed clear divergent effects in both conditions ( P < 0.05). These effects were reflected by PCr/Pi ratio ( P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia ( P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.

Control mechanisms in blood fluidity: role of adenosine triphosphate

1963 ◽  
Vol 18 (6) ◽  
pp. 1105-1110 ◽  
Author(s):  
L. O. Pilgeram ◽  
D. A. Loegering
Keyword(s):  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
High Energy ◽  
Control Mechanisms ◽  
High Energy Phosphate ◽  
Cellular Mechanisms ◽  
Blood Fluidity ◽  
Phosphate Linkage ◽  
Glass Surfaces

A possible role for cellular energy metabolism in the control of the blood clotting mechanism has been shown. High-energy phosphate was found to strongly inhibit the recalcification time of plasma prepared with siliconized or glass surfaces. The nucleotide, adenosine triphosphate, in crystalline form and chromatographically pure, will inhibit or completely prevent coagulation in vitro. Reactivity is based primarily on the high-energy phosphate linkage and secondarily upon the nucleoside, adenosine. The principal site of action for ATP is on an unidentified precursor of thromboplastin. Available evidence indicates an important role for energy metabolism in the cellular mechanisms which effect a control over thromboplastin generation and its possible thrombotic and arteriosclerotic sequelae. cellular control mechanisms; blood fluidity; thrombosis arteriosclerosis; aging Submitted on July 1, 1963

Cerebral high-energy compounds: changes in anoxia

1962 ◽  
Vol 202 (1) ◽  
pp. 77-79 ◽  
Author(s):  
Richard N. Lolley ◽  
Frederick E. Samson
Keyword(s):  
Ion Exchange ◽  
Rat Brain ◽  
Adenosine Triphosphate ◽  
Energy Flow ◽  
Inorganic Phosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Guanosine Triphosphate ◽  
Inosine Monophosphate ◽  
Flow Through

Acid-soluble phosphates of rat brain during anoxia were determined by ion-exchange and chemical procedures. There is a general shift during anoxia of triphosphate nucleotides to monophosphates and a very rapid breakdown of phosphoryl-creatine. However, total phosphate leaving the high-energy phosphate pool is not equal to the changes in inorganic phosphate; inorganic phosphate change is much larger than high-energy phosphate change in early anoxia and much smaller in extended anoxia. The patterns of guanosine triphosphate and uridine triphosphate changes are more complex than adenosine triphosphate changes. Nicotinamideadenine dinucleotide levels are steady until late anoxia, at which time they decrease slightly. Cytidine monophosphate is the only cytidine nucleotide detected. Inosine nucleotide concentrations in control animals were below the limit of the method, but in late anoxia inosine monophosphate appeared. The data show that the energy flow through the phosphates in brain is rapid and involves phosphate compounds other than the acid-soluble nucleotides and phosphoryl-creatine.

PHOSPHORYLATION COUPLED TO THE OXIDATION OF SULFITE AND 2-MERCAPTOETHANOL IN EXTRACTS OF THIOBACILLUS THIOPARUS

1967 ◽  
Vol 13 (7) ◽  
pp. 873-884 ◽  
Author(s):  
E. A. Davis ◽  
E. J. Johnson
Keyword(s):  
Electron Donor ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Thiobacillus Thioparus ◽  
Ph Values ◽  
Cell Extracts ◽  
Endogenous Level ◽  
Sulfite Oxidation

The effect of 10−4 M 2, 4-dinitrophenol (DNP) on the production of high energy phosphate bonds during sulfite and 2-mercaptoethanol (2-ME) oxidation by cell extracts of Thiobacillus thioparus was determined. Phosphorylation was measured indirectly by14CO2fixation and directly by32PO4esterification. DNP-sensitive phosphorylation was demonstrated by coupling sulfite oxidation with the concomitant phosphorylation of adenosine monophosphate (AMP) to14CO2fixation beginning with ribose-5-phosphate. Esterification of32PO4was measured at pH values of 6.4, 7.2, and 8.0 with AMP and adenosine diphosphate (ADP) as the phosphate acceptor and sulfite as the electron donor. The optimal pH for the greatest DNP-sensitive phosphorylation was 7.2 with AMP. DNP at 10−4 M significantly reduced32PO4esterification at all pH values tested and with the three ADP concentrations employed. Maximum DNP-sensitive phosphorylation of ADP was demonstrated with 5 μmoles of ADP at pH 7.2. The maximum P:O ratio was 0.13. With 2-ME as the nonphysiological electron donor and AMP as the phosphate acceptor, no phosphorylation above the endogenous level was measured at the three pH values tested. With ADP as the phosphate acceptor and 2-ME as the electron donor,32PO4esterification significantly above the endogenous level was demonstrated at pH 6.4 with 5 μmoles of ADP; this phosphorylation was sensitive to 10−4 M DNP.

Bioenergetics of acute vasogenic edema

1980 ◽  
Vol 53 (4) ◽  
pp. 470-476 ◽  
Author(s):  
Leslie N. Sutton ◽  
Frank Welsh ◽  
Derek A. Bruce
Keyword(s):  
White Matter ◽  
Adenosine Triphosphate ◽  
Vasogenic Edema ◽  
Lactate Concentration ◽  
High Energy ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Content Type ◽  
Cold Lesion ◽  
Fine Print

✓ The bioenergetic mechanisms of vasogenic edema were studied by measuring concentrations of adenosine triphosphate (ATP), phosphocreatine (CrP), and lactate in rapidly frozen edematous white matter in cats. When edema was produced using a cold lesion, it was found that both ATP and CrP were reduced to one-half of control values, and that lactate was elevated. When a correction was applied for dilution, however, it was found that high-energy phosphates were equal to control values, and that lactate was even more significantly elevated. This pattern contrasted with that seen in white-matter ischemia, in which CrP is depressed out of proportion to ATP. Finally, it was found that the white-matter lactate concentration in the plasma infusion model of edema was increased. It is concluded that vasogenic edema induces an increase in lactate, but does not deplete high-energy phosphate compounds in affected white matter.

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