scholarly journals High-energy phosphate metabolism and energy liberation associated with rapid shortening in frog skeletal muscle

1981 ◽  
Vol 321 (1) ◽  
pp. 423-436 ◽  
Author(s):  
E. Homsher ◽  
M. Irving ◽  
A. Wallner
Keyword(s):  
Skeletal Muscle ◽  
High Energy ◽  
Energy Liberation ◽  
Phosphate Metabolism ◽  
Frog Skeletal Muscle ◽  
High Energy Phosphate ◽  
High Energy Phosphate Metabolism

scholarly journals Skeletal muscle high energy phosphate metabolism in patients with obesity and impaired fasting blood glucose

2012 ◽  
Vol 14 (S1) ◽  
Author(s):  
Gurusher S Panjrath ◽  
Michael Schär ◽  
AbdEl-Monem El-Sharkawy ◽  
Steven P Schulman ◽  
Kerry Stewart ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Fasting Blood Glucose ◽  
High Energy ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
High Energy Phosphate 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.

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