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Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. [1] Symptoms may include weakness, trouble breathing, and loss of appetite. [1]
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[3] [27] The final step in treatment is to calculate the patients free water deficit, and to replace it at a steady rate using a combination of oral or IV fluids. [3] [27] The rate of replacement of fluids varies depending on how long the patient has been hypernatremic. Lowering the sodium level too quickly can cause cerebral edema.
γ-L-Glutamyl-L-cysteine, also known as γ-glutamylcysteine (GGC), is a dipeptide found in animals, plants, fungi, some bacteria, and archaea.It has a relatively unusual γ-bond between the constituent amino acids, L-glutamic acid and L-cysteine and is a key intermediate in the γ-glutamyl cycle first described by Meister in the 1970s.
The diagnosis of hyperphosphatemia is made through measuring the concentration of phosphate in the blood. A phosphate concentration greater than 1.46 mmol/L (4.5 mg/dL) is indicative of hyperphosphatemia, though further tests may be needed to identify the underlying cause of the elevated phosphate levels. [5]
(α-1,4 glycogen chain) n + Pi ⇌ (α-1,4 glycogen chain) n-1 + α-D-glucose-1-phosphate. [2] Glycogen is left with one fewer glucose molecule, and the free glucose molecule is in the form of glucose-1-phosphate. In order to be used for metabolism, it must be converted to glucose-6-phosphate by the enzyme phosphoglucomutase.
This enzyme belongs to the family of isomerases, specifically the phosphotransferases (phosphomutases), which transfer phosphate groups within a molecule. The systematic name of this enzyme class is alpha-D-glucose 1,6-phosphomutase (glucose-cofactor). Other names in common use include glucose phosphomutase, and glucose-1-phosphate ...
Glycerol kinase catalyzes the transfer of a phosphate from ATP to glycerol thus forming glycerol 3-phosphate: ATP + glycerol <=> ADP + sn-glycerol 3-phosphate. Adipocytes lack glycerol kinase so they cannot metabolize the glycerol produced during triacyl glycerol degradation. This glycerol is instead shuttled to the liver via the blood where it is: