The permissive effect of cortisol on insulin action in liver glycogenesis is observed in hepatocyte culture in the laboratory, although the mechanism for this is unknown. Bone and collagen
Cortisol reduces bone formation, favoring long-term development of osteoporosis (progressive bone disease). The mechanism behind this is two-fold: cortisol stimulates the production of RANKL by osteoblasts which stimulates, through binding to RANK receptors, the activity of osteoclasts – cells responsible for calcium resorption from bone – and also inhibits the production of osteoprotegerin (OPG) which acts as a decoy receptor and captures some RANKL before it can activate the osteoclasts through RANK. In other words, when RANKL binds to OPG, no response occurs as opposed to the binding to RANK which leads to the activation of osteoclasts. It transports potassium out of cells in exchange for an equal number of sodium ions (see above). This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine. Cortisol down-regulates the synthesis of collagen. Amino acid
Cortisol raises the free amino acids in the serum by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis. Cortisol (as opticortinol) may inversely inhibit IgA precursor cells in the intestines of calves. Cortisol also inhibits IgA in serum, as it does IgM; however, it is not shown to inhibit IgE. Electrolyte balance
Cortisol decreases glomerular filtration rate, and renal plasma flow from the kidneys thus increasing phosphate excretion, as well as increasing sodium and water retention and potassium excretion by acting on mineralocorticoid receptors.
Diagnosis
The diagnosis for argininemia can usually be done using fetal blood sample. One can look for the following indicators as to the presence of the condition:
Plasma ammonia concentration. Urinary orotic acid concentration
Red blood cell arginase enzyme activity (measurement)

Treatment
The treatment for infants (individuals) with argininemia is the following, including medications:

References
Further reading
(editors), Jean-Marie Saudubray, Georges van den Berghe, John H. Walter; Berghe, Georges van den; Walter, John H. (2012). Inborn metabolic diseases diagnosis and treatment (5th ed.). Berlin: Springer. ISBN 9783642157202. Retrieved 28 November 2016. {{cite book}}: |last1= has generic name (help)
Piña-Garza, J. Eric (2013). Fenichels Clinical pediatric neurology a signs and symptoms approach (7th ed.). Oxford: Saunders. ISBN 978-1455748129. Retrieved 28 November 2016. == External links ==