Dexamethasone is a corticosteroid that prevents the release of substances in the body that cause inflammation. Dexamethasone is used to treat many different inflammatory conditions such as allergic disorders, skin conditions,ulcerative colitis , arthritis, lupus, psoriasis, or breathing disorders. Moreover, chronic dexamethasone therapy is required in several cases such as pediatric nephrotic syndrome, graft-versus-host disease etc. What are the sequential biochemical and/or molecular mechanisms involved in dexamethasone mediated diabetes?
biochemical mecanism of dexametasone mediated diabetes is gluconeogenesis. Gluconeogenesis is the glucose maintaining from muscles.
gluconeogenesis [gloo″ko-ne″o-jen´ĕ-sis]
the synthesis of glucose from noncarbohydrate sources, such as amino acids and glycerol. It occurs primarily in the liver and kidneys whenever the supply of carbohydrates is insufficient to meet the body's energy needs. Gluconeogenesis is stimulated by cortisol and other glucocorticoids and by the thyroid hormone thyroxine. Formerly called glyconeogenesis.
biochemical mecanism of dexametasone mediated diabetes is gluconeogenesis. Gluconeogenesis is the glucose maintaining from muscles.
gluconeogenesis [gloo″ko-ne″o-jen´ĕ-sis]
the synthesis of glucose from noncarbohydrate sources, such as amino acids and glycerol. It occurs primarily in the liver and kidneys whenever the supply of carbohydrates is insufficient to meet the body's energy needs. Gluconeogenesis is stimulated by cortisol and other glucocorticoids and by the thyroid hormone thyroxine. Formerly called glyconeogenesis.
According to Bazuine M et al., (2004) dexamethasone inhibits the activation of GLUT4 in plasma membrane by a p38 MAPK-dependent phosphorylation.
Adding to Binnur Tüzün, in moleular level dexamethasone induces gluconeogenesis by trans-activation of PEPCK, TAT and G6 P ase.
Loss of glu4, upregulation gluconeogenesis, impairments in insulin signalling with compromised akt activation , visceral adipogenesity, increase in the pool of precursors for gluconeogenesis due to protein breakdown, adipocyte differentiation via lipin that in time causes sufficient inflàmmatory response which in turn reduce insulin sensitivity.
Mechanisms run deep. Duration of excess cortisol plays an important role.
Am glad you asked it. Any particular interest in glucocorticoid induced insulin resistance?
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