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Glucocorticoid deficiency can be caused by inherited genetic disorders that affect the production of cortisol in the adrenal glands, such as familial glucocorticoid deficiency (FGD). [3] FGD is a group of monogenic recessive disorders caused by disease-causing variants in genes involved in cortisol biosynthesis. [ 4 ]
The mutations in the MRAP gene caused the congenital disorder familial glucocorticoid deficiency type 2 (FGD-2). FGD-2 is an autosomal recessive disease with early childhood onset of recurrent infections, hypoglycaemia, skin hyperpigmentation, and failure to thrive due to low glucocorticoids levels. If left untreated, it could be fatal.
Glucocorticoid deficiency 1 is an adrenocortical failure characterized by low levels of plasma cortisol produced by the adrenal gland despite high levels of plasma ACTH. This is an inherited disorder with several different causes which define the type.
The glucocorticoids provide a reliable substitute for cortisol, thereby reducing ACTH levels. Reducing ACTH also reduces the stimulus for continued hyperplasia and overproduction of androgens. In other words, glucocorticoid replacement is the primary method of reducing the excessive adrenal androgen production in both sexes.
MRAP2 is found in the adrenal gland where MRAP is known to regulate MC 2 surface expression and function. [21] In vivo studies had revealed MRAP2 to interact with MC 2 leading to an increase in the receptor surface expression as well as enhancing the response of the receptor to adrenocorticotropic hormone (ACTH) stimulation. [6]
The glucocorticoid receptor (GR or GCR) also known as NR3C1 (nuclear receptor subfamily 3, group C, member 1) is the receptor to which cortisol and other glucocorticoids bind. The GR is expressed in almost every cell in the body and regulates genes controlling the development , metabolism , and immune response .
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The adrenocorticotropic hormone receptor or ACTH receptor also known as the melanocortin receptor 2 or MC 2 receptor is a type of melanocortin receptor (type 2) which is specific for ACTH. [5] A G protein–coupled receptor located on the external cell plasma membrane, it is coupled to G αs and upregulates levels of cAMP by activating adenylyl ...