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1 MN551 Unit 7 Discussion Student name Institution Course Professor Due date

2 Part 2 The dexamethasone test involves the administration of a synthetic glucocorticoid (e., cortisol). Knowing what you do about negative feedback mechanisms, how might this test be used to assess pituitary function? According to Guyton and Hall (2021), the dexamethasone suppression test is a significant diagnostic tool that is used to examine the function of the pituitary gland as well as the negative feedback loop that controls cortisol production in the body. During this particular examination, the patient will be given the synthetic glucocorticoid known as dexamethasone. Both structurally and functionally, dexamethasone is quite similar to the hormone cortisol. According to Guyton and Hall's research (2021), when dexamethasone is administered to a living organism, it acts as an exogenous source of the glucocorticoid. In those whose hypothalamic-pituitary-adrenal (HPA) axis, which regulates the production of cortisol, is working appropriately, the presence of dexamethasone should set off a powerful negative feedback reaction (Guyton & Hall, 2021). According to Guyton and Hall 2021, dexamethasone sends a signal to the hypothalamus and pituitary gland, telling them to decrease the amount of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) that they produce and release. As a direct consequence of this, the adrenal glands' natural capacity to produce endogenous cortisol is reduced. This decrease of cortisol levels suggests that the HPA axis is operating correctly, and that the pituitary gland is capable of reacting adequately to the exogenous glucocorticoid (Guyton & Hall, 2021). Dexamethasone fails to adequately suppress cortisol production in cases of pituitary dysfunction, such as in Cushing's disease, in which the pituitary overproduces ACTH. This is a clear indication of pituitary hyperactivity and an underlying problem with the negative feedback regulation of cortisol secretion (Guyton & Hall, 2021).

3 Describe how the steroid hormones, like cortisol, are metabolized in the body. What are the advantages of using a 24-hour urine test to measure this hormone? Various metabolic processes take place in the liver and other organs to break down steroid hormones like cortisol. The removal and inactivation of cortisol are the results of a series of enzymatic processes. To begin, the enzyme 11-hydroxysteroid dehydrogenase type 2 (11- HSD2) may convert cortisol into cortisone, an inactive version of cortisol (Romero and Beattie, 2022). Moreover, cortisol may be broken down by reduction, oxidation, and conjugation. It is the water-soluble compounds produced by these processes that are ultimately eliminated from the body through the urinary tract (Romero and Beattie, 2022). There are various benefits to using a 24-hour urine test to determine cortisol levels in clinical evaluation. By measuring cortisol levels continuously throughout time, this technique gives a more accurate depiction of an individual's hormonal balance. Since cortisol levels normally follow a circadian rhythm, with greater concentrations in the morning and lower concentrations in the evening, this enables for the assessment of diurnal fluctuations in cortisol production (Scheun et al., 2018). And although blood testing may provide you a "snapshot" of your cortisol levels at any one time, the 24-hour urine test is less susceptible to short-term variations. Because it measures total cortisol output, it is useful for detecting imbalances in the endocrine system that can lead to diseases like Cushing's syndrome (excessive cortisol production) and Addison's disease (insufficient cortisol production) (Scheun et al., 2018). Protein-based and steroid-based hormones trigger cellular responses in different ways. What are the differences between the mechanism of action of ACTH and cortisol on target cells?

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4 The structural distinctions between protein-based hormones and steroid-based hormones cause them to trigger cellular responses in different ways. The stress hormones ACTH (adrenocorticotropic hormone) and cortisol (the stress hormone) serve as examples of this discrepancy. Cortisol is a steroid hormone, whereas ACTH is a protein hormone. ACTH predominantly exerts its effects on cells via binding to melanocortin receptors (MCRs) on their surface. When ACTH binds to its receptor, it sets off a series of actions inside the cell. In order to activate protein kinase A (PKA), MCR activation must first raise intracellular cyclic adenosine monophosphate (cAMP) levels (de Souza et al., 2023) in the cell. The protein kinase A (PKA) phosphorylates intracellular targets, setting in motion signaling pathways that eventually promote cortisol production and secretion by the adrenal cortex. Cortisol is released very immediately after stress or ACTH activation, thanks to this signaling mechanism (de Souza et al., 2023) that works at a high speed. In contrast, cortisol acts differently since it is a steroid hormone. Glucocorticoid receptors (GRs) are intracellular receptors that cortisol binds to after diffusing across the cell membrane (Silver et al., 2021). Once in the nucleus, the cortisol-GR complex may regulate gene expression. In the promoter regions of target genes, it binds to DNA sequences known as glucocorticoid response elements (GREs) (Silver et al., 2021). Gene transcription is altered as a result of this DNA interaction, and this in turn affects the production of a wide range of proteins involved in metabolic and anti-inflammatory activities (Silver et al., 2021). Since cortisol's wide-ranging physiological effects are mediated by proteins, the hormone's manifestations tend to be gradual and long-lasting compared to ACTH's (Silver et al., 2021).

5 References de Souza, C. F., Stopa, L. R. S., Martins, A. B., Wunderlich, A. L. M., Lopes, G. M., de Fatima Silva, F., ... & Uchoa, E. T. (2023). Glucocorticoids contribute to metabolic and liver impairments induced by lactation overnutrition in male adult rats. Frontiers in Physiology , 14 , 1161582. Guyton, A. C., & Hall, J. E. (2021). Chapter 80: Parathyroid hormone, calcitonin, calcium, and phosphate metabolism, vitamin D, bone, and teeth. Textbook of medical physiology. 14th ed. Philadelphia, PA: Elsevier , 997. Romero, L. M., & Beattie, U. K. (2022). Common myths of glucocorticoid function in ecology and conservation. Journal of Experimental Zoology Part A: Ecological and Integrative Physiology , 337 (1), 7-14. Silver, Z., Abbott-Tate, S., Hyland, L., Sherratt, F., Woodside, B., & Abizaid, A. (2021). Ghrelin receptor signaling is not required for glucocorticoid-induced obesity in female mice. The Journal of Endocrinology , 250 (2), 37-48. Scheun, J., Greeff, D., & Ganswindt, A. (2018). Non-invasive monitoring of glucocorticoid metabolite concentrations in urine and faeces of the Sungazer (Smaug giganteus). PeerJ , 6 , e6132.

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