Ability of thyroid hormone to "permit" epinephrine-induced release of fatty acids from adipose-tissue cells. The thyroid hormones exert this effect by causing an increased number of epinephrine receptors on the cell.
The events initiated by the binding of a hormone to its receptor—that is, the mechanisms by which the hormone elicits a cellular response—are one or more of the signal transduction pathways that apply to all chemical messengers, as described in Chapter 7 (see Figures 7-12 and 7-13). In other words, there is nothing unique about the mechanisms initiated by hormones as compared to those utilized by neuro-transmitters and paracrine/autocrine agents, and so they are only briefly reviewed at this point (see Table 10-2).
As stated above, the receptors for peptide hormones and the catecholamine hormones are located on the outer surface of the target cell's plasma membrane. When activated by hormone binding, the receptors trigger one or more of the signal transduction pathways described for plasma-membrane receptors in Chapter 7 (see Figure 7-13). That is, the activated receptors directly influence: (1) ion channels that are part of the receptors; (2) enzyme activity that is part of the receptor; (3) activity of cytoplasmic JAK kinases associated with the receptor; or (4) G proteins coupled in the plasma membrane to effector proteins—ion channels and enzymes—that generate second messengers. The opening or closing of ion channels changes the electrical potential across the membrane and, when a calcium channel is involved, changes the cytosolic concentration of this important ionic second messenger. The changes in enzyme activity produce—most
Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition
Principles of Hormonal Control Systems CHAPTER TEN
commonly by phosphorylation catalysed by protein kinase enzymes—changes in the conformation and hence the activity of various cellular proteins. In some cases the signal transduction pathways also lead to activation (or inhibition) of particular genes, causing a change in the rate of synthesis of the proteins coded for by these genes.
Effects of Steroid and Thyroid Hormones Structurally, the steroid hormones, the thyroid hormones, and the steroid derivative 1,25-dihydroxyvitamin D3 are all closely related, and their receptors, which are intracellular, constitute the steroid-hormone receptor superfamily. As described in Chapter 7 (see Figure 7-12), the binding of hormone to one of these receptors leads to activation (or in some cases, inhibition) of particular genes, causing a change in the rate of synthesis of the proteins coded for by those genes. The ultimate result of changes in the concentrations of these proteins is an enhancement or inhibition of particular processes carried out by the cell, or a change in the rate of protein secretion by the cell.
Surprisingly, in addition to having intracellular receptors, some target cells also have plasma-membrane receptors for certain of the steroid hormones. In such cases the signal-transduction pathways initiated by the plasma-membrane receptors elicit rapid nongenomic cell responses while the intracellular receptors mediate a delayed response, requiring new protein synthesis.
Administration of very large quantities of a hormone for medical purposes may have effects that are never seen in a normal healthy person. They are called pharmacological effects, and they can also occur in diseases when excessive amounts of hormones are secreted. Pharmacological effects are of great importance in medicine, since hormones are often used in large doses as therapeutic agents. Perhaps the most common example is that of the adrenal cortical hormone cortisol, which is administered in large amounts to suppress allergic and inflammatory reactions.
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