Hypothalamicpituitarythyroid Axis Components and Function

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The thyroid gland, composed of two central lobes connected by an isthmus, synthesizes the hormones thyroxine (T4) and triiodothyronine (T3). These iodine-containing compounds serve as global regulators of the body's metabolic rate, and are also critical for brain development. The release and synthesis of these hormones is ultimately controlled by signals from the CNS.

The hypothalamic-pituitary-thyroid (HPT) axis is composed of three main parts, as its name suggests. The tripeptide (pGlu-His-Pro-NH2) thyr-otropin-releasing hormone (TRH) is synthesized predominantly in the PVN of the hypothalamus and stored in nerve terminals in the median eminence, where it is released into the vessels of the hypothalamo-hypophyseal portal system (Figure 4.3). TRH is then transported to the sinusoids in the anterior pituitary, where it binds to thyrotropes and releases the peptide thyroid-stimulating hormone (TSH) into the systemic circulation. TRH is heteroge-neously distributed in the brain, which strongly suggests a role for this peptide as a neurotransmitter as well as a releasing hormone. Thus TRH itself can produce direct effects on the CNS independent of its actions on pituitary thyrotrophs. The HPT axis exhibits an ultradian rhythm, where TSH secretion, and consequently T3 and T4 levels, rise in the afternoon and evening, peak sometime after midnight and decline throughout the day [2].

Figure 4.3 Overview of the feedback system of the hypothalamic-pituitary-thyroid (HPT) axis. Thyroid-releasing hormone (TRH) from the hypothalamus stimulates thyroid stimulating hormone (TSH) from the pituitary, which stimulates thyroid hormone release. As circulating thyroid hormone levels increase, they inhibit further release of TSH and TRH. Other hypothalamic-pituitary-end organ axes exhibit similar feedback control mechanisms

Figure 4.3 Overview of the feedback system of the hypothalamic-pituitary-thyroid (HPT) axis. Thyroid-releasing hormone (TRH) from the hypothalamus stimulates thyroid stimulating hormone (TSH) from the pituitary, which stimulates thyroid hormone release. As circulating thyroid hormone levels increase, they inhibit further release of TSH and TRH. Other hypothalamic-pituitary-end organ axes exhibit similar feedback control mechanisms

TSH is a 28-kDA glycoprotein composed of two non-covalently linked protein chains, TSH-a and TSH-p. The a subunit is identical to the a subunit contained in other pituitary hormones, including follicle-stimulating hormone, luteinizing hormone and human chorionic gonadotropin. Upon release from the pituitary, TSH circulates through the blood and exerts its effects via binding to the TSH receptor in the thyroid, a G-protein-coupled receptor that stimulates the activation of adenylate cyclase.

Upon stimulation by TSH, the thyroid gland releases the iodinated amino acids T3 and T4. Of the two hormones, T3 is much more physiologically active. Although debate still exists in the literature, T4 is often considered a prohormone that becomes active after monodeiodination in peripheral tissues. T3 directly promotes gene expression through binding to thyroid response elements (TREs) located in the promoter regions of a diverse number of genes. T3 also directly regulates the HPT axis by inhibiting TSH release and gene expression in the pituitary, and TRH gene expression in the hypothalamus [3]. This is characteristic of the end-product negative feedback seen in the hypothalamic-pituitary-end organ axes. In the circulation, these hormones are primarily bound to a carrier-protein, thyroglobulin, though it is the unbound form of these hormones that is metabolically active. Thyroid hormones have numerous effects on metabolism and increase heat production, oxygen consumption, lipid metabolism, intestinal absorption of carbohydrates, cardiac function and in regulating the activity of the Na+ — K+ ATPase. All of these functions are consistent with increasing metabolic rate.

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