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Thyroid control

Blood Calcium Ion Level. In normal adults, the blood Ca " level is estabhshed by an equiUbrium between blood Ca " and the more soluble intercrystalline calcium salts of the bone. Additionally, a subtle and intricate feedback mechanism responsive to the Ca " concentration of the blood that involves the less soluble crystalline hydroxyapatite comes into play. The thyroid and parathyroid glands, the fiver, kidney, and intestine also participate in Ca " control. The salient features of this mechanism are summarized in Figure 2 (29—31). [Pg.376]

Factors controlling calcium homeostasis are calcitonin, parathyroid hormone(PTH), and a vitamin D metabolite. Calcitonin, a polypeptide of 32 amino acid residues, mol wt - SGOO, is synthesized by the thyroid gland. Release is stimulated by small increases in blood Ca " concentration. The sites of action of calcitonin are the bones and kidneys. Calcitonin increases bone calcification, thereby inhibiting resorption. In the kidney, it inhibits Ca " reabsorption and increases Ca " excretion in urine. Calcitonin operates via a cyclic adenosine monophosphate (cAMP) mechanism. [Pg.376]

Metabolic Functions. The functions of the thyroid hormones and thus of iodine are control of energy transductions (121). These hormones increase oxygen consumption and basal metaboHc rate by accelerating reactions in nearly all cells of the body. A part of this effect is attributed to increase in activity of many enzymes. Additionally, protein synthesis is affected by the thyroid hormones (121,122). [Pg.386]

Fig. 1. Mechanisms controlling free thyroid-hormone levels. Fig. 1. Mechanisms controlling free thyroid-hormone levels.
Amphibians. Amphibians are highly susceptible to endocrine disruption during development of the larval form and during metamorphosis. The action of metamorphosis is triggered and controlled by the thyroid gland via an increase in triiodothyronine and a decrease in thyroxine, and differs greatly between oviparous and viviparous species. Experimentally, it has been shown that disruption during this sensitive period can lead to malformations and adverse impacts on immune and reproductive functions. [Pg.72]

The thyroid gland, located in the base of the neck, exerts i key role on growth and metabolism. In contrast with that of some of the other endocrine glands, this control is effected Ihrough a pair of relatively simple molecules, thyroxine, and its close congener, triiodothyronine. Cases of thyroid deficien-cy (hypothyroidism) are common enough to warrant the production... [Pg.95]

Hyperthyroidism, that is, the overproduction of thyroid hormones, is usually treated by surgical removal of the thyroid gland. Before such a procedure is undertaken, the hyperthyroidism is usually first brought under control by treatment with so-called antithyroid agents. [Pg.240]

Cellular functions are controlled by extracellular signals such as hormones, neurotransmitters, odorants, light and other chemical or physical stimuli. Only a few of these signal molecules, e.g., the highly lipid-soluble steroids or thyroid hormones, can diffiise across the... [Pg.1236]

The formation of FMN and FAD is ATP-dependent and takes place predominantly in liver, kidney, and heart. It is controlled by thyroid hormones [2]. [Pg.1289]

Luft, R., Ikkos, D., Palmieri, G., Emster, L., Aftelius, B. (1962). A case of severe hypermetabolism of non-thyroid origin with a defect in the maintenance of mitochondrial respiratory control A correlated clinical, biochemical and morphological study. J. Clin. Invest. 41, 1776-1804. [Pg.152]

Thyroid-associated ophthalmopathy (TAO) is present in 90% of patients with the classical triad of Graves disease (goiter, ophthalmopathy, dermopathy) but these features may follow independent courses and successful control of the hyperthyroidism improves TAO in less than 5% cases. Immunosuppression has been used since theories of the etiology of TAO include the presence of circulating antibodies to both thyroid and ocular muscle fibers, and of thyroglobulin-antithy-roglobulin complexes with high affinity for extraocular muscles. [Pg.338]

There are few absolute contraindications for deep peeling, with the exception of physical or mental instability. During pregnancy and lactation any cosmetic intervention is considered to be undesirable. We have safely peeled patients with hypertension, diabetes mellitus, thrombocytopenia, thyroid malfunction, etc, as long as their disease is well controlled and stable. All pa-... [Pg.72]

Figure 25-8. Control of adipose tissue lipolysis. (TSH, thyroid-stimulating hormone FFA, free fatty acids.) Note the cascade sequence of reactions affording amplification at each step. The lipolytic stimulus is "switched off" by removal of the stimulating hormone the action of lipase phosphatase the inhibition of the lipase and adenylyl cyclase by high concentrations of FFA the inhibition of adenylyl cyclase by adenosine and the removal of cAMP by the action of phosphodiesterase. ACTFI,TSFI, and glucagon may not activate adenylyl cyclase in vivo, since the concentration of each hormone required in vitro is much higher than is found in the circulation. Positive ( ) and negative ( ) regulatory effects are represented by broken lines and substrate flow by solid lines. Figure 25-8. Control of adipose tissue lipolysis. (TSH, thyroid-stimulating hormone FFA, free fatty acids.) Note the cascade sequence of reactions affording amplification at each step. The lipolytic stimulus is "switched off" by removal of the stimulating hormone the action of lipase phosphatase the inhibition of the lipase and adenylyl cyclase by high concentrations of FFA the inhibition of adenylyl cyclase by adenosine and the removal of cAMP by the action of phosphodiesterase. ACTFI,TSFI, and glucagon may not activate adenylyl cyclase in vivo, since the concentration of each hormone required in vitro is much higher than is found in the circulation. Positive ( ) and negative ( ) regulatory effects are represented by broken lines and substrate flow by solid lines.
The thyroid is able to concentrate T against a strong electrochemical gradient. This is an energy-dependent process and is linked to the Na -K ATPase-dependent thyroidal T transporter. The ratio of iodide in thyroid to iodide in serum (T S ratio) is a reflection of the activity of this transporter. This activity is primarily controlled by TSH and ranges from 500 1 in animals chronically stimulated with TSH to 5 1 or less in hy-pophysectomized animals (no TSH). The T S ratio in humans on a normal iodine diet is about 25 1. [Pg.449]


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