Central nervous system , thyroid hormones

It has also been mentioned that salt iodization efficacy, the preferred strategy for IDD, might be influenced by ID, because this disorder impairs thyroid metabolism (WHO, 2001, Zimmermann et al., 2000). It has been observed that two initial steps in thyroid hormone synthesis are catalyzed by Fe-dependent thyroid peroxidase (TPO). One Fe-defl-ciency anemia study in rats showed reduced TPO activity, and decreased plasma T4 and triiodothyronine (T3) levels (Hess et al, 2002). IDA may also alter the central nervous systems thyroid metabolism control, and reduce T4 to T3 peripheral conversion (Beard etal, 1998), modify nuclear T3 binding (Smith et al, 1994), and increase circulating thyrotropin (TSH) (Beard et at, 1990). The therapeutic response to oral iodized oil is impaired in children with IDA compared with Fe-sufficient children (Zimmermann et al, 2000). 

Angiotensin II, administered into the central nervous system, increases the release of luteinizing hormone, adrenocortical hormone, thyroid-releasing hormone, (3-endorphin, vasopressin, and oxytocin from the anterior pituitary. In contrast, centrally administered angiotensin II inhibits the release of anterior pituitary growth hormone and prolactin. 

There is no such clear cut difTcrcnlialiun as metamorphosis in the mammal, but development is an extremely complex process and has been shown to depend upon the presence of adequate amounts of thyroid hormones. Deficient development, especially of the central nervous system, is marked in ehildren suffering from thyroid deficiency early in life, ansi this inadequacy cannot be overcome completely by medication commenced after the first few weeks. In the adult, thyroxine is important in the maintenance of energy turnover in most of the tissues of the body, such as the heart, skeletal muscle, liver, and kidney, Other physiological functions, most notably brain aclivity and reproduction, are also dependent upon thyroxine, although the metabolic rales of the tissues concerned in these functions do not seem to be altered. 

Fifth, certain kallikreins, such as human kallikrein 6, are highly expressed in the central nervous system. It has previously been shown that hK6, and possibly some other kallikreins, are implicated in inflammatory reactions within the central nervous system that lead to demyelination. The association of hK6 and some other kallikreins with AD and multiple sclerosis points to the possibility that some of these enzymes may play important roles within the central nervous system. In addition, many of these enzymes have been found in endocrine tissues such as the islets of Langerhans, thyroid, pituitary, and others, pointing to the possibility that they may participate in prohormone or hormone processing. 

Such events show how the immune, endocrine and central nervous systems are integrated in their responses to any form of stress. It is well established that physical or psychosocial stress causes increased secretions of prolactin, growth hormones, thyroid, and gonadal hormones, in addition to ACTH. Endogenous opioids are secreted under such conditions and function as immunomodulators, while also elevating the pain threshold. Receptors for such hormones exist on immunocompetent cells, along with receptors for catecholamines, serotonin and acetylcholine. 

In addition to the obvious deactivating role of deiodinases, there has been recent evidence that a relationship exists between regulation of deiodination of thyroid hormones in target cells and the intracellular effects of T4 and T3 on pituitary and hypothalamus function. In the rat pituitary, and probably the human, type-II deiodinase-catalyzed conversion of T4 to T3 is a prerequisite for inhibition of TRH release. rT3, produced from T4 by type-III deiodinase, is a potent inhibitor of type-II deiodinase. In a postulated regulatory circuit, rT3 formed from T4 by type-III deiodinase in surrounding CNS (Central Nervous System) tissue enters the pituitary and inhibits type-II enzyme. The resulting decrease in T3 concentration, in turn, causes an increase in TSH secretion49. 

Q3 The thyroid hormones thyroxine and triiodothyronine have many metabolic effects. In adults they increase metabolic rate, oxygen and calorie consumption, stimulate carbohydrate metabolism and turnover of protein, deplete fat stores and increase catabolism of free fatty acids. Thyroid hormones stimulate heart rate and force and increase pulmonary ventilation, gastrointestinal motility and central nervous system (CNS) activity. Actions on the heart can result in an increased incidence of dysrhythmias. Thyroid hormones are critical for the normal growth and development of the infant, particularly in respect of skeletal growth and maturation of the CNS. 

CalzaL, EemandezM,Giuhani A, D Intino S, Pirondi S, SivihaS, Paradisi M, Desordi N, Giardino L (2005) Thyroid hormone and remyelination in adult central nervous system A lesson from an inflammatory-demy-ehnating disease. Brain Res Brain Res Rev 48 339-346. 

The organization of the endocrine system can best be described in relation to the central nervous system. Three levels of endocrine tissues can be distinguished on the basis of their association with the central nervous system (Figure 30-12). The first level consists of those that are (or were) derived from nerve cells these include the hypothalamus, adrenal medulla, thyroid C-cell, and gastrointestinal enterochromaffin cells. The hypothalamus and adrenal medulla still retain their neural connections and can therefore be regarded as endocrine extensions of the nervous system. The C-cell and the gut cells, however, are APUD cells and lack neural connections. These four tissues produce hormonal peptides or amines having, like neurotransmitters, rapid-onset, short-term effects. 

Less common etiologies include central nervous system lesions that physically compress the pituitary stalk and interrupt tonic hypothalamic dopamine secretion, resulting in hyperprolactinemia. Increased thyroid-releasing hormone (TRH) concentrations in hypothyroidism can stimulate prolactin secretion and cause hyperprolactinemia. During conditions of renal or liver compromise, the... 

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