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Hormones trophic

ACTH = adrenocortico-trophic hormone T4 = thyroxine T3 = triiodothyronine E, = estradiol T = testosterone I7,20/IP = 17,20/1-dihydroxy-4-pregnen-3-one KT = Il-ketotestosterone VTG = vitellogenin. [Pg.31]

A trophic hormone acts on another endocrine gland to stimulate secretion of its hormone. For example, thyrotropin, or thyroid-stimulating hormone (TSH), stimulates the secretion of thyroid hormones. Adrenocorticotropin, or adrenocorticotropic hormone (ACTH), stimulates the adrenal cortex to secrete the hormone cortisol. Both trophic hormones are produced by the pituitary gland in fact, many trophic hormones are secreted by the pituitary. The pituitary gland is sometimes referred to as the "master gland" because its hormones regulate the activity of other endocrine glands. [Pg.115]

The hypothalamic releasing factors regulate release of the anterior pituitary trophic hormones 844... [Pg.843]

The hypothalamic releasing factors regulate release of the anterior pituitary trophic hormones. As summarized in Figure 52-1, the releasing factors are produced in various neuronal groups within the hypothalamus and are transported to the median eminence for release into the portal circulation to the anterior pituitary. Neurons in the hypothalamus also produce the hormones oxytocin and vasopressin, which are released by the posterior pituitary into the blood. Therefore, it is not surprising that behavior and experience, which influence the hypothalamus, sometimes alter the secretion of these hypothalamic releasing factors and hormones. [Pg.844]

The vascular wall is a target for sexual hormones. In the particular case of estrogens, specific receptors have been found in both endothelium and vascular smooth muscle cells (VSMC) (Venkov et al. 1996 Karas et al. 1994). The trophic effects of estrogens on the endothelium have been advocated as crucial against initiation and promotion of atherosclerosis. Thus, cellular and animal models,... [Pg.222]

According to results from clinical trials, the agonistic effects of tamoxifen detected in animals were also observed in the human uterus as it produces a trophic effect and an increase in the incidence of endometrial pathology, which is related to endometrial thickening (> 4 mm). Its use seems to be associated with an increase in endometrial cancer, which is related to the length of treatment and the accumulated dose of tamoxifen. Nevertheless, these tumors do not seem to be more aggressive or to have a worse prognosis than those found in women who do not follow this treatment or who receive hormone therapy. [Pg.294]

Certain tissues of the female reproductive tract, which are subject to the trophic action of hormones, exhibit a high frequency of neoplasia. Cancer of the breast, the second most common form of cancer in American women, and the rarer endometrial cancer in women, are often responsive to treatments with estrogens or progestins. The toxicity of these hormonal treatments compared with standard cancer chemotherapy is low. [Pg.711]

The anterior lobe secretes various trophic hormones, the posterior lobe is responsible for the secretion of oxytocin and antidiuretic hormone (vasopressin) and middle lobe secretes melanocyte-stimulating hormone (MSH) which may affect the synthesis of melanin. [Pg.269]

Anterior lobe of pituitary is the master gland of the endocrine system as a whole because it produces peptide trophic hormones which affect the other ductless/endocrine glands. The anterior lobe secretes the following hormones ... [Pg.269]

Perheentupa J. Hormonal background of the hypertension and fluid derangements associated with adrenocortico-trophic hormone treatment of infants. Eur J Pediatr 1989 148(8) 737—41. [Pg.99]

Figure 18.3. Endocrine-immune inter-relationship in depression. In depression, the hypothalamic-pituitary-adrenal (HPA) axis is up-regulated with a down-regulation of its negative feedback controls. Corticotrophin releasing factor (CRF) is hypersecreted from the hypothalamus and induces the release of adrenocortico-trophic hormone (ACTH) from the pituitary. ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands adrenal hypertrophy can also occur. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose. The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release. Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission. Figure 18.3. Endocrine-immune inter-relationship in depression. In depression, the hypothalamic-pituitary-adrenal (HPA) axis is up-regulated with a down-regulation of its negative feedback controls. Corticotrophin releasing factor (CRF) is hypersecreted from the hypothalamus and induces the release of adrenocortico-trophic hormone (ACTH) from the pituitary. ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands adrenal hypertrophy can also occur. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose. The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release. Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission.
The release of cholesterol from cholesterol esters occurs extra-mitochondrially by means of a cholesterol ester hydrolase in adrenals, ovaries and testicular Ley dig cells (see Ref. 6 for review). This enzyme has been studied mostly in adrenal preparations, and is known to be activated and de-activated by reversible phosphorylation [14] and that the phosphorylation was brought about by a c-AMP-dependent protein kinase [15]. Hence, ACTH stimulation of cholesterol ester activity in the adrenal occurs via the kinase and, in a similar way, trophic hormone stimulation of ovarian and testicular cholesterol ester hydrolases may occur and provide a large pool of cholesterol for steroidogenesis [16-18],... [Pg.5]

The transport of cholesterol to, and its side-chain cleavage in, the mitochondria are the most important steps in the hormonal control of steroidogenesis. The enzymatic activities in the endoplasmic reticulum are also under hormonal control. However, expression of hormonal effects in this compartment requires several hours and is therefore part of the chronic, trophic effects of LH [3,4,32],... [Pg.166]


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See also in sourсe #XX -- [ Pg.115 ]




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