Prolonged effects of tumor necrosis factor-α on anterior pituitary hormone release

Harel, Gideon; Shamoun, Dalal S.; Kane, John P.; Magner, James A.; Szabó, Márta

doi:10.1016/0196-9781(95)00019-g

Cited by 30 publications

(21 citation statements)

References 22 publications

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“…Both IL1b and TNFa decrease basal TSHb release independently of T 3 uptake and action in the pituitary cells (Harel et al 1995, Wassen et al 1996. Interestingly, acute energy deprivation has no effect on TSHb release from pituitary cells in culture, consistent with the in vivo studies discussed above showing that the TSHb decrease during chronic inflammation is only partly explained by decreased food intake (Boelen et al 2006).…”

Section: Illness Induced Alterations In Pituitary Tshb Expressionsupporting

confidence: 74%

The molecular basis of the non-thyroidal illness syndrome

Vries¹,

Fliers²,

Boelen³

2015

Journal of Endocrinology

153

116

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The 'sick euthyroid syndrome' or 'non-thyroidal illness syndrome' (NTIS) occurs in a large proportion of hospitalized patients and comprises a variety of alterations in the hypothalamus-pituitary-thyroid (HPT) axis that are observed during illness. One of the hallmarks of NTIS is decreased thyroid hormone (TH) serum concentrations, often viewed as an adaptive mechanism to save energy. Downregulation of hypophysiotropic TRH neurons in the paraventricular nucleus of the hypothalamus and of TSH production in the pituitary gland points to disturbed negative feedback regulation during illness. In addition to these alterations in the central component of the HPT axis, changes in TH metabolism occur in a variety of TH target tissues during NTIS, dependent on the timing, nature and severity of the illness. Cytokines, released during illness, are known to affect a variety of genes involved in TH metabolism and are therefore considered a major determinant of NTIS. The availability of in vivo and in vitro models for NTIS has elucidated part of the mechanisms involved in the sometimes paradoxical changes in the HPT axis and TH responsive tissues. However, the pathogenesis of NTIS is still incompletely understood. This review focusses on the molecular mechanisms involved in the tissue changes in TH metabolism and discusses the gaps that still require further research.

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Section: Illness Induced Alterations In Pituitary Tshb Expressionsupporting

confidence: 74%

The molecular basis of the non-thyroidal illness syndrome

Vries¹,

Fliers²,

Boelen³

2015

Journal of Endocrinology

153

116

View full text Add to dashboard Cite

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“…On this basis, we favor the possibility that tumor cells stimulate the production of certain cytokines from inflammatory and immune cells that elicit the endocrine responses detected. There are multiple candidate mediators that increase corticosterone levels when applied in vivo (Besedovsky et al, 1986(Besedovsky et al, , 1991: TNF, which inhibits prolactin release (Harel et al, 1995), and TNF, IL-1, IL-6 and interferon, which inhibit insulin secretion (Rabinovitch et al, 1990;del Rey and Besedovsky, 1987). …”

Section: Table II -Hormone Levels In Animals Bearing Autochthonous Tumentioning

confidence: 99%

“…Furthermore, it is well established that insulin, prolactin and corticosterone exert synergistic effects on neoplastic transformation (Ball et al, 1988;Singh et al, 1980;Giovannucci, 1995;Tran et al, 1996;Haraguchi et al, 1992) and tumor cell growth, e.g., by inducing the expression of different oncogenes in mammary epithelial cells (Romagnolo et al, 1993;Haraguchi et al, 1997;Wennbo et al, 1997). In addition, levels of insulin, corticosterone and prolactin are influenced by cytokines derived from inflammatory and other types of immune cell, which therefore may mediate changes in the levels of these hormones during tumor development (Besedovsky et al, 1991;Harel et al, 1995;Rabinovitch et al, 1990;del Rey and Besedovsky, 1987).…”

mentioning

confidence: 97%

Endocrine host responses during early and late phases of tumor development

et al. 2000

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“…However, in the treatment of hemipituitaries, it results in a dose-related increase in ACTH, GH, and thyroid-stimulating hormone (TSH) secretion, while PRL secretion is not affected [17], although it causes its release in dispersed anterior pituitary cell culture [18]. In cultured rat anterior pituitary cells, chronic treatment suppressed basal and growth hormone-releasing hormone-stimulated GH release, basal and thyroid-releasing hormone-induced PRL, and basal TSH, while it enhanced the maximal TSH response to thyroid-releasing hormone [19]. In the normal human pituitary, it activates the PRL promoter [20].…”

Section: Relevant Cytokines In the Anterior Pituitarymentioning

confidence: 99%

Regulation of Pituitary Function by Cytokines

et al. 2009

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Research performed on the pituitary has proven that cytokines play an important role in maintaining pituitary physiology, affecting not only cell proliferation but also hormone secretion. The effects of cytokines can be autocrine or paracrine. This review gives an overview on the effects of the most studied cytokines in the pituitary. Special interest is focused on interleukin-6 (IL-6) because it has the distinctive characteristic of stimulating pituitary tumor cell growth, but has the opposite effect on normal pituitary cells. On the other hand, IL-6 is a cytokine of interest in the pituitary because recent work has shown that it promotes and maintains senescence in certain types of tumors. Given that the majority of pituitary adenomas are microadenomas and the fact that clinically inapparent pituitary tumors are quite common, senescence, perhaps mediated by IL-6, is an attractive mechanism for explaining the benign nature of pituitary tumors.

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Prolonged effects of tumor necrosis factor-α on anterior pituitary hormone release

Cited by 30 publications

References 22 publications

The molecular basis of the non-thyroidal illness syndrome

The molecular basis of the non-thyroidal illness syndrome

Endocrine host responses during early and late phases of tumor development

Regulation of Pituitary Function by Cytokines

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