Thyroid Hormone Receptor Expression in the "Sick Euthyroid" Syndrome

Williams, Gareth R.; Franklyn, Jayne A.; Neuberger, James; Sheppard, M. C.

doi:10.1016/s0140-6736(89)92930-9

Cited by 61 publications

(21 citation statements)

References 30 publications

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“…SRC-1 and other coactivators in the heart (Feingold et al 2004). In agreement with these studies, but in contrast to the findings of Williams et al 1989, Boelen et al (2004b reported a rapid decrease in liver Thrb1 mRNA after LPS administration in an animal model. A lowering of THRb1 mRNA in response to inflammatory cytokines also occurs in vitro using a hepatoma cell line (Yu & Koenig 2000).…”

Section: Expression Of Thrs In Illnesssupporting

confidence: 87%

“…Early work in patients with liver failure or chronic renal failure showed increased THRa and THRb mRNA expression in peripheral mononuclear cells and liver tissue taken from biopsy (Williams et al 1989). More recently, data from models of acute illness have been published, which have included mice treated with LPS or cytokines (Beigneux et al 2003, Boelen et al 2004b, Feingold et al 2004) and patients with septic shock (Rodriguez-Perez et al 2008) and in each model, THR expression is diminished.…”

Section: Expression Of Thrs In Illnessmentioning

confidence: 99%

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Mechanisms behind the non-thyroidal illness syndrome: an update

Warner

Beckett²

2009

Journal of Endocrinology

350

317

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The mechanisms behind the changes in serum triiodothyronine (T 3 ), thyroxine (T 4 ) and TSH that occur in the nonthyroidal illness syndrome (NTIS) are becoming clearer. Induction of a central hypothyroidism occurs due to a diminution in hypothalamic thyrotropin-releasing hormone. This can be signalled by a decrease in leptin caused by malnutrition and possibly a localised increase in hypothalamic T 3 catalyzed by altered expression of hypothalamic iodothyronine deiodinases D2 and D3. Data from D1 and D2 knockout mice suggest that these enzymes may have little contribution to the low serum T 3 found in acute illness. The decline in serum T 3 and T 4 in models of acute illness precedes the fall in hepatic D1, suggesting that much of the initial fall in these hormones may be attributable to an acute phase response giving rise to a reduction in the thyroid hormone binding capacity of plasma. When measured by reliable methods, changes in serum free T 4 and free T 3 are modest in comparison to the fall seen in total thyroid hormone. Thyroid hormone transporter expression is up-regulated in many models of the NTIS, thus if diminished tissue uptake of hormone occurs in vivo, it is likely to be the result of impaired transporter function caused by diminished intracellular ATP or plasma inhibitors of transporter action. In man, chronic illness leads to an upregulation of thyroid hormone receptor (THR) expression at least in liver and renal failure. In contrast, human and animal models of sepsis and trauma indicate that expression of THRs and their coactivators are decreased in acute illness.

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Section: Expression Of Thrs In Illnesssupporting

confidence: 87%

Section: Expression Of Thrs In Illnessmentioning

confidence: 99%

Mechanisms behind the non-thyroidal illness syndrome: an update

Warner

Beckett²

2009

Journal of Endocrinology

350

317

View full text Add to dashboard Cite

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“…In his review, Chopra concludes that patients with a mild, of short duration, NTIS may be euthyroid, and this is consistent with the pioneer work of Williams et al [68] revealing increased T3 receptor expression in patients with NTIS as a plausible explanation for their clinical euthyroid status despite low circulating T4 levels; on the contrary, those suffering a severe and prolonged NTIS may actually be tissue hypothyroid and represent the subgroup that might benefit from T4 supplementation treatment [69].…”

Section: Resultsmentioning

confidence: 54%

The nonthyroidal illness syndrome in the non-critically ill patient

Παππά

Vagenakis

Alevizaki

2010

European Journal of Clinical Investigation

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Background The nonthyroidal illness syndrome (NTIS) is a very common clinical entity among hospitalized patients and has been reported in practically every severe illness and acute or chronic stressful event. There is a large body of data associating the presence of NTIS with the severity of the underlying disease. Most of these studies concern intensive care unit (ICU) patients, whereas the non-critically ill patients outside the ICU setting are less well studied.

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“…In addition to the reduction in the expression of T 3 -dependent proteins, hypothyroidism has been reported to be associated with an increase in T 3 receptor expression as compensation for the low thyroid hormone concentration [27, 28]. Unoccupied T 3 receptors repress some genes that are stimulated by T 3 .…”

Section: Discussionmentioning

confidence: 99%

Effects of Thyroid Hormone and Hypoxia on 2,3-Bisphosphoglycerate, Bisphosphoglycerate Synthase and Phosphoglycerate Mutase in Rabbit Erythroblasts and Reticulocytes in vivo

González-Cinca

Ossa²,

Carreras³

et al. 2004

Horm Res Paediatr

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Objectives: The effects of triiodothyronine (T₃) and hypoxia on 2,3-bisphosphoglycerate (2,3-BPG) studied in vitro are unclear. To clarify these effects we selected a more physiologic approach: the in vivo study in rabbits. We also present the changes produced by T₃ and hypoxia on phosphoglycerate mutase (PGAM), which requires 2,3-BPG as a cofactor, and 2,3-BPG synthase (BPGS), the enzyme responsible for 2,3-BPG synthesis in erythroblasts and reticulocytes. Methods: Hyperthyroidism was induced by daily T₃ injection (250 µg/kg), hypoxia by a mixture of 90% nitrogen and 10% oxygen and hypothyroidism by propylthiouracil (PTU) added to drinking water. Results: Both T₃ administration and hypoxic conditions increased 2,3-BPG levels and BPGS mRNA levels and activity in erythroblasts but not in reticulocytes. Unlike BPGS, both PGAM mRNA levels and activity were increased in erythroblasts and reticulocytes under hyperthyrodism and hypoxia. The antihormone PTU produced opposite effects to T₃. Conclusion: The results presented here suggest that both hyperthyroidism and hypoxia modulate in vivo red cell 2,3-BPG content by changes in the expression of BPGS. Similarly, the changes in PGAM activity are also explained by changes in its expression.

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Thyroid Hormone Receptor Expression in the "Sick Euthyroid" Syndrome

Cited by 61 publications

References 30 publications

Mechanisms behind the non-thyroidal illness syndrome: an update

Mechanisms behind the non-thyroidal illness syndrome: an update

The nonthyroidal illness syndrome in the non-critically ill patient

Effects of Thyroid Hormone and Hypoxia on 2,3-Bisphosphoglycerate, Bisphosphoglycerate Synthase and Phosphoglycerate Mutase in Rabbit Erythroblasts and Reticulocytes in vivo

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