Searchable abstracts of presentations at key conferences in endocrinology

ea0029s59.3 | Obesity and thyroid function | ICEECE2012

Type 2 deiodinase in muscle during health and disease

Boelen A.

One of the major routes for metabolism of thyroid hormones is by deiodination through the iodothyronine deiodinases, an enzyme family consisting of three members, types 1 (D1), 2 (D2) and type 3 (D3). The outer ring of thyroxin (T4) can be deiodinated by D2, leading to the formation of active hormone, triiodothyronine (T3). D2 is expressed predominantly in the brain and pituitary, but also in brown adipose tissue and muscle. Within the cell, D2 is localiz...

ea0026s13.2 | Endocrine response to critical illness | ECE2011

Thyroid hormone metabolism in inflammation and sepsis

Boelen A

During illness changes in thyroid hormone metabolism occur, collectively known as the non-thyroidal illness syndrome (NTIS). NTIS is characterized by low serum thyroid hormone levels, while TSH and TRH expression do not increase, indicating a disturbance of the normal thyroid hormone feedback regulation.Although the common view was that NTIS results in overall downregulation of metabolism in order to save energy, recent work has shown that genes involved...

ea0044s10.3 | Clinical thyroidology update | SFEBES2016

Sick Euthyroid Syndrome

Boelen Anita

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 plasma triiodothyronine (T3) levels, in severe illness accompanied by low plasma thyroxine (T4) and increased plasma reverse T3 (rT3) concentrations. Downregulation of hy...

ea0034s5.3 | Endocrine consequences of major trauma | SFEBES2014

Thyroid hormone economy during critical illness

Boelen Anita

During illness changes in thyroid hormone metabolism occur, collectively known as the non-thyroidal illness syndrome (NTIS). NTIS is characterized by low serum thyroid hormone levels, while TSH and TRH expression do not increase, indicating a disturbance of the normal thyroid hormone feedback regulation.Although the common view was that NTIS results in overall downregulation of metabolism in order to save energy, recent work has shown that genes involved...

ea0084op-04-17 | Oral Session 4: Basic 1 | ETA2022

Age and diet regulate intrahepatic thyroid hormone concentration in a mouse model of non-alcoholic fatty liver disease (NAFLD)

Bruinstroop Eveline , Boelen Anita , Yen Paul , Singh Brijesh

Background: Previously, we showed that thyroid hormone (TH) supplementation reduced hepatosteatosis in patients with non-alcoholic fatty liver disease (NAFLD) and was more effective in older patients. We hypothesized that intrahepatic TH concentrations may decrease with age. To investigate this issue, we examined the effects of age on intrahepatic TH concentrations in a mouse model of NAFLD.Methods: Intrahepatic TH levels and deiodinase activity were mea...

ea0065s4.2 | Thyroid hormone a key regulator in inflammation | SFEBES2019

Thyroid hormone in inflammation

van der Spek Anne H , Fliers Eric , Boelen Anita

Thyroid hormone levels are strongly affected by inflammation. In a wide spectrum of diseases, ranging from critical illness in the ICU to ischemic stroke, a decrease in circulating T3 and T4 is observed without the expected increase in TSH. This disruption of the negative feedback system of the hypothalamic–pituitary–thyroid (HPT) axis is accompanied by various changes in thyroid hormone metabolism at the cellular and tissue level. C...

ea0092op-07-01 | Oral Session 7: Thyroid hormone receptors | ETA2023

Monocyte and macrophage function is impaired in patients with resistance to thyroid hormone due to a mutation in thyroid hormone receptor ALPHA

van der Spek Anne , Agostini Maura , Boelen Anita , Chatterjee Krishna

Resistance to thyroid hormone due to a mutation in thyroid hormone receptor alpha (RTHα) is a syndrome whose features include delayed growth and neurocognitive development. Macrophages, which derive from circulating monocytes and have recently been recognized as important thyroid hormone target cells, are innate immune cells that are capable of adopting a wide range of phenotypes. Assuming the right phenotype in the right setting is crucial as macrophage dysfunction has b...

ea0081p206 | Thyroid | ECE2022

Discordance between fT4 and TSH concentrations during levothyroxine treatment

Jansen Heleen , Bult Marijn , Bisschop Peter H. , Boelen Anita , C Heijboer Annemieke , Hillebrand Jacquelien

Introduction: Physicians in our hospital notified the laboratory staff of a number of patients at the outpatient clinic with increased free T4 (fT4) concentrations without (complete) suppression of thyroid stimulating hormone (TSH). This phenomenon appeared to occur more frequently following implementation of a new automated fT4 immunoassay. The discordance between fT4 and TSH concentrations may be explained by analytical issues (not further explained here), incorrect referenc...

ea0022h2.5 | Oral Communications Highlights 2 | ECE2010

Effects of leptin administration on starvation-induced alterations in hepatic thyroid hormone metabolism in mice

Boelen Anita , Van Beeren Mieke , Vos Xander , Surovtseva Olga , Kwakkel Joan , Fliers Eric

Fasting induces profound metabolic changes in order to decrease energy expenditure and to conserve energy. One of the major adaptations is downregulation of the hypothalamus–pituitary–thyroid (HPT) axis, characterized by decreased serum thyroid hormone levels without an increase in serum TSH or in TRH expression in the hypothalamic paraventricular nucleus (PVN). Leptin has been proposed as a critical signal initiating the neuroendocrine response to fasting as it decr...

ea0092ps2-19-07 | Thyroid Hormone Transport & Metabolism Basic | ETA2023

Absence of MCT8 and OATP1C1 in mouse oligodendroglia cells results in delayed myelination

Richter Joshua-Joel , Markova Boyka , Boelen Anita , Mayerl Steffen , Heuer Heike

Inactivation of the thyroid hormone transporters Mct8/Oatp1c1 in mice causes a profound TH deficiency in the CNS due to an impaired TH transport across brain barrier cells. As oligodendrocyte maturation and myelin formation requires proper thyroid hormone (TH) signaling, Mct8/Oatp1c1 double knock-out (DKO) mice exhibit a persistent state of hypomyelination similar to the situation in MCT8 deficient patients. Yet, to which extent proper myelination is dependent on the presence ...