Physiological role and regulation of iodothyronine deiodinases: A 2011 update

Marsili, Alessandro; Zavacki, Ann Marie; Harney, John W.; Larsen, P. Reed

doi:10.1007/bf03347465

Cited by 83 publications

(49 citation statements)

References 146 publications

(144 reference statements)

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“…Thus, the changes observed in the current multigenerational study, primarily T 4 , represent a reduction in the circulating thyroid hormone functional reserve pool rather than a decrease in circulating pool of the ultimate T 3 hormone (Larsen and Zavacki 2012;Marsili et al, 2011). This interpretation is consistent with the lack of any evidence of overt thyroid disease such asovert hypothyroidism as evidenced by lack of histopathology and changes in circulating TSH and T 3 .…”

Section: Discussionsupporting

confidence: 81%

“…Serum T 4 represents a circulating thyroid hormone reserve since it is a pro-hormone, with T 3 being the ultimate hormone (Larsen and Zavacki 2012;Marsili et al, 2011). Thus, the changes observed in the current multigenerational study, primarily T 4 , represent a reduction in the circulating thyroid hormone functional reserve pool rather than a decrease in circulating pool of the ultimate T 3 hormone (Larsen and Zavacki 2012;Marsili et al, 2011).…”

Section: Discussionmentioning

confidence: 88%

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A reproductive, developmental and neurobehavioral study following oral exposure of tetrabromobisphenol A on Sprague-Dawley rats

2015

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The objectives of these GLP US EPA OPPTS 970.3800 and 970.3700 studies were to examine the effects of tetrabromobisphenol A (TBBPA) at oral doses of 10, 100 or 1000 mg/kg BW/day over the course of 2 generations on growth as well as behavioral, neurological and neuropathologic functions in offspring. In a separate study the influence of oral TBBPA (0, 100, 300 or 1000 mg/kg BW/d) was examined on embryonic/fetal development from gestation days (GDs) 0-19. In the reproductive study, exposure to ≥ 100-mg/kg BW/d TBBPA resulted in a decrease in circulating, peripheral thyroxine (T4) levels in rats that were not accompanied by any marked alterations in triiodothyronine (T3) and thyroid stimulating hormone (TSH). These findings are explainable on the basis of induction of rat liver catabolism, a phenomenon that may be species-specific and not relevant for humans. TBBPA at up to 1000 mg/kg BW/d was not associated with any significant non-neurological effects on reproduction, growth and development. A subtle reduction, of unknown biological relevance, in the thickness of the parietal cortices of 11-day-old F2 pups in the 1000 mg/kg BW/d group was noted. This change was not accompanied by evidence of micro-anatomic changes. No estrogenic effects sufficient to affect macro and micro anatomy, fertility, reproduction, development, survival or behavior were detected in the embryofetal development study or in the multigenerational study. No other TBBPA-related effects on developmental neurotoxicity/neuropathology were detected. In the developmental study no TBBPA related change in mortality rate was observed in any of the dams. No other significant test article-related effects were noted. The no observed effect level (NOEL) for maternal and developmental toxicity was 1000 mg/kg BW/d, the highest dose evaluated.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 88%

A reproductive, developmental and neurobehavioral study following oral exposure of tetrabromobisphenol A on Sprague-Dawley rats

2015

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“…The main hormones secreted by the gland are Thyroxine (T 4 ), which has limited biological activity and triiodothyronine (T 3 ) which is more potent but with a shorter half-life. T 4 is converted to T 3 by the enzyme thyroxine 5'-deiodinase [165]. Thyroid hormones are regulated by thyroid stimulating hormone (TSH) secreted by the anterior pituitary gland, which in turn is regulated by TRH produced by the hypothalamus [166, 167].…”

Section: Overview Of Tissues and Hormones Controlling Metabolismmentioning

confidence: 99%

Metabolism disrupting chemicals and metabolic disorders

Heindel

Blumberg

Cave

et al. 2017

Reproductive Toxicology

820

651

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The recent epidemics of metabolic diseases, obesity, type 2 diabetes(T2D), liver lipid disorders and metabolic syndrome have largely been attributed to genetic background and changes in diet, exercise and aging. However, there is now considerable evidence that other environmental factors may contribute to the rapid increase in the incidence of these metabolic diseases. This review will examine changes to the incidence of obesity, T2D and non-alcoholic fatty liver disease (NAFLD), the contribution of genetics to these disorders and describe the role of the endocrine system in these metabolic disorders. It will then specifically focus on the role of endocrine disrupting chemicals (EDCs) in the etiology of obesity, T2D and NAFLD while finally integrating the information on EDCs on multiple metabolic disorders that could lead to metabolic syndrome. We will specifically examine evidence linking EDC exposures during critical periods of development with metabolic diseases that manifest later in life and across generations.

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“…Thyroxine (T 4 ) is the major secretory product of the thyroid gland and it is a precursor of the active form of the hormone, the 3,5,3 0 -triiodothyronine (T 3 ), which is mainly produced in peripheral tissues by 5 0 -deiodination of T 4 (9). Thyroid hormone production is controlled by the thyroid-stimulating hormone (TSH) that is secreted by the anterior pituitary gland.…”

Section: The Thermogenic Effect Of Thyroid Hormonesmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: The crosstalk between thyroid gland and adipose tissue: signal integration in health and disease

Santini

Marzullo

Rotondi

et al. 2014

European Journal of Endocrinology

202

185

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Obesity and thyroid diseases are common disorders in the general population and they frequently occur in single individuals. Alongside a chance association, a direct relationship between 'thyroid and obesity' has been hypothesized. Thyroid hormone is an important determinant of energy expenditure and contributes to appetite regulation, while hormones and cytokines from the adipose tissue act on the CNS to inform on the quantity of energy stores. A continuous interaction between the thyroid hormone and regulatory mechanisms localized in adipose tissue and brain is important for human body weight control and maintenance of optimal energy balance. Whether obesity has a pathogenic role in thyroid disease remains largely a matter of investigation. This review highlights the complexity in the identification of thyroid hormone deficiency in obese patients. Regardless of the importance of treating subclinical and overt hypothyroidism, at present there is no evidence to recommend pharmacological correction of the isolated hyperthyrotropinemia often encountered in obese patients. While thyroid hormones are not indicated as anti-obesity drugs, preclinical studies suggest that thyromimetic drugs, by targeting selected receptors, might be useful in the treatment of obesity and dyslipidemia.

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Physiological role and regulation of iodothyronine deiodinases: A 2011 update

Cited by 83 publications

References 146 publications

A reproductive, developmental and neurobehavioral study following oral exposure of tetrabromobisphenol A on Sprague-Dawley rats

A reproductive, developmental and neurobehavioral study following oral exposure of tetrabromobisphenol A on Sprague-Dawley rats

Metabolism disrupting chemicals and metabolic disorders

MECHANISMS IN ENDOCRINOLOGY: The crosstalk between thyroid gland and adipose tissue: signal integration in health and disease

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