Advances in Our Understanding of Thyroid Hormone Action at the Cellular Level*

Oppenheimer, Jack H.; Schwartz, Harold L.; Mariash, Cary N.; Kinlaw, William B.; Wong, Norman C.W.; Freake, Hedley C.

doi:10.1210/edrv-8-3-288

Cited by 457 publications

(212 citation statements)

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“…TH acts by means of a nuclear family of receptors (Yaoita et al, 1990;Kanamori and Brown, 1992;Shi et al, 1992), which interact with chromatin (Oppenheimer et al, 1987) to modulate the transcription of TH-responsive genes.…”

Section: Cell Death and Secondary Myogenesismentioning

confidence: 99%

Xenopusmuscle development: From primary to secondary myogenesis

Chanoine

Hardy

2002

Developmental Dynamics

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Xenopus myogenesis is characterized by specific features, different from those of mammalian and avian systems both at the cellular level and in gene expression patterns. During early embryogenesis, after the initial molecular signals inducing mesoderm, the myogenic determination factors XMyoD and XMyf-5 are activated in presomitic mesoderm in response to mesoderm-inducing factors. After these first inductions of the myogenic program, forming muscles in Xenopus can have different destinies, some of these resulting in cell death before adulthood. In particular, it is quite characteristic of this species that, during metamorphosis, the primary myotomal myofibers completely die and are progressively replaced by secondary "adult" multinucleated myofibers. This feature offers the unique opportunity to totally separate the molecular analysis of these two distinct types of myogenesis. The aim of this review is to summarize our knowledge on the cellular and molecular events as well as the epigenetic regulations involved in the construction of Xenopus muscles during development. Developmental Dynamics 226:12-23, 2003.

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Section: Cell Death and Secondary Myogenesismentioning

confidence: 99%

Xenopusmuscle development: From primary to secondary myogenesis

Chanoine

Hardy

2002

Developmental Dynamics

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“…Thyroid hormones act specifically by regulating the genes that underlie major neurodevelopmental events, including neurogenesis, axon and dendrite formation, neuronal migration, synaptogenesis and myelination (10)(11)(12)(13)(14) . Thyroid hormones are also involved in the regulation of BMR and macronutrient metabolism (15) .…”

mentioning

confidence: 99%

Iodine deficiency during pregnancy: a national cross-sectional survey in Latvia

Konrāde

Kalere

Strēle

et al. 2015

Public Health Nutr.

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Objective: Low iodine intake during pregnancy may cause thyroid dysfunction, which results in inadequate fetal brain development. In the absence of a universal salt iodization programme, we conducted a nationwide survey of iodine deficiency in pregnant women in Latvia. Design: A countrywide twenty-cluster survey, with at least twenty women per cluster. Participants completed a questionnaire on dietary habits concerning iodine intake (n 739). Thyroid function (thyroid-stimulating hormone, free thyroxine and thyroperoxidase antibodies) was measured (n 550). Urinary iodine was measured using the ammonium persulfate method (n 696). Setting: The survey was performed in all regions of Latvia during the spring and autumn seasons in 2013. Subjects: Pregnant women (n 829). Results: The median creatinine (Cr)-standardized urinary iodine concentration (UIC) was 80·8 (interquartile range (IQR) 46·1-130·6) µg/g Cr or 69·4 (IQR 53·9-92·6) µg/l during pregnancy, and 81 % of pregnant women had UIC levels below the WHO recommended range of 150-250 µg/g Cr. The UIC was lowest during the first trimester of pregnancy, 56·0 (IQR 36·4-100·6) µg/g Cr, reaching higher concentrations of 87·5 (IQR 46·4-141·7) µg/g Cr and 86·9 (IQR 53·8-140·6) µg/g Cr in the second and third trimesters, respectively. Women taking supplements containing ≥150 µg iodine (6·8 % of respondents) had non-significantly higher UIC than did women without supplementation (96·2 v. 80·3 µg/g Cr, respectively, P = NS). Thyroperoxidase antibody concentration did not correlate significantly with UIC: Spearman's ρ = − 0·012, P = 0·78. Conclusions: The median UIC indicates iodine deficiency in pregnant women in Latvia. Iodine supplementation (150 µg daily) and regular UIC monitoring should be suggested to overcome iodine deficiency and to reach the recommended levels without inducing autoimmune processes.

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“…Thyroid hormone is known to affect the hepatic expression of genes involved in lipid homeostasis (9). Thus, we used qRT-PCR to measure the expression of candidate genes known to be T3-regulated and/or to play important roles in lipid homeostasis at different developmental and postnatal time points.…”

Section: Perinatal Liver D2 Affects the Expression Of Genes Involved mentioning

confidence: 99%

“…The liver is a canonical target of thyroid hormone, with T3 stimulating lipogenesis, fatty acid oxidation, bile acid, and cholesterol metabolism (9). In addition, clinical studies have shown that thyrotoxicosis increases hepatic glucose production and reduces hepatic insulin sensitivity (10,11).…”

mentioning

confidence: 99%

Perinatal deiodinase 2 expression in hepatocytes defines epigenetic susceptibility to liver steatosis and obesity

Fonseca

Fernandes

McAninch

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Thyroid hormone binds to nuclear receptors and regulates gene transcription. Here we report that in mice, at around the first day of life, there is a transient surge in hepatocyte type 2 deiodinase (D2) that activates the prohormone thyroxine to the active hormone triiodothyronine, modifying the expression of ∼165 genes involved in broad aspects of hepatocyte function, including lipid metabolism. Hepatocyte-specific D2 inactivation (ALB-D2KO) is followed by a delay in neonatal expression of key lipid-related genes and a persistent reduction in peroxisome proliferator-activated receptor-γ expression. Notably, the absence of a neonatal D2 peak significantly modifies the baseline and long-term hepatic transcriptional response to a high-fat diet (HFD). Overall, changes in the expression of approximately 400 genes represent the HFD response in control animals toward the synthesis of fatty acids and triglycerides, whereas in ALB-D2KO animals, the response is limited to a very different set of only approximately 200 genes associated with reverse cholesterol transport and lipase activity. A whole genome methylation profile coupled to multiple analytical platforms indicate that 10-20% of these differences can be related to the presence of differentially methylated local regions mapped to sites of active/suppressed chromatin, thus qualifying as epigenetic modifications occurring as a result of neonatal D2 inactivation. The resulting phenotype of the adult ALB-D2KO mouse is dramatic, with greatly reduced susceptibility to diet-induced steatosis, hypertriglyceridemia, and obesity.deiodinase | thyroid hormone | lipids | steatosis | obesity

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Advances in Our Understanding of Thyroid Hormone Action at the Cellular Level*

Cited by 457 publications

References 0 publications

Xenopusmuscle development: From primary to secondary myogenesis

Xenopusmuscle development: From primary to secondary myogenesis

Iodine deficiency during pregnancy: a national cross-sectional survey in Latvia

Perinatal deiodinase 2 expression in hepatocytes defines epigenetic susceptibility to liver steatosis and obesity

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