scholarly journals β-Blocker inhibits myocardial infarction-induced brown adipose tissue D2 activation and maintains a low thyroid hormone state in rats

2018 ◽  
Author(s):  
Fernando A. C. Seara ◽  
Iracema G. Araujo ◽  
Güínever E. Império ◽  
Michelle P. Marassi ◽  
Alba C. M. Silva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Cardiac Function ◽  
Brown Adipose Tissue ◽  
Sham Group ◽  
Low T3 ◽  
Brown Adipose ◽  
Serum T3 ◽  
Serum T4

AbstractConsidering the recognized role of thyroid hormones on the cardiovascular system during health and disease, we hypothesized that type 2 deiodinase (D2) activity, the main activation pathway of thyroxine (T4)-to-triiodothyronine (T3), could be an important site to modulate thyroid hormone status, which would then constitute a possible target for β-adrenergic blocking agents in a myocardial infarction (MI) model induced by left coronary occlusion in rats. Despite a sustained and dramatic fall in serum T4 concentrations (60-70%), the serum T3 concentration fell only transiently in the first week post-infarction (53%) and returned to control levels at 8 and 12 weeks after surgery compared to Sham group (P<0.05). Brown adipose tissue (BAT) D2 activity (fmoles T4/min.mg ptn) was dramatically increased by approximately 77% in the 8th week and approximately 100% in the 12th week in the MI group compared to that of the Sham group (P<0.05). Beta-blocker treatment (propranolol given in the drinking water, 0.5 g/L) maintained a low T3 state in MI animals, dampening both BAT D2 activity (44% reduction) and serum T3 (66% reduction in serum T3) compared to that of the non-treated MI group 12 weeks after surgery (P<0.05). Propranolol improved cardiac function (assessed by echocardiogram) in MI group compared to MI-non treated one by 40 and 57 % 1 and 12 weeks after treatment respectively (P<0.05). Our data suggest that the beta-adrenergic pathway may contribute to BAT D2 hyperactivity and T3 normalization after MI in rats. Propranolol treatment maintains low T3 state and improves cardiac function additionally.

scholarly journals Correction: Thyroid Hormone Activates Brown Adipose Tissue and Increases Non-Shivering Thermogenesis—A Cohort Study in a Group of Thyroid Carcinoma Patients

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0209225
Author(s):  
Evie P. M. Broeders ◽  
Guy H. E. J. Vijgen ◽  
Bas Havekes ◽  
Nicole D. Bouvy ◽  
Felix M. Mottaghy ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cohort Study ◽  
Thyroid Hormone ◽  
Thyroid Carcinoma ◽  
Brown Adipose Tissue ◽  
Brown Adipose ◽  
Shivering Thermogenesis

Regulation of brown adipose tissue lipogenesis by thyroid hormone and the sympathetic nervous system

1993 ◽  
Vol 265 (2) ◽  
pp. E252-E258 ◽  
Author(s):  
W. J. Yeh ◽  
P. Leahy ◽  
H. C. Freake
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Thyroid Hormone ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthase ◽  
Northern Analysis ◽  
Brown Adipose ◽  
Sympathetic Nervous

Thyroid hormone regulates lipogenesis differently in rat liver and brown adipose tissue (BAT). In the hypothyroid state, lipogenesis is suppressed in liver but enhanced in BAT. Here we investigated the mechanisms underlying increased lipogenesis in hypothyroid BAT. Housing the animals at 28 degrees C decreased lipogenesis in hypothyroid BAT to euthyroid levels. Denervation resulted in a 90% reduction in lipogenesis in hypothyroid BAT such that levels were lower than in euthyroid tissue. Thyroid hormone treatment of hypothyroid rats stimulated fatty acid synthesis in denervated BAT, as in liver, but decreased it in intact BAT. Steady-state levels of mRNA encoding acetyl-CoA carboxylase, fatty-acid synthase, and spor 14 were measured in similar animals by Northern analysis. The expression of these mRNAs mirrored the lipogenic data, showing that both thyroid hormone and the sympathetic nervous system work at a pretranslational level in this tissue. These data suggest that the increased BAT lipogenesis found with hypothyroidism is mediated by the sympathetic nervous system to counter the reduction in metabolic rate in these animals.

Inhibition of Type 1 Iodothyronine Deiodinase by Bisphenol A

2019 ◽  
Vol 51 (10) ◽  
pp. 671-677 ◽  
Author(s):  
Maurício Martins da Silva ◽  
Carlos Frederico Lima Gonçalves ◽  
Leandro Miranda-Alves ◽  
Rodrigo Soares Fortunato ◽  
Denise P. Carvalho ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Bisphenol A ◽  
Brown Adipose Tissue ◽  
Tissue Type ◽  
Deiodinase Activity ◽  
Brown Adipose

AbstractPlastics are ubiquitously present in our daily life and some components of plastics are endocrine-disrupting chemicals, such as bisphenol A and phthalates. Herein, we aimed to evaluate the effect of plastic endocrine disruptors on type 1 and type 2 deiodinase activities, enzymes responsible for the conversion of the pro-hormone T4 into the biologically active thyroid hormone T3, both in vitro and in vivo. Initially, we incubated rat liver type 1 deiodinase and brown adipose tissue type 2 deiodinase samples with 0.5 mM of the plasticizers, and the deiodinase activity was measured. Among them, only BPA was capable to inhibit both type 1 and type 2 deiodinases. Then, adult male Wistar rats were treated orally with bisphenol A (40 mg/kg b.w.) for 15 days and hepatic type 1 deiodinase and brown adipose tissue type 2 deiodinase activities and serum thyroid hormone concentrations were measured. In vivo bisphenol A treatment significantly reduced hepatic type 1 deiodinase activity but did not affect brown adipose tissue type 2 deiodinase activity. Serum T4 levels were higher in bisphenol A group, while T3 remained unchanged. T3/T4 ratio was decreased in rats treated with bisphenol A, reinforcing the idea that peripheral metabolism of thyroid hormone was affected by bisphenol A exposure. Therefore, our results suggest that bisphenol A can affect the metabolism of thyroid hormone thus disrupting thyroid signaling.

Brown Adipose Tissue (BAT) detection by 18F-FDG PET and thyroid hormone level(s)—a systematic review

Endocrine ◽  
2018 ◽  
Vol 62 (2) ◽  
pp. 496-500 ◽  
Author(s):  
Prasanna Santhanam ◽  
Rexford S Ahima ◽  
Jennifer S Mammen ◽  
Luca Giovanella ◽  
Giorgio Treglia
Keyword(s):  
Systematic Review ◽  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Brown Adipose Tissue ◽  
Fdg Pet ◽  
Hormone Level ◽  
Thyroid Hormone Level ◽  
Brown Adipose ◽  
18F Fdg ◽  
Bat Detection

scholarly journals Brown adipose tissue prevents glucose intolerance and cardiac remodeling in high-fat-fed mice after a mild myocardial infarction

2021 ◽  
Author(s):  
Carmem Peres Valgas da Silva ◽  
Vikram K. Shettigar ◽  
Lisa A. Baer ◽  
Eaman Abay ◽  
Kendra L. Madaris ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Body Composition ◽  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Cardiac Function ◽  
Cardiac Remodeling ◽  
Exercise Intolerance ◽  
Metabolic Function ◽  
High Fat ◽  
Brown Adipose

Abstract Background Obesity increases the risk of developing impaired glucose tolerance (IGT) and type 2 diabetes (T2D) after myocardial infarction (MI). Brown adipose tissue (BAT) is important to combat obesity and T2D, and increasing BAT mass by transplantation improves glucose metabolism and cardiac function. The objective of this study was to determine if BAT had a protective effect on glucose tolerance and cardiac function in high-fat diet (HFD) fed mice subjected to a mild MI. Methods Male C57BL/6 mice were fed a HFD for eight weeks and then divided into Sham (Sham-operated) and +BAT (mice receiving 0.1 g BAT into their visceral cavity). Sixteen weeks post-transplantation, mice were further subdivided into ±MI (Sham; Sham-MI; +BAT; +BAT-MI) and maintained on a HFD. Cardiac (echocardiography) and metabolic function (glucose and insulin tolerance tests, body composition and exercise tolerance) were assessed throughout 22 weeks post-MI. Quantitative PCR (qPCR) was performed to determine the expression of genes related to metabolic function of perigonadal adipose tissue (pgWAT), subcutaneous white adipose tissue (scWAT), liver, heart, tibialis anterior skeletal muscle (TA); and BAT. Results +BAT prevented the increase in left ventricle mass (LVM) and exercise intolerance in response to MI. Similar to what is observed in humans, Sham-MI mice developed IGT post-MI, but this was negated in +BAT-MI mice. IGT was independent of changes in body composition. Genes involved in inflammation, insulin resistance, and metabolism were significantly altered in pgWAT, scWAT, and liver in Sham-MI mice compared to all other groups. Conclusions BAT transplantation prevents IGT, the increase in LVM, and exercise intolerance following MI. MI alters the expression of several metabolic-related genes in WAT and liver in Sham-MI mice, suggesting that these tissues may contribute to the impaired metabolic response. Increasing BAT may be an important intervention to prevent the development of IGT or T2D and cardiac remodeling in obese patients post-MI.

Selenium and iodine deficiencies: effects on brain and brown adipose tissue selenoenzyme activity and expression

1997 ◽  
Vol 155 (2) ◽  
pp. 255-263 ◽  
Author(s):  
JH Mitchell ◽  
F Nicol ◽  
GJ Beckett ◽  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Glutathione Peroxidase ◽  
Brown Adipose Tissue ◽  
Iodine Deficiency ◽  
Uncoupling Protein ◽  
Compensatory Mechanisms ◽  
Iodothyronine Deiodinase ◽  
Brown Adipose ◽  
The Brain

Adequate dietary iodine supplies and thyroid hormones are needed for the development of the central nervous system (CNS) and brown adipose tissue (BAT) function. Decreases in plasma thyroxine (T4) concentrations may increase the requirement for the selenoenzymes types I and II iodothyronine deiodinase (ID-I and ID-II) in the brain and ID-II in BAT to protect against any fall in intracellular 3,3',5 tri-iodothyronine (T3) concentrations in these organs. We have therefore investigated selenoenzyme activity and expression and some developmental markers in brain and BAT of second generation selenium- and iodine-deficient rats. Despite substantial alterations in plasma thyroid hormone concentrations and thyroidal and hepatic selenoprotein expression in selenium and iodine deficiencies, ID-I, cytosolic glutathione peroxidase (cGSHPx) and phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activities and expression remained relatively constant in most brain regions studied. Additionally, brain and pituitary ID-II activities were increased in iodine deficiency regardless of selenium status. This can help maintain tissue T3 concentrations in hypothyroidism. Consistent with this, no significant effects of iodine or selenium deficiency on the development of the brain were observed, as assessed by the activities of marker enzymes. In contrast, BAT from selenium- and iodine deficient rats had impaired thyroid hormone metabolism and less uncoupling protein than in tissue from selenium- and iodine-supplemented animals. Thus, the effects of selenium and iodine deficiency on the brain are limited due to the activation of the compensatory mechanisms but these mechanisms are less effective in BAT.

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