Thyroid hormone signaling in energy homeostasis and energy metabolism

McAninch, Elizabeth A.; Bianco, Antonio C.

doi:10.1111/nyas.12374

Cited by 183 publications

(157 citation statements)

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“…Typically, Dio2 converts T4 to its active metabolite, T3 (37). The Dio2-mediated increase in T3 levels can enhance the cyclic AMP (cAMP) response.…”

Section: Discussionmentioning

confidence: 99%

β-Lapachone Prevents Diet-Induced Obesity by Increasing Energy Expenditure and Stimulating the Browning of White Adipose Tissue via Downregulation of miR-382 Expression

et al. 2016

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There has been great interest in the browning of fat for the treatment of obesity. Although b-lapachone (BLC) has potential therapeutic effects on obesity, the fat-browning effect and thermogenic capacity of BLC on obesity have never been demonstrated. Here, we showed that BLC stimulated the browning of white adipose tissue (WAT), increased the expression of brown adipocyte-specific genes (e.g., uncoupling protein 1 [UCP1]), decreased body weight gain, and ameliorated metabolic parameters in mice fed a high-fat diet. Consistently, BLC-treated mice showed significantly higher energy expenditure compared with control mice. In vitro, BLC increased the expression of brown adipocyte-specific genes in stromal vascular fraction-differentiated adipocytes. BLC also controlled the expression of miR-382, which led to the upregulation of its direct target, Dio2. Upregulation of miR-382 markedly inhibited the differentiation of adipocytes into beige adipocytes, whereas BLC recovered beige adipocyte differentiation and increased the expression of Dio2 and UCP1. Our findings suggest that the BLC-mediated increase in the browning of WAT and the thermogenic capacity of BAT significantly results in increases in energy expenditure. Browning of WAT by BLC was partially controlled via the regulation of miR-382 targeting Dio2 and may lead to the prevention of diet-induced obesity.

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“…Typically, Dio2 converts T4 to its active metabolite, T3 (37). The Dio2-mediated increase in T3 levels can enhance the cyclic AMP (cAMP) response.…”

Section: Discussionmentioning

confidence: 99%

β-Lapachone Prevents Diet-Induced Obesity by Increasing Energy Expenditure and Stimulating the Browning of White Adipose Tissue via Downregulation of miR-382 Expression

et al. 2016

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“…Deiodinases 1 or 2 (D1, D2) convert T 4 to T 3 in various tissues and their activity is differentially regulated in a condition-and tissue-specific manner (McAninch & Bianco 2014). TH have crucial roles in basal metabolic rate, thermogenesis, lipid and carbohydrate metabolism, indicating that the hypothalamus-pituitary-thyroid (HPT) axis is an important player in energy homeostasis (Hollenberg 2008, Fliers et al 2014, McAninch & Bianco 2014, Mullur et al 2014.…”

Section: Introductionmentioning

confidence: 99%

“…TH have crucial roles in basal metabolic rate, thermogenesis, lipid and carbohydrate metabolism, indicating that the hypothalamus-pituitary-thyroid (HPT) axis is an important player in energy homeostasis (Hollenberg 2008, Fliers et al 2014, McAninch & Bianco 2014, Mullur et al 2014. The activity of the HPT axis is stringently regulated by neuronal stimuli impinging on TRH neurons and by the negative-feedback effects of TH on TRH and TSH synthesis and release (Hollenberg 2008, Fekete & Lechan 2014, Schematic localization of TRH endocrine and nonendocrine cell bodies and TRH receptor fields in the hypothalamus and pituitary and of afferents to TRH neurons.…”

Section: Introductionmentioning

confidence: 99%

Regulation of TRH neurons and energy homeostasis-related signals under stress

Joseph‐Bravo

Jaimes-Hoy

Charlí

2015

Journal of Endocrinology

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Energy homeostasis relies on a concerted response of the nervous and endocrine systems to signals evoked by intake, storage, and expenditure of fuels. Glucocorticoids (GCs) and thyroid hormones are involved in meeting immediate energy demands, thus placing the hypothalamo-pituitary-thyroid (HPT) and hypothalamo-pituitary-adrenal axes at a central interface. This review describes the mode of regulation of hypophysiotropic TRHergic neurons and the evidence supporting the concept that they act as metabolic integrators. Emphasis has been be placed on i) the effects of GCs on the modulation of transcription of Trh in vivo and in vitro, ii) the physiological and molecular mechanisms by which acute or chronic situations of stress and energy demands affect the activity of TRHergic neurons and the HPT axis, and iii) the less explored role of non-hypophysiotropic hypothalamic TRH neurons. The partial evidence gathered so far is indicative of a contrasting involvement of distinct TRH cell types, manifested through variability in cellular phenotype and physiology, including rapid responses to energy demands for thermogenesis or physical activity and nutritional status that may be modified according to stress history.

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“…They influence these activities by regulating the synthesis and activation of membrane transporter proteins, deiodinase enzymes, and their cellular receptors [2]. Beside their effects on the metabolic pathways, thyroid hormones are also known to regulate insulin secretion and action [3].…”

Section: Introductionmentioning

confidence: 99%