scholarly journals The Small Polyphenolic Molecule Kaempferol Increases Cellular Energy Expenditure and Thyroid Hormone Activation

Diabetes ◽  
2007 ◽  
Vol 56 (3) ◽  
pp. 767-776 ◽  
Author(s):  
W. S. da-Silva ◽  
J. W. Harney ◽  
B. W. Kim ◽  
J. Li ◽  
S. D.C. Bianco ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Energy Expenditure ◽  
Cellular Energy

Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation

Nature ◽  
2006 ◽  
Vol 439 (7075) ◽  
pp. 484-489 ◽  
Author(s):  
Mitsuhiro Watanabe ◽  
Sander M. Houten ◽  
Chikage Mataki ◽  
Marcelo A. Christoffolete ◽  
Brian W. Kim ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Energy Expenditure ◽  
Bile Acids

scholarly journals Thyroid Hormone Mediated Modulation of Energy Expenditure

2015 ◽  
Vol 16 (7) ◽  
pp. 16158-16175 ◽  
Author(s):  
Janina Vaitkus ◽  
Jared Farrar ◽  
Francesco Celi
Keyword(s):  
Thyroid Hormone ◽  
Energy Expenditure

scholarly journals Liver X receptor β controls thyroid hormone feedback in the brain and regulates browning of subcutaneous white adipose tissue

2015 ◽  
Vol 112 (45) ◽  
pp. 14006-14011 ◽  
Author(s):  
Yifei Miao ◽  
Wanfu Wu ◽  
Yubing Dai ◽  
Laure Maneix ◽  
Bo Huang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Energy Expenditure ◽  
White Adipose Tissue ◽  
Uncoupling Protein ◽  
Thyroid Stimulating Hormone ◽  
Vital Role ◽  
Normal Diet ◽  
Subcutaneous White Adipose Tissue ◽  
Brown Adipose

The recent discovery of browning of white adipose tissue (WAT) has raised great research interest because of its significant potential in counteracting obesity and type 2 diabetes. Browning is the result of the induction in WAT of a newly discovered type of adipocyte, the beige cell. When mice are exposed to cold or several kinds of hormones or treatments with chemicals, specific depots of WAT undergo a browning process, characterized by highly activated mitochondria and increased heat production and energy expenditure. However, the mechanisms underlying browning are still poorly understood. Liver X receptors (LXRs) are one class of nuclear receptors, which play a vital role in regulating cholesterol, triglyceride, and glucose metabolism. Following our previous finding that LXRs serve as repressors of uncoupling protein-1 (UCP1) in classic brown adipose tissue in female mice, we found that LXRs, especially LXRβ, also repress the browning process of subcutaneous adipose tissue (SAT) in male rodents fed a normal diet. Depletion of LXRs activated thyroid-stimulating hormone (TSH)-releasing hormone (TRH)-positive neurons in the paraventricular nucleus area of the hypothalamus and thus stimulated secretion of TSH from the pituitary. Consequently, production of thyroid hormones in the thyroid gland and circulating thyroid hormone level were increased. Moreover, the activity of thyroid signaling in SAT was markedly increased. Together, our findings have uncovered the basis of increased energy expenditure in male LXR knockout mice and provided support for targeting LXRs in treatment of obesity.

scholarly journals The Role of Nuclear Receptor Corepressors NCoR1 and SMRT on Physiologic Function in the Adult Mouse

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A979-A979
Author(s):  
Megan J Ritter ◽  
Izuki Amano ◽  
Lorraine Soares De Oliveira ◽  
Kristen R Vella ◽  
Anthony Neil Hollenberg
Keyword(s):  
Thyroid Hormone ◽  
Energy Expenditure ◽  
Nuclear Receptor ◽  
Adult Mouse ◽  
Thyroid Hormone Receptor ◽  
Rapid Development ◽  
Lethal Phenotype ◽  
Organ Systems ◽  
Physiologic Function

Abstract Thyroid hormone (TH) plays an essential role in maintaining homeostasis and regulating metabolism in all organ systems beginning with embryogenesis and continuing throughout life. TH action is mediated by the thyroid hormone receptor (TR), which is a nuclear receptor, and it’s coregulators. The nuclear receptor corepressor 1 (NCoR1) and the silencing mediator of retinoid and thyroid hormone receptors (SMRT) are two critical corepressors of the TR that inhibit gene transcription in the absence of TH. Repression is mediated by complexing with histone deacetylase 3 (HDAC3), which is stabilized by NCoR1 and SMRT. NCoR1 and SMRT are critical for maintaining metabolic homeostasis and act to mediate energy expenditure, insulin sensitivity, and body weight. We sought to elucidate the roles of NCoR1 and SMRT in maintaining global physiologic function in the adult mouse. In order to study the post-natal role of these corepressors, we used a tamoxifen-inducible Cre recombinase (UBC-Cre-ERT2) to knock-out (KO) NCoR1, SMRT, or NCoR1 and SMRT together in adult mice because global deletion of either corepressor during embryogenesis is lethal. Mice were injected with tamoxifen at 8 weeks of age to KO either NCoR1 (NCoR1-KO; NKO), SMRT (SMRT-KO; SKO), or both NCoR1 and SMRT (double KO; DKO) and metabolic parameters were analyzed. While postnatal deletion of either NCoR1 or SMRT did not impact mortality, KO of both NCoR1 and SMRT resulted in a rapidly lethal phenotype heralded by weight loss, hypoglycemia and hypothermia. Metabolic phenotyping confirmed a loss of body mass and in particular fat mass in addition to a reduction in energy expenditure and increase in fecal caloric density. Further analysis showed the rapid development of hepatosteatosis and disturbances in lipid metabolism with a profound increase in beta-oxidation. We also found a reduction in HDAC3 protein levels in the DKO mice but no rapidly lethal phenotype in HDAC3 KO mice. Overall, we show that NCoR1 and SMRT together are critical for life as their deletion results in a rapidly lethal phenotype. While NCoR1 and SMRT are required to stabilize the corepressor complex, including HDAC3, HDAC3 KO resulted in a distinct and separate phenotype.

scholarly journals Energy Expenditure during Cell Spreading Induces AMPK Activation and Regulates the Mechanoresponse of Stem Cells

2019 ◽  
Author(s):  
Jing Xie ◽  
Min Bao ◽  
Xinyu Hu ◽  
Werner J. H. Koopman ◽  
Wilhelm T. S. Huck
Keyword(s):  
Energy Expenditure ◽  
Cell Fate ◽  
Focal Adhesions ◽  
Cell Spreading ◽  
Mitochondrial Fragmentation ◽  
Cell Contractility ◽  
Genetic Ablation ◽  
Cellular Energy ◽  
Atp Levels ◽  
Amp Activated Protein Kinase

AbstractCells respond to the mechanical properties of the extracellular matrix (ECM) through formation of focal adhesions (FAs), re-organization of the actin cytoskeleton and adjustment of cell contractility. These are energy-demanding processes, but a potential causality between mechanical cues and cellular (energy) metabolism remains largely unexplored. Here, we demonstrate that cytoskeletal reorganization and FA formation during cell spreading on stiff substrates lead to a drop in intracellular ATP levels, thereby activating AMP-activated protein kinase (AMPK). The latter then triggers rapid mitochondrial fragmentation and an increase in ATP levels to reinforce cell tension and regulate nuclear localization of YAP/TAZ and Runx2. Genetic ablation of AMPK Thr-172 phosphorylation lowered cellular ATP content and strongly reduced responses to substrate stiffness. Together, these findings reveal the importance of energy expenditure in regulating the mechanoresponse of cells, and point to AMPK as a key mediator of stem cell fate in response to ECM mechanics.

scholarly journals Quantifying energy expenditure in childhood: utility in managing pediatric metabolic disorders

2019 ◽  
Vol 110 (5) ◽  
pp. 1186-1191
Author(s):  
Laura P E Watson ◽  
Katherine S Carr ◽  
Michelle C Venables ◽  
Carlo L Acerini ◽  
Greta Lyons ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Energy Expenditure ◽  
Thyroid Hormone Receptor ◽  
Pediatric Population ◽  
Resting Energy Expenditure ◽  
Prediction Equation ◽  
Healthy Population ◽  
Prediction Equations ◽  
Z Scores ◽  
Healthy Participants

ABSTRACT Background Energy expenditure prediction equations are used to estimate energy intake based on general population measures. However, when using equations to compare with a disease cohort with known metabolic abnormalities, it is important to derive one's own equations based on measurement conditions matching the disease cohort. Objective We aimed to use newly developed prediction equations based on a healthy pediatric population to describe and predict resting energy expenditure (REE) in a cohort of pediatric patients with thyroid disorders. Methods Body composition was measured by DXA and REE was assessed by indirect calorimetry in 201 healthy participants. A prediction equation for REE was derived in 100 healthy participants using multiple linear regression and z scores were calculated. The equation was validated in 101 healthy participants. This method was applied to participants with resistance to thyroid hormone (RTH) disorders, due to mutations in either thyroid hormone receptor β or α (β: female n = 17, male n = 9; α: female n = 1, male n = 1), with deviation of REE in patients compared with the healthy population presented by the difference in z scores. Results The prediction equation for REE = 0.061 * Lean soft tissue (kg) − 0.138 * Sex (0 male, 1 female) + 2.41 (R2 = 0.816). The mean ± SD of the residuals is −0.02 ± 0.44 kJ/min. Mean ± SD REE z scores for RTHβ patients are −0.02 ± 1.26. z Scores of −1.69 and −2.05 were recorded in male (n = 1) and female ( n = 1) RTHα patients. Conclusions We have described methodology whereby differences in REE between patients with a metabolic disorder and healthy participants can be expressed as a z score. This approach also enables change in REE after a clinical intervention (e.g., thyroxine treatment of RTHα) to be monitored.

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