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Hypothalamic mTOR pathway mediates thyroid hormone-induced hyperphagia in hyperthyroidism
The Journal of pathology, 2012-06, Vol.227 (2), p.209-222
Varela, Luis
Martínez-Sánchez, Noelia
Gallego, Rosalía
Vázquez, María J
Roa, Juan
Gándara, Marina
Schoenmakers, Erik
Nogueiras, Rubén
Chatterjee, Krishna
Tena-Sempere, Manuel
Diéguez, Carlos
López, Miguel
2012
Details
Autor(en) / Beteiligte
Varela, Luis
Martínez-Sánchez, Noelia
Gallego, Rosalía
Vázquez, María J
Roa, Juan
Gándara, Marina
Schoenmakers, Erik
Nogueiras, Rubén
Chatterjee, Krishna
Tena-Sempere, Manuel
Diéguez, Carlos
López, Miguel
Titel
Hypothalamic mTOR pathway mediates thyroid hormone-induced hyperphagia in hyperthyroidism
Ist Teil von
The Journal of pathology, 2012-06, Vol.227 (2), p.209-222
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2012
Link zum Volltext
Quelle
Wiley Online Library - AutoHoldings Journals
Beschreibungen/Notizen
Hyperthyroidism is characterized in rats by increased energy expenditure and marked hyperphagia. Alterations of thermogenesis linked to hyperthyroidism are associated with dysregulation of hypothalamic AMPK and fatty acid metabolism; however, the central mechanisms mediating hyperthyroidism‐induced hyperphagia remain largely unclear. Here, we demonstrate that hyperthyroid rats exhibit marked up‐regulation of the hypothalamic mammalian target of rapamycin (mTOR) signalling pathway associated with increased mRNA levels of agouti‐related protein (AgRP) and neuropeptide Y (NPY), and decreased mRNA levels of pro‐opiomelanocortin (POMC) in the arcuate nucleus of the hypothalamus (ARC), an area where mTOR co‐localizes with thyroid hormone receptor‐α (TRα). Central administration of thyroid hormone (T3) or genetic activation of thyroid hormone signalling in the ARC recapitulated hyperthyroidism effects on feeding and the mTOR pathway. In turn, central inhibition of mTOR signalling with rapamycin in hyperthyroid rats reversed hyperphagia and normalized the expression of ARC‐derived neuropeptides, resulting in substantial body weight loss. The data indicate that in the hyperthyroid state, increased feeding is associated with thyroid hormone‐induced up‐regulation of mTOR signalling. Furthermore, our findings that different neuronal modulations influence food intake and energy expenditure in hyperthyroidism pave the way for a more rational design of specific and selective therapeutic compounds aimed at reversing the metabolic consequences of this disease. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.3984
Titel-ID: cdi_crossref_primary_10_1002_path_3984
Format
–
Schlagworte
Agouti-Related Protein - genetics
,
AMP-Activated Protein Kinases - metabolism
,
AMPK
,
Animals
,
Biological and medical sciences
,
Disease Models, Animal
,
Eating - drug effects
,
Endocrinopathies
,
energy balance
,
Feeding Behavior - drug effects
,
food intake
,
Hyperphagia - enzymology
,
Hyperphagia - etiology
,
Hyperphagia - genetics
,
Hyperphagia - physiopathology
,
Hyperphagia - prevention & control
,
hyperthyroidism
,
Hyperthyroidism - chemically induced
,
Hyperthyroidism - complications
,
Hyperthyroidism - enzymology
,
Hyperthyroidism - genetics
,
Hyperthyroidism - physiopathology
,
hypothalamus
,
Hypothalamus - drug effects
,
Hypothalamus - enzymology
,
Hypothalamus - physiopathology
,
Investigative techniques, diagnostic techniques (general aspects)
,
Male
,
Medical sciences
,
mTOR
,
Neural Pathways - drug effects
,
Neural Pathways - enzymology
,
Neuropeptide Y - genetics
,
Non tumoral diseases. Target tissue resistance. Benign neoplasms
,
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
,
Phosphorylation
,
Pro-Opiomelanocortin - genetics
,
Protein Kinase Inhibitors - pharmacology
,
Rats
,
Rats, Sprague-Dawley
,
RNA, Messenger - metabolism
,
Signal Transduction - drug effects
,
Sirolimus - pharmacology
,
Thyroid Hormone Receptors alpha - metabolism
,
Thyroid. Thyroid axis (diseases)
,
Time Factors
,
TOR Serine-Threonine Kinases - antagonists & inhibitors
,
TOR Serine-Threonine Kinases - metabolism
,
Triiodothyronine
,
Weight Loss
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