Triiodothyronine induces the transcription of the uncoupling protein gene and stabilizes its mRNA in fetal rat brown adipocyte primary cultures.

Confluent fetal rat brown adipocytes in primary culture showed an almost undetectable level of uncoupling protein (UCP) mRNA and a low mitochondrial content of functional UCP. Treatment of confluent cells with 10 nM triiodothyronine in a serum-free medium, in the absence of noradrenergic stimulation...

Descripción completa

Detalles Bibliográficos
Autores: Guerra, C, Roncero, C, Porras, A, Fernández, M, Benito, M
Tipo de recurso: artículo
Fecha de publicación:1996
País:España
Institución:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/23075
Acceso en línea:https://hdl.handle.net/20.500.12105/23075
Access Level:acceso abierto
Palabra clave:Adipose Tissue, Brown
Animals
Carrier Proteins
Cells, Cultured
Cycloheximide
Gene Expression Regulation
Guanosine Diphosphate
Ion Channels
Membrane Proteins
Mitochondria
Mitochondrial Proteins
Norepinephrine
Protein Synthesis Inhibitors
RNA, Messenger
Rats
Transcription, Genetic
Triiodothyronine
Uncoupling Protein 1
Descripción
Sumario:Confluent fetal rat brown adipocytes in primary culture showed an almost undetectable level of uncoupling protein (UCP) mRNA and a low mitochondrial content of functional UCP. Treatment of confluent cells with 10 nM triiodothyronine in a serum-free medium, in the absence of noradrenergic stimulation, increased the amount of UCP mRNA in a time-dependent manner. This effect was due to an increased UCP gene transcription rate and UCP mRNA stabilization, resulting in a higher content of immunoreactive mitochondrial UCP and functional UCP (detected by its ability to bind GDP). Thus, triiodothyronine might play a significant physiological role in the UCP expression throughout fetal development, when brown adipose tissue starts to differentiate and UCP is primarily expressed.