ABSTRACT
OBJECTIVE: To examine the effect of different doses of triiodothyronine (T3) on mRNA levels of thyroid hormone receptors, TRα and TRß, at different times. MATERIALS AND METHODS: 3T3-L1 adipocytes were incubated with T3 (physiological dose: F; supraphysiological doses: SI or SII), or without T3 (control, C) for 0.5, 1, 6, or 24h. TRα and TRß mRNA was detected using real-time polymerase chain reaction. RESULTS: F increased TRß mRNA levels at 0.5h. After 1h, TRα levels increased with F and SI and TRß levels decreased with SII compared with C, F, and SI. After 6h, both genes were suppressed at all concentrations. In 24h, TRα and TRß levels were similar to those of C group. CONCLUSIONS: T3 action with F began at 1h for TRα and at 0.5h for TRß. These results suggest the importance of knowing the times and doses that activate T3 receptors in adipocytes.
Subject(s)
Adipocytes/drug effects , Antigenic Modulation/immunology , Thyroid Hormone Receptors alpha/metabolism , Thyroid Hormone Receptors beta/metabolism , Triiodothyronine/administration & dosage , Adipocytes/metabolism , Animals , Cell Line , Drug Administration Schedule , RNA, Messenger/analysis , Thyroid Hormone Receptors alpha/genetics , Thyroid Hormone Receptors beta/genetics , Triiodothyronine/pharmacologyABSTRACT
OBJECTIVE: To examine the effect of different doses of triiodothyronine (T3) on mRNA levels of thyroid hormone receptors, TRα and TRβ, at different times. MATERIALS AND METHODS: 3T3-L1 adipocytes were incubated with T3 (physiological dose: F; supraphysiological doses: SI or SII), or without T3 (control, C) for 0.5, 1, 6, or 24h. TRα and TRβ mRNA was detected using real-time polymerase chain reaction. RESULTS: F increased TRβ mRNA levels at 0.5h. After 1h, TRα levels increased with F and SI and TRβ levels decreased with SII compared with C, F, and SI. After 6h, both genes were suppressed at all concentrations. In 24h, TRα and TRβ levels were similar to those of C group. CONCLUSIONS: T3 action with F began at 1h for TRα and at 0.5h for TRβ. These results suggest the importance of knowing the times and doses that activate T3 receptors in adipocytes.
OBJETIVO: Examinar o efeito de diferentes doses de triiodotironina (T3) sobre a expressão gênica dos receptores TRα e TRβ em diferentes tempos. MATERIAIS E MÉTODOS: Adipócitos, 3T3-L1, foram incubados com T3 nas doses fisiológica (F, 10nM) e suprafisiológicas (SI, 100nM ou SII, 1000nM) ou veículo (controle, C) durante 0,5, 1, 6 ou 24h. mRNA dos TRs foram detectados utilizando PCR em tempo real. RESULTADOS: Níveis de TRβ aumentaram em F em 0,5h. Após 1h, níveis de TRα aumentaram em F e SI comparado ao C, enquanto TRβ diminuiu no SII comparado com C, F, e SI. Após 6h, ambos os genes foram suprimidos em todas concentrações. Em 24h, níveis de TRα e TRβ retornaram aos do C. CONCLUSÕES: Ação do T3 em F iniciou-se em 1h para TRα e 0,5h para TRβ. Esses resultados são importantes para determinar tempo inicial e dose de T3 em que os receptores de HT são ativados em adipócitos.
Subject(s)
Animals , Adipocytes/drug effects , Antigenic Modulation/immunology , Thyroid Hormone Receptors alpha/metabolism , Thyroid Hormone Receptors beta/metabolism , Triiodothyronine/administration & dosage , Adipocytes/metabolism , Cell Line , Drug Administration Schedule , RNA, Messenger/analysis , Thyroid Hormone Receptors alpha/genetics , Thyroid Hormone Receptors beta/genetics , Triiodothyronine/pharmacologyABSTRACT
Adiponectin is the most abundant plasma protein synthesized mostly by adipose tissue and is an insulin-sensitive hormone, playing a central role in glucose and lipid metabolism. Adiponectin effects are mediated via two receptors, adipoR1 and adipoR2. Several hormones and diet components that are involved in insulin resistance may impair insulin sensitivity at least in part by decreasing adiponectin and adiponectin receptors. Adiponectin expression and serum levels are associated with the amount and type of fatty acids and carbohydrate consumed. Other food items, such as vitamins, alcohol, sodium, green tea, and coffee, have been reported to modify adiponectin levels. Several hormones, including testosterone, estrogen, prolactin, glucocorticoids, catecholamines, and growth hormone, have been shown to inhibit adiponectin production, but the studies are still controversial. Even so, adiponectin is a potential therapeutic target in the treatment of diabetes mellitus and other diseases associated with hypoadiponectinemia.
