Thyroid hormone receptors (TR) are members of the nuclear receptor superfamily. There are at least two TR isoforms, TRα and TRβ, which act as mediators of thyroid hormone in tissues. However, the relative expression of each TR isoform in target tissues is still elusive. Herein, we have developed an RT-PCR and restriction enzyme digestion method to determine the expression of TRα1 and TRβ 1. We analyzed the expression of TR isoforms in 3T3-L1 preadipocytes induced to differentiate by an adipogenic cocktail in the presence or absence of 100 nM triiodothyronine (T3). The TRα1 isoform was predominantly expressed in 3T3-L1 adipocytes, and its expression was increased at the stage of development concomitant with the emergence of lipid droplets. Little, if any, TRβ1 mRNA was detected in adipocytes. Administration of T3 to the differentiating 3T3-L1 cells enhanced the accumulation of triglyceride. The expression profile of TRα1 in T3-treated adipocytes was similar to that in non-treated cells. The transcripts of adipogenic factors, CCAAT/enhancer binding protein β (C/EBPβ) and peroxisome proliferator activated receptor γ (PPARγ), were not altered by T3. Lipid binding protein, aP2, that is downstream of these transcription factors was also unaffected by T3. In contrast, the lipogenic enzyme, glyceraldehyde-3-phosphate dehydrogenase mRNA was significantly increased in the presence of T3. Therefore, T3 appears to be a hormone capable of modulating the expression of lipogenic enzyme and augments the accumulation of lipid droplets. We conclude that the TRα isoform might play an important role in the generation and maintenance of the mature adipocyte phenotype, regulating the expression of lipogenic enzymes. © 2004 Society for Endocrinology.
CITATION STYLE
Jiang, W., Miyamoto, T., Kakizawa, T., Sakuma, T., Nishio, S. I., Takeda, T., … Hashizume, K. (2004). Expression of thyroid hormone receptor α in 3T3-L1 adipocytes; triiodothyronine increases the expression of lipogenic enzyme and triglyceride accumulation. Journal of Endocrinology, 182(2), 295–302. https://doi.org/10.1677/joe.0.1820295
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