Triiodothyronine differentially modulates the LH and FSH synthesis and secretion in male rats.

Hypothyroidism and thyrotoxicosis produce adverse effects in male reproduction by unknown mechanisms. We investigated whether triiodothyronine (T3) modulates luteinizing hormone (LH) and follicle stimulating hormone (FSH) synthesis/secretion, by inducing different thyroid states. In hypothyroidism, the content of Lhb and Fshb mRNAs was increased, while their association to ribosomes and the protein content were reduced and the serum LH and FSH concentrations were augmented and decreased, respectively.

T(3) rapidly regulates several steps of alpha subunit glycoprotein (CGA) synthesis and secretion in the pituitary of male rats: Potential repercussions on TSH, FSH and LH secretion.

TSH, FSH and LH share the same glycoprotein alpha chain (CGA) as part of their protein structure. Therefore, it is possible that thyroid and gonadal dysfunction may affect the CGA expression. This study evaluated several steps of CGA synthesis and secretion in thyrotrophs and gonadotrophs of control and hypothyroid rats, acutely or chronically-treated with T3.

Triiodothyronine rapidly alters the TSH content and the secretory granules distribution in male rat thyrotrophs by a cytoskeleton rearrangement-independent mechanism.

Rapid actions of T3 on TSH synthesis in posttranscriptional steps, such as polyadenylation and translation rate, have already been described. The focus of this paper was to characterize rapid actions of T3 on TSH secretion and the involvement of actin and microtubule cytoskeleton in this process. For that, sham-operated (SO) and thyroidectomized (Tx) rats were subjected to acute or chronic treatment with T3.

Hypothyroidism in adult male rats alters posttranscriptional mechanisms of luteinizing hormone biosynthesis.

Background: Studies in men are not consistent regarding the effects of thyroid hormone on the production of gonadotropins. In hypothyroidism consequent to diverse causes, an increase or no change in serum luteinizing hormone (LH) have been reported. The attempt to explain the mechanisms involved in this pathology using rats as an experimental model also seems to repeat this divergence, since hypothyroidism has been shown to induce hypogonadotropic hypogonadism, a hypergonadotropic state, or not to affect the basal levels of LH.

T3 rapidly increases SLC2A4 gene expression and GLUT4 trafficking to the plasma membrane in skeletal muscle of rat and improves glucose homeostasis.

Background: Glucose transporter 4 (GLUT4) is highly expressed in muscle and fat tissue, where triiodothyronine (T(3)) induces solute carrier family 2 facilitated glucose transporter member 4 (SLC2A4) gene transcription. T(3) was also shown to rapidly increase glucose uptake in myocytes exposed to cycloheximide, indicating that it might act nongenomically to regulate GLUT4 availability. We tested this hypothesis by evaluating, in thyroidectomized rats (Tx rats), the acute and/or chronic T(3) effects on GLUT4 mRNA expression and polyadenylation, protein content, and trafficking to the plasma membrane (PM) in skeletal muscle, as well as on blood glucose disappearance rate (kITT) after insulin administration.