[Regulation of thyrotropin synthesis and secretion]. / Regulação da síntese e secreção de tireotrofina.

The set point of thyrotropin (TSH) secretion is determined by the balance of a positive regulation of thyrotropin releasing hormone (TRH) and the strong negative regulation exerted by thyroid hormones. In addition, there are other regulators superimposed on this main axis such as somatostatin and dopamine, which act as inhibitors of TSH secretion, and central alpha-adrenergic pathways that are predominantly stimulatory and involved in the cold-induced thyroid activation. Nutritional status and leptin also regulate TSH by stimulating TRH neurons through direct and indirect mechanisms. Stress is also involved in lowering TRH/TSH secretion possibly through glucocorticoids, cytokines and opioids. Recently, a new regulatory pathway has been proposed, via peptides produced in pituitary, acting in an autocrine/paracrine manner. Among those, more consistent data are available on neuromedin B, gastrin-releasing peptide and pituitary leptin, which act as local inhibitors of TSH release. Neonatal programming of TSH secretion set point is also discussed.

Regulação da síntese e secreção de tireotrofina / Regulation of thyrotropin synthesis and secretion

A secreção de tireotrofina (TSH) é determinada pelo efeito estimulatório do hormônio hipotalâmico estimulador de tireotrofina (TRH) e pela retroalimentação negativa exercida pelos hormônios tireóideos (HT). Superpostos, atuam outros reguladores e aferências do sistema nervoso central. Somatostatina e dopamina inibem a secreção de TSH, já as vias alfa-adrenérgicas centrais são predominantemente estimuladoras e participariam no estímulo da secreção de TSH pelo frio. O estado nutricional modula o eixo através da leptina, por vias diretas e indiretas. O estresse induz redução da secreção de TSH, e discute-se a participação dos glicocorticóides, citocinas e opiáceos. Recentemente, evidenciou-se que fatores locais produzidos na adenohipófise podem atuar de forma autócrina/parácrina, modulando a secreção de TSH. Dentre estes, destacam-se a neuromedina B e o peptídeo liberador de gastrina, que atuam como inibidores locais da secreção de TSH. Discute-se ainda, as alterações do TSH decorrentes da programação neonatal, por hormônios ou desnutrição.

Lower faecal egg excretion in chemically-induced diabetic mice infected with Schistosoma mansoni due to impaired egg maturation

The effect of streptozotocin-induced diabetes mellitus was studied in mice infected with Schistosoma mansoni. Faecal egg excretion was lower in diabetic mice but worm load and total amount of eggs in the intestine tissue were equal to the control group. Evaluation of an oogram showed a great number of immature dead eggs and a low number of mature eggs in diabetic mice. It was therefore concluded that faecal egg excretion was lower in diabetic mice due to impaired egg maturation