RESUMO
Melatonin is widely available as a supplement, usually for sleep disorders. The consumption of melatonin supplements has increased considerably in recent years. An overlooked aspect of melatonin's administration is the resulting increase in prolactin secretion, via its action on hypothalamic dopaminergic neurons. We believe that since the effect of melatonin on prolactin is tangible, the laboratory finding of hyperprolactinemia could be encountered more often, given the increase in melatonin's use. This is an issue that merits further study.
RESUMO
Aging and its underlying pathophysiological background has always attracted the attention of the scientific society. Defined as the gradual, time-dependent, heterogeneous decline of physiological functions, aging is orchestrated by a plethora of molecular mechanisms, which vividly interact to alter body homeostasis. The ability of an organism to adjust to these alterations, in conjunction with the dynamic effect of various environmental stimuli across lifespan, promotes longevity, frailty or disease. Endocrine function undergoes major changes during aging, as well. Specifically, alterations in hormonal networks and concomitant hormonal deficits/excess, augmented by poor sensitivity of tissues to their action, take place. As hypothalamic-pituitary unit is the central regulator of crucial body functions, these alterations can be translated in significant clinical sequelae that can impair the quality of life and promote frailty and disease. Delineating the hormonal signaling alterations that occur across lifespan and exploring possible remedial interventions could possibly help us improve the quality of life of the elderly and promote longevity.
Assuntos
Envelhecimento/metabolismo , Sistema Endócrino/metabolismo , Estresse Oxidativo , Adjuvantes Imunológicos/uso terapêutico , Androgênios/uso terapêutico , Antioxidantes/uso terapêutico , Ritmo Circadiano , Desidroepiandrosterona/uso terapêutico , Diabetes Mellitus Tipo 2/metabolismo , Dietoterapia , Terapia de Reposição de Estrogênios , Retroalimentação Fisiológica , Feminino , Preservação da Fertilidade , Gonadotropinas/metabolismo , Terapia de Reposição Hormonal , Humanos , Hiperandrogenismo/metabolismo , Hipertireoidismo/metabolismo , Hipertireoidismo/terapia , Hipoglicemiantes/uso terapêutico , Hipogonadismo/tratamento farmacológico , Hipogonadismo/metabolismo , Sistema Hipotálamo-Hipofisário/metabolismo , Hipotireoidismo/tratamento farmacológico , Hipotireoidismo/metabolismo , Células Secretoras de Insulina/metabolismo , Masculino , Menopausa/metabolismo , Reserva Ovariana , Medicina de Precisão , Qualidade de Vida , Transplante de Células-Tronco , Células-Tronco , Testosterona/uso terapêutico , Glândula Tireoide , Equilíbrio HidroeletrolíticoRESUMO
The recommended daily intake of iodide, is 150 µg for adolescents and adults, 250 µg for pregnancy and lactation. Thyroid gland is an effective collector of iodine. The active iodine uptake along the basolateral membrane of thyroid cell is followed by its transport to the apical edge of the cell and then to the follicle lumen. TSH acts through cAMP and stimulates NIS gene expression and protein synthesis. The major proportion of iodine in the thyroid gland is bound to Thyroglobulin. The non-organic intrathyroidal iodine is usually low, but significantly greater compared to plasma. Large doses of iodine reduce both the uptake and the organification (Wolff-Chaikoff effect) and cause partial inhibition of Tg proteolysis. The thyroid gland has several protective mechanisms resulting on the maintenance of normal thyroid function despite wide fluctuations of the daily iodine intake. Ingestion of several commonly used drugs and food conservatives results in acute or chronic excessive iodine intake. Failure to escape from the iodine induced organification inhibition can cause hypothyroidism, which is temporary and subsides after iodine exposure ceases. Iodine excess may also establish a status of excessive thyroid hormone synthesis and release, thus inducing autonomic thyroid function in iodopenic areas or can contribute to the development of iodine-induced hyperthyroidism in iodine abundant areas. The anti-arrhythmic Amiodarone, is a benzofuranic product with a very high iodine content, is associated with either hypo- or hyperthyroidism development. In the presence of defective auto-protective mechanisms, excessive iodine ingestion can divert the normal thyroid function.
Assuntos
Hipertireoidismo/etiologia , Hipotireoidismo/etiologia , Iodo/administração & dosagem , Iodo/efeitos adversos , Glândula Tireoide/fisiologia , Neoplasias da Glândula Tireoide/etiologia , Oligoelementos/administração & dosagem , Oligoelementos/efeitos adversos , Adolescente , Adulto , Amiodarona/efeitos adversos , Antiarrítmicos/efeitos adversos , Feminino , Humanos , Iodo/metabolismo , Gravidez , Recomendações Nutricionais , Tireoglobulina/metabolismo , Tireotropina/metabolismo , Oligoelementos/metabolismoRESUMO
OBJECTIVE: Adequate dietary iodine intake is necessary for normal thyroid gland function at all times, and most particularly during pregnancy. Increased iodine loss is cited, among other factors, as responsible for the increased iodine demand in this period. Our aim was to compare renal iodine excretion between women during all three pregnancy trimesters with that of their spouses and thereby to estimate the iodine intake in an a large sample of pregnant women in urban areas in Greece. DESIGN: Four hundred twenty-four healthy pregnant women were included prospectively (residents of Athens n=218, residents of Patras n=206). The spouses of 177 of these women following the same diet were also studied. Determinations included serum FT4, TSH and aTPO and urinary iodine excretion (UIE). RESULTS: No difference was found either in median UIE throughout pregnancy or between the UIE of the pregnant women and their spouses during the trimesters. Throughout pregnancy, mild iodine deficiency was noted and was classified as mild in 60%, moderate in 30% and severe in 10% of the women studied. Users of iodized salt had significantly higher median UIE compared with non-users. Serum FT4 levels decreased and TSH increased as pregnancy progressed. CONCLUSIONS: Our study indicates that renal iodine excretion is not increased during pregnancy. This finding needs to be confirmed by further investigation in other populations with different iodine intakes. Thus, increased iodine requirements in pregnancy are possibly due to extra-renal causes. The population of pregnant women in Greek urban areas is mildly-and often moderately and severely-iodopenic and needs to be treated accordingly.