Modulação da função tireóidea após privação de sono paradoxal em ratos adrenalectomizados ou tratados com propranolol

Abstract

Modern life is shortening the sleep time and the consequences of this decreased has been studied in humans and animal models. Nevertheless, the effects of sleep deprivation in thyroid function are rarely studied. Our group pioneered in demonstrating the effects of paradoxcal sleep deprivation in the thyroid function; previous stududy related to thyroid function did full sleep deprivation. In this study, our objective was evaluating if the recent data we observed effects on thyroid function after paradoxcal sleep deprivation were due to the sleep deprivation or secondary to an hyperadrenocorticism and/or β-adrenergic hyperstimulation. Male rats (250-300g) from UFRRJ, animal care were kept in light-dark cycles (7-19h), controlled temperature (22° ± 2°C) with food and water ad libitum. For the propranolol protocol, the animals were distributed in 6 groups: 1 control (C), with a regular sleep pattern; 2 control treated with propranolol (C+P); 3 sleep deprived for 24h (P24); 4 sleep deprived for 24h with a 24h rebound period (P24R); 5 P24 treated with propranolol (P24+P) and 6 P24R treated with propranolol (P24R+P). All animals were treated with a 30mg/Kg dosage of propranolol benzoate or water in the control groups, for 14 days. For the adrenalectomy protocol, (Ax), the animals were anesthetized e adrenalectomized, or Shan, after 10 days of surgery the animals were divided as: Sham, sleep deprived for 24h or 96 with their respective rebound periods (P24, P96, P24R and P96R) e sleep deprived Ax for 24 e 96 hours with their respective rebound periods (AxP24, Ax P96, AxP24R e AxP96 and AxP96R). All animals were euthanized on the same day; blood was collected for T3, T4, TSH e corticosterone analisys; liver(F) and thyroid(T) for type 1 deiodinase (D1), hypophysis (H), brown adipose tissue (TAM), hypothalamus (HP) for type 2deiodinase (D2) activity. The entire procedure was approved by UFRRJ Ethics Committee 003/2015. T4 decreased in both protocols, T3 had no change in the propranolol protocol, where the D1 increases at the F in all groups and sees no changes in the T; D2 increases on TAM only in P24+P and P24R+P at the HP, while in the H D2 decreased on C+P and P24+P but normalizes after the rebound period. Corticosterone decreased in all Ax e AxP24, yet on Ax96 this decrease normalized. TSH increased in Ax e and normalized in AxP24 e AxP24R when compared to Sham. We can conclude that the decrease in T4 is independent to an adrenergic hyperactivation, for neither the adrenalectomia nor the β-adrenergic block were effective in maintaining T4 levels and sleep deprivation leads to a failure in the feedback mechanism once the diminished T4 doesnt stimulate a TSH increase and that T3 probably suffers no alteration due to the increase in T4-T3's peripheral conversion.