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Sleep deprivation alters thyroid hormone economy in rats
Author(s) -
Rodrigues Nayana Coutinho,
da Cruz Natália Santos,
de Paula Nascimento Cristine,
da Conceição Rodrigo Rodrigues,
da Silva Alba Cenélia Matos,
Olivares Emerson Lopes,
Marassi Michelle Porto
Publication year - 2015
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2014.083303
Subject(s) - endocrinology , sleep deprivation , medicine , sleep (system call) , hormone , triiodothyronine , thyroid , hypothalamic–pituitary–thyroid axis , rapid eye movement sleep , privation , sleep restriction , circadian rhythm , psychiatry , computer science , operating system , electroencephalography
New FindingsWhat is the central question of this study? The relationship between the thyroid system and sleep deprivation has seldom been assessed in the literature, and mounting evidence exists that sleep disturbances influence human lifestyles. The aim of this study was to investigate the hypothalamic–pituitary–thyroid axis and thyroid hormone metabolism in sleep‐deprived and sleep‐restricted rats.What is the main finding and its importance? Central hypothyroidism and high thyroxine (T 4 ) to 3,5,3′‐triiodothyronine (T 3 ) activation in brown adipose tissue were observed following sleep deprivation. Sleep‐restricted rats exhibited normal thyroid‐stimulating hormone and T 4 concentrations despite increased circulating T 3 . Sleep recovery for 24 h did not normalize the high T 3 concentrations, suggesting that high T 3 is a powerful counterregulatory mechanism activated following sleep deprivation.Modern life has shortened sleep time, and the consequences of sleep deprivation have been examined in both human subjects and animal models. As the relationship between thyroid function and sleep deprivation has not been fully investigated, the aim of this study was to assess the hypothalamic–pituitary–thyroid axis and thyroid hormone metabolism following paradoxical sleep deprivation (PSD) and sleep restriction (SR) in rats. The effects of a 24 h rebound period were also studied. Male Wistar rats (200–250 g, n = 10 per group) were subjected to sleep deprivation via the modified multiple platform method. Rats were assigned to the following seven groups: control, PSD for 24 or 96 h, 24 or 96 h of sleep deprivation with rebound (PSD24R and PSD96R), SR for 21 days (SR21) and SR21 with rebound (SR21R). Blood samples were collected to determine the 3,5,3′‐triiodothyronine (T 3 ), thyroxine (T 4 ) and thyroid‐stimulating hormone concentrations. Brown adipose tissue iodothyronine deiodinase type 2 (D2) activity was also evaluated. Body weight gain was dramatically reduced (by ∼50–100%) in all sleep‐deprived and sleep‐restricted rats; rebound restored this parameter in only the PSD24R group. The serum TSH and T 4 concentrations decreased, whereas T 3 increased in both the PSD24 and PSD96 groups compared with control animals ( P < 0.05). Only PSD24R and PSD96R normalized T 4 and thyroid‐stimulating hormone concentrations, respectively, independently of the higher circulating T 3 concentrations (∼20–30%) noted in all groups compared with control animals ( P < 0.05). Brown adipose tissue D2 activity increased in the PSD 24 and 96 h groups (∼10 times), and PSD24R was more effective than PSD96R at restoring basal brown adipose tissue D2 activity. Our data suggest that thyroid hormone metabolism adapts to sleep deprivation‐induced hypothalamic–pituitary–thyroid alterations and increases T 4 to T 3 activation peripherally, thereby increasing circulating T 3 in rats.