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Tokyo Adachi Hospital, Adachi, Tokyo, Japan
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rhythms ( Kohsaka et al. 2007 ). The levels of several hormones and cytokines show a circadian rhythm ( Andrews & Folk 1964 , Barter et al. 1971 , Vaughan et al. 1976 , Kaneko et al. 1980 , Arvidson et al. 1994 , Sinha et al. 1996
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timing signals for living organisms on Earth. Consequently, according to these signals, the endogenous circadian rhythms within organisms are entrained to the solar day ( Pittendrich 1960 , Refinetti 2010 , Fonken et al. 2013 ). While the central
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there are no studies at present in the literature investigating a possible BDNF circadian rhythm in humans, we studied the BDNF levels throughout 24 h in healthy men, in order to detect the possible relative changes in plasma BDNF protein. Additionally
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Department of Animal Science, University of California, Davis, California 95616, U.S.A.
(Received 8 October 1974)
Few studies have dealt with diurnal cortisol rhythm in sheep (McNatty, Cashmore & Young, 1972; McNatty & Young, 1973). The present results elucidate further the circadian rhythm of ovine plasma cortisol and describe the effect of sudden and continuous cage restraint.
Experimental methods and conditions were reported in detail by Holley & Evans (1974). Six mature rams were sampled at 4 h intervals for 32 days. On day 17 the animals were placed singly in small cages. Throughout the experiment the sheep received lucerne pellets at 16.00 h and the lighting schedule was maintained at 14 h light: 10 h darkness. Plasma cortisol was determined in duplicate without correction for other steroids as described by Bassett & Hinks (1969) and adjusted for extraction efficiency.
Fig. 1. Daily percentage variations (means ± s.e.m.) in plasma cortisol
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Pharmacological doses of glucocorticoids inhibit thyroid function in man and laboratory animals due to suppression of thyrotrophin (TSH) secretion (Wilber & Utiger, 1969). Administration of prednisolone or dexamethasone for 1–2 days results in a suppression of basal serum TSH levels in normal subjects and in patients with primary hypothyroidism, whilst the pituitary TSH reserve capacity, as assessed by the response to synthetic thyrotrophin releasing hormone (TRH), remains unaltered (Wilber & Utiger, 1969; Besser, Ratcliffe, Kilborn, Ormston & Hall, 1971; Haigler, Pittman & Hershman, 1971). However, impairment of serum TSH response to administered TRH does occur in patients treated with glucocorticoids for 1 or more months (Otsuki, Dakoda & Baba, 1973). These studies suggest that glucocorticoids may inhibit TSH secretion at both hypothalamic and pituitary levels but the main effect of the short-term treatment is suppression of TRH production.
Nicoloff, Fisher & Appleman (1970) found that the circadian rhythm of thyroidal
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Rats with a 4-day oestrous cycle were given a single dose of atropine (100, 300, 500 or 700 mg/kg body wt) at 13.00 h on the days of oestrus, dioestrus 1, dioestrus 2 or pro-oestrus and were autopsied on the next expected day of oestrus. The doses of atropine (in mg/kg body wt) necessary to block ovulation during the cycle were 300 at oestrus, 100 at dioestrus 1 or 2 and 700 at pro-oestrus. A single dose of atropine (100 mg/kg) at oestrus, dioestrus 1 or dioestrus 2 was given at 09.00, 13.00, 17.00 or 21.00 h, autopsy again being performed on the next expected day of oestrus. The ability of atropine to block ovulation appeared to have a circadian rhythm, with a maximum blockade at 13.00 h on dioestrus 1 and dioestrus 2 and a minimum at 21.00 h on the same days. Hormone replacement (human chorionic gonadotrophin at oestrus, dioestrus 1 or 2, oestradiol benzoate at dioestrus 2 or progesterone at pro-oestrus) re-established normal ovulation in rats whose ovulation was blocked with atropine (100 mg/kg) on dioestrus 1 at 13.00 h. When ovulation was blocked with atropine but no hormone replacement had been given, rats ovulated 24 h after the next expected day of oestrus.
Results obtained in these experiments suggest the existence of a circadian rhythm of gonadotrophin secretion thoughout the oestrous cycle and a close relationship between that rhythm and the cholinergic system.
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adrenal hormones play a pivotal role in mitigating or enhancing the effects of clock genes on their own targets. The exact role of glucocorticoids in this context has yet to be fully elucidated. However, it is generally accepted that their circadian rhythm
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ABSTRACT
Melatonin was measured by radioimmunoassay in homogenates of pineal glands from quail (Coturnix coturnix japonica) kept under different photoperiods and in darkness. Under 8-, 12- and 16-h daylengths melatonin levels were increased during the dark period, the duration of the increase depending on the duration of the dark period. As the daylength was increased the peak occurred closer to lights-off, reflecting the more rapid melatonin rise under the longer photoperiods. The pineal melatonin rhythm continued in darkness with an amplitude relative to that seen under a light/dark cycle of slightly less than one-half after 2 days in darkness and one-third after 6 days in darkness. The corresponding average periods of the rhythm were 25·5 h and 25·7 h. These results show that there is a circadian rhythm of melatonin in the pineal gland of the quail which is entrained by light/dark cycles and which continues in darkness.
J. Endocr. (1985) 107, 317–324
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ABSTRACT
Using a metaphase arrest technique, mitotic activity was quantified in the adrenal cortex over a 24-h period in 14-day-old male Sprague–Dawley rats before functional rhythmicity of the hypothalamic pituitary-adrenal (HPA) axis is established, and after its onset, in 6- to 7-week-old rats. At all times, proliferative activity was greater in the younger animals, as previously reported. A significant circadian rhythm was identified in both groups, but the timing of the peak differed, lying between 17.00 and 21.00 h at 14 days and 11.00 and 15.00 h at 6–7 weeks. These results raise the possibility that functional rhythmicity of the HPA axis may alter an inherent proliferative rhythm.
Journal of Endocrinology (1989) 120, 307–310
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relate to increased adiposity and the development of other parameters of metabolic syndrome ( Báez-Ruiz et al. 2017 ). Although many evidence suggests that the desynchronization of circadian rhythm increases the risk of cardiometabolic disorders
