Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats.
ABSTRACT The main systemic disorders resulting from prolonged sleep deprivation in laboratory animals are a negative energy balance, low circulating thyroid hormones, and host defense impairments. Low thyroid hormones previously have been found caused by altered regulation at the level of the hypothalamus with possible pituitary involvement. The present studies investigated the effects of sleep deprivation on other major anabolic hormonal systems. Plasma growth hormone (GH) concentrations and major secretory bursts were characterized. Insulin-like growth factor I (IGF-I) was evaluated as an integrative marker of peripheral GH effector activity. Prolactin (PRL) was assessed by basal concentrations and by stimulating the pituitary with exogenous thyrotropin-releasing hormone. Leptin was studied for its linkage to metabolic signs of sleep loss and its correspondence to altered neuroendocrine regulation in other disease states. Last, plasma corticosterone was measured to investigate the degree of hypothalamic-pituitary-adrenal activation. Sleep deprivation was produced by the disk-over-water method, a well-established means of selective deprivation of sleep and noninterference with normal waking behaviors. Hormone concentrations were determined in sham comparisons and at intervals during baseline and experimental periods lasting at least 15 days in partially and totally sleep-deprived rats. The results indicate that high-amplitude pulses of GH were nearly abolished and that concentrations of GH, IGF-I, PRL, and leptin all were suppressed by sleep deprivation. Corticosterone concentration was relatively unaffected. Features of these results, such as low GH and low IGF-I, indicate failed negative feedback and point to hypothalamic mechanisms as containing the foci responsible for peripheral signs.
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ABSTRACT: Leptin, the product of obese (ob) gene, has been reported to affect the secretion of all six anterior pituitary hormones, but data are especially scarce regarding the interplay between leptin and prolactin (PRL). Thus, in this study we examined and compared in vivo the effects of acute and chronic administrations of recombinant mouse leptin on PRL secretion in male rats. Normally-fed and 3-day-fasted rats received an intraperitoneal bolus injection of leptin [1.0 mg/kg body weight (BW)] or vehicle only. The leptin treatment was without effect on plasma PRL levels up to 5 h postadministration. Food deprivation for 3 days significantly decreased both PRL and leptin levels. This decrease in plasma PRL was prevented by a 3-day constant infusion of 75 microg/kg BW/day of leptin, which maintained plasma leptin levels similar to those of normally-fed rats. The administration of three times the higher dose of leptin (225 microg/kg BW/day) to fasted rats led to further increases in both PRL and leptin in the plasma. Thus, a dose-dependent stimulatory effect of chronic leptin treatment on PRL secretion was indicated. This study demonstrates that chronic, but not acute, administration of leptin stimulates PRL secretion in the rat.Brain Research 01/2001; 887(2):426-31. · 2.88 Impact Factor
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ABSTRACT: Recent advances indicate that a robust physiologic system acts to maintain relative constancy of weight in mammals. A key component of this system is leptin. Leptin is an adipocyte hormone that functions as the afferent signal in a negative feedback loop regulating body weight. In addition, leptin functions as a key link between nutrition and the function of most, if not all other physiologic systems. When at their set point, individuals produce a given amount of leptin and in turn maintain a state of energy balance. Weight gain results in an increased plasma leptin level, which elicits a biologic response characterized in part by a state of negative energy balance. Weight loss among both lean and obese subjects results in decreased plasma levels of leptin, which lead to a state of positive energy balance and a number of other physiologic responses. In humans, both the intrinsic sensitivity to leptin and its rate of production vary and both appear to contribute to differences in weight. Further studies of leptin, its receptor, and the molecular components of this system are likely to have a major impact on our understanding of obesity and the interplay between nutrition and physiology.Nutrition Reviews 11/2002; 60(10 Pt 2):S1-14; discussion S68-84, 85-7. · 4.60 Impact Factor
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ABSTRACT: Patients often complain about insufficient sleep or chronic insomnia in the belief that they need 8 hours of sleep. Treatment strategies may be guided by what sleep durations predict optimal survival and whether insomnia might signal mortality risks. In 1982, the Cancer Prevention Study II of the American Cancer Society asked participants about their sleep duration and frequency of insomnia. Cox proportional hazards survival models were computed to determine whether sleep duration or frequency of insomnia was associated with excess mortality up to 1988, controlling simultaneously for demographics, habits, health factors, and use of various medications. Participants were more than 1.1 million men and women from 30 to 102 years of age. The best survival was found among those who slept 7 hours per night. Participants who reported sleeping 8 hours or more experienced significantly increased mortality hazard, as did those who slept 6 hours or less. The increased risk exceeded 15% for those reporting more than 8.5 hours sleep or less than 3.5 or 4.5 hours. In contrast, reports of "insomnia" were not associated with excess mortality hazard. As previously described, prescription sleeping pill use was associated with significantly increased mortality after control for reported sleep durations and insomnia. Patients can be reassured that short sleep and insomnia seem associated with little risk distinct from comorbidities. Slight risks associated with 8 or more hours of sleep and sleeping pill use need further study. Causality is unproven.Archives of General Psychiatry 03/2002; 59(2):131-6. · 13.77 Impact Factor