Animals ; Hippocampus ; metabolism ; Long-Term Potentiation ; Male ; Neurogranin ; biosynthesis ; Rats ; Rats, Wistar ; Sleep Deprivation ; metabolism

Sleep is a physiologic state of decreased metabolism and serves a reparative role, marked by increased glycogen stores and peptide synthesis. Normal sleep is characterized by reduced glucose turnover by the brain and other metabolically active tissues, particularly during non-rapid eye movement sleep. Circadian and sleep-related changes in glucose tolerance occur in normal subjects. Sleep duration has decreased over the last several decades, and with this have come cross-sectional and longitudinal data suggesting a link between short sleep duration and the prevalence of type 2 diabetes. Forced decreased sleep duration in healthy individuals has linked to impaired glucose homeostasis. Moreover, short sleep duration has been associated with obesity. Obstructive sleep apnea syndrome is characterized by diminished or abrogated airflow, which results in intermittent hypoxia and sleep fragmentation. This disorder appears to be associated with impaired glucose tolerance. Thus, the quality and quantity of sleep may have a profound effect on type 2 diabetes; therefore, these relationships should be carefully assessed in primary and endocrinology clinics.
Anoxia ; Brain ; Diabetes Mellitus ; Endocrinology ; Eye Movements ; Glucose ; Glycogen ; Homeostasis ; Metabolism ; Obesity ; Prevalence ; Sleep Apnea, Obstructive ; Sleep Deprivation

Sleep and public health has close relationship. Life in modern society makes human sleep deprived state. Sleep deprivation could induce cognitive deficits, heart diseases, glucose metabolic disorders, and decrease quality of life. Moreover, shift worker should work in mismatched circadian rhythm environment. Errors due to sleep deprivation, mismatched circadian rhythm, and various sleep disorders including sleep apnea could be tremendous hazard to public. By understanding sleep physiology, we can prevent sleep deprivation induced accidents and health problems. Sleep specialists have role of education and detection of patients with sleep disorders
Circadian Rhythm ; Glucose Metabolism Disorders ; Heart Diseases ; Humans ; Public Health ; Quality of Life ; Sleep Apnea Syndromes ; Sleep Deprivation ; Sleep Wake Disorders ; Specialization

OBJECTIVETo study the effect of chronic rapid eye movement sleep deprivation on energy metabolism, FT3, FT4 in serum.

METHODSRapid eye movement sleep deprivation of rats were deprived by flower pot, and then the energy metabolism were detected. The FT3, FT4 level in serum was determined by radioimmunoassay kit.

RESULTSRats after sleep deprivation displayed food intake increased from (75.06 +/- 25.37)g/(d x kg) to (122.30 +/- 20.43)g/(d x kg), body weight substantially decreased from (360.89 +/- 43.01) g to (295.97 +/- 37.95) g, body temperature from (37.62 +/- 1.12) degrees C up to the first (39.00 +/- 0.87) degrees C and then reduced to (37.72 +/- 0.84) degrees C, the basal metabolism rate increased significantly from (1.69 +/- 0.36) mlO2/(g x h) to (2.40 +/- 0.09) mlO2/(g x h), compared with the control group( P < 0.05). Sleep deprivation also resulted significantly lower serum thyroxine levels in comparison with the control, serum free triiodothyronine (FT3) level reduced from (3.38 +/- 0.88) pmol/L to (2.38 +/- 0.83) pmol/L, then free thyroxine(FT4) decreased from (14.62 +/- 3.62) pmol/L to (8.26 +/- 2.80) pmol/L (P < 0.05).

CONCLUSIONRapid eye movement sleep deprivation can change energy metabolism remarkable, as well as the alteration of FT3, FT4 levels in serum.

Animals ; Energy Metabolism ; physiology ; Male ; Rats ; Rats, Wistar ; Sleep Deprivation ; blood ; metabolism ; Sleep, REM ; physiology ; Thyroxine ; blood ; Time Factors ; Triiodothyronine ; analogs & derivatives ; blood

OBJECTIVETo observe the expression of cannabinoid receptor 1 (CB1R) mRNA and pathological changes in rat hippocampus after deprivation of rapid eye movement (REM) sleep.

METHODSTotally 42 Sprague-Dawley male rats were randomly divided into cage control (CC), tank control (TC) and the sleep deprivation groups (SD). The SD and TC rats were sacrificed at the end of 1 d, 3 d and 5 d sleep deprivation periods, respectively. The modified multiple platform methods were established for the REM sleep deprivation. CB1R mRNA was measured by reverse transcription-polymerase chain reaction (RT-PCR). The hippocampus sections of different stages were observed with electron microscope.

RESULTIn SD 1 d group, the expression of CB1R mRNA was significantly increased compared with the CC, TC, SD 3 d and SD 5 d groups (P <0.05) while in SD 3 d group it was reduced. The expression of CB1R mRNA of SD 5 d group was significantly higher than that of the SD 3 d group (P <0.05). Neuron apoptosis was found in SD 3 d and SD 5 d groups.

CONCLUSIONSleep deprivation can cause brain injury with the changes of CB1R mRNA expression.

Animals ; Hippocampus ; metabolism ; ultrastructure ; Male ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1 ; biosynthesis ; genetics ; Sleep Deprivation ; metabolism ; pathology ; Sleep, REM

OBJECTIVETo observe the changes of mitochondria stress in locus coeruleus and the tyrosine hydroxylasic projection after long-term sleep deprivation.

METHODSSleep deprivation mice model was set up by employing "novel environments" method. The expression of NAD -dependent deacetylase Sirtuin type 3 (SIRT3), which regulates mitochondrial energy production and oxidative stress, and heat shock protein 60 (HSP60), a major biomarker of mitochondrial stress, and the tyrosine hydroxylasic projection from locus coeruleus were analyzed after a 5-day sleep deprivation.

RESULTSCompared to the control group, the expression of SIRT3 in locus coeruleus was significantly decreased in respouse to long-term sleep deprivation, while the expression of HSP60 was significantly increased. In addition, relative to control group, pereentage area of the tyrosine hydroxylasic projection to anterior cingulate cortex was substantial decreased in long-term sleep deprivation group.

CONCLUSIONLong-term sleep deprivation induced the decreased level of SIRT3 expression and the elevation of mitochondrial stress in locus coenileus, which may further lead to the loss of tyrosine hydroxylasic projection in mice.

Animals ; Chaperonin 60 ; metabolism ; Locus Coeruleus ; metabolism ; physiology ; Mice ; Mitochondria ; metabolism ; Mitochondrial Proteins ; metabolism ; Oxidative Stress ; physiology ; Sirtuin 3 ; metabolism ; Sleep Deprivation ; Tyrosine ; metabolism

OBJECTIVETo explore the difference between adolescent and adult C57BL/6J mice in response to rapid eye movement sleep (REMS) deprivation in terms of anxiety behavior and hippocampal NO level.

METHODSBoth adolescent and adult C57BL/6J mice were divided into normal control (NC) group, wide platform (WP) group, and 24-hour REMS deprivation group, each group consisting of 15 mice. REMS deprivation models were established using a small platform in water tank, and the elevated plus maze test was used to examine anxiety behavior of the mice. After behavioral tests, the mice were sacrificed to examine hippocampal NO levels using enzyme-linked immunosorbent assay, and hippocampal nNOS protein expression was detected with Western blotting.

RESULTSThe adolescent C57BL/6J mice showed no obvious differences in anxiety behaviors between the 3 groups, but NO level and nNOS expression in the hippocampus was significantly higher in REMSD group than in NC and WP groups (P<0.01). The adult mice in REMSD group, compared with those in the other two groups, exhibited significantly increased total number of arm entry (P<0.01), lowered number of open arm entry and reduced open arm time (P<0.01), increased number of close arm entry and prolonged close arm time (P<0.01 or 0.05); no obvious differences in NO level or nNOS expression in the hippocampus were found in the 3 groups of adult mice.

CONCLUSIONREMS deprivation produces different effects on anxiety-related behaviors between adolescent and adult mice possibly in relation to their different responses in terms of NO levels and nNOS expression in the hippocampus.

Animals ; Anxiety ; Hippocampus ; chemistry ; Mice ; Mice, Inbred C57BL ; Nitric Oxide ; chemistry ; Nitric Oxide Synthase Type I ; metabolism ; Sleep Deprivation ; Sleep, REM

OBJECTIVETo explore the effects of retinol acid (RA) and triiodothyronine (T3) on alleviating the impairment of cognitive function by sleep deprivation (SD).

METHODSMale Wistar rats were divided into 4 groups: control group (C group), sleep deprivation group (SD group), sleep deprivation + RA group (SD + RA group) and sleep deprivation + T3 group (SD + T3 group). Open field test (OFT) was used to observe the nervous behavior of the rats after SD and electrophysiological brain stereotactic method was used to test long-term potentiation (LTP) in dentate gyrus (DG) of the rats. Ng protein expression was determined by Western blot.

RESULTSCompared with the SD group, the number of crossing in OFT, the changes of amplitude of population spike (PS) and the expression of Ng protein in hippocampus were higher significantly in the SD + RA and SD + T3 groups. All of these had not significant difference comparing with the C group.

CONCLUSIONRA and T3 may alleviate the restrain state of neural system after SD by augmenting the expression of Ng protein in hippocampus.

Animals ; Cognition ; drug effects ; Dentate Gyrus ; metabolism ; Long-Term Potentiation ; Male ; Neurogranin ; metabolism ; Rats ; Rats, Wistar ; Sleep Deprivation ; metabolism ; psychology ; Triiodothyronine ; pharmacology ; Vitamin A ; pharmacology

OBJECTIVETo determine the effects of ginsenosides Rb1(GSRb1) on learning and memory and expression of somatostatin (SS) in the hippocampus and the frontal cortex in rat model of sleep deprivation (SD).

METHODSRats were randomized into groups of SD 2 d, SD 4 d, SD 6 d, and SD 0 d, while each group was sub-divided into GSRb1 group and normal saline (NS) sub-groups. Rats were intraperitoneal administered with 30 mg/(kg*d) of GSRb1 or NS for 7 d, then the learning and memory abilities were examined by measuring average swimming speed and mean escape latency using Morris maze.Expression of somatostatin was detected with immunohistochemical method and image analysis in the hippocampus and the frontal cortex.

RESULTSCompared with SD 0 d rats, SD rats exhibited significant decrease in the average swimming speed and increase in the escape latency (P <0.01). The expression of somatostatin in the hippocampus was decreased significantly in SD 2 d, SD 4 d and SD 6 d rats (P<0.05). However, decrease was only observed in SD 4 d and SD 6 d rats in the frontal cortex (P <0.05). Parallel comparison between NS control and GSRb1 treated rats demonstrated that rats treated with GSRb1 in each subgroup exhibited faster swimming speed and shorter escape latency (P <0.05). Meanwhile, the expression of somatostatin was increased in SD 2 d, SD 4 d and SD 6 d rats in the hippocampus and in SD 4 d and SD 6 d rats in the frontal cortex (P <0.05), respectively.

CONCLUSIONGSRb1 enhances the expression of somatostatin in sleep deprivation rats and subsequently may improve learning and memory abilities of rats.

Animals ; Brain ; metabolism ; Disease Models, Animal ; Ginsenosides ; pharmacology ; Learning ; drug effects ; Male ; Memory ; drug effects ; Rats ; Rats, Sprague-Dawley ; Sleep Deprivation ; metabolism ; Somatostatin ; metabolism

Animals ; Glutamine ; blood ; metabolism ; Male ; Physical Conditioning, Animal ; physiology ; Physical Exertion ; physiology ; Rats ; Rats, Sprague-Dawley ; Sleep Deprivation ; metabolism ; physiopathology ; Thymus Gland ; metabolism ; Time Factors