scholarly journals Partial sleep deprivation by environmental noise increases food intake and body weight in obesity-resistant rats

Obesity ◽  
2013 ◽  
Vol 21 (7) ◽  
pp. 1396-1405 ◽  
Author(s):  
Vijayakumar Mavanji ◽  
Jennifer A. Teske ◽  
Charles J. Billington ◽  
Catherine M. Kotz
2010 ◽  
Vol 298 (3) ◽  
pp. E726-E734 ◽  
Author(s):  
Paulo José Forcina Martins ◽  
Marina Soares Marques ◽  
Sergio Tufik ◽  
Vânia D'Almeida

Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25–35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.


eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Surabhi Bhutani ◽  
James D Howard ◽  
Rachel Reynolds ◽  
Phyllis C Zee ◽  
Jay Gottfried ◽  
...  

Sleep deprivation has marked effects on food intake, shifting food choices toward energy-dense options. Here we test the hypothesis that neural processing in central olfactory circuits, in tandem with the endocannabinoid system (ECS), plays a key role in mediating this relationship. We combined a partial sleep-deprivation protocol, pattern-based olfactory neuroimaging, and ad libitum food intake to test how central olfactory mechanisms alter food intake after sleep deprivation. We found that sleep restriction increased levels of the ECS compound 2-oleoylglycerol (2-OG), enhanced encoding of food odors in piriform cortex, and shifted food choices toward energy-dense food items. Importantly, the relationship between changes in 2-OG and food choices was formally mediated by odor-evoked connectivity between the piriform cortex and insula, a region involved in integrating feeding-related signals. These findings describe a potential neurobiological pathway by which state-dependent changes in the ECS may modulate chemosensory processing to regulate food choices.


2010 ◽  
Vol 91 (6) ◽  
pp. 1550-1559 ◽  
Author(s):  
Laurent Brondel ◽  
Michael A Romer ◽  
Pauline M Nougues ◽  
Peio Touyarou ◽  
Damien Davenne

2015 ◽  
Vol 4 (1) ◽  
Author(s):  
Deby Nelsya Eka Putri ◽  
Ellyza Nasrul ◽  
Machdawaty Masri

AbstrakPengurangan durasi tidur menurunkan kadar leptin dan meningkatkan kadar ghrelin sehingga merangsang nafsu makan dan meningkatkan kemungkinan terjadinya obesitas pada manusia. Pada tikus akan menyebabkan peningkatan asupan makanan tetapi terjadi penurunan berat badan yang disebabkan karena aktivitas yang tinggi pada tikus. Tujuan penelitian ini adalah untuk melihat pengaruh kurang tidur 24 jam, 48 jam dan 72 jam terhadap berat badan pada tikus Wistar jantan. Jenis penelitian adalah true experimental research dengan rancangan randomized post control group terhadap 14 ekor tikus Wistar yang dibagi atas kelompok kontrol, kelompok perlakuan 24 jam, 48 jam dan 72 jam. Tikus dikondisikan mengalami paradoxycal sleep deprivation dengan metode modified multiple platform. Asupan makanan diberikan ad libitum dan berat badan diukur setelah pengurangan durasi tidur selama 24 jam, 48 jam, dan 72 jam.Analisis data menggunakan uji Saphiro-Wilk Test dan One-Way ANOVA. Rerata berat badan setelah pengurangan durasi tidur 24 jam adalah 193,6±17,9 gram; setelah 48 jam 179,6±17,3 gram; dan setelah 72 jam 176,7±15,9 gram dibandingkan dengan kontrol 219.6±11,3 gram. Pengurangan durasi tidur 48 jam dan 72 jam dibandingkan dengan kontrol bermakna (p<0,05). Dapat disimpulkan bahwa terjadi penurunan berat badan pada pengurangan durasi tidur selama 48 jam dan 72 jam.Kata kunci: kurang tidur, berat badan, tikus wistarAbstractSleep deprivation lowers level of leptin and increases level of ghrelin which stimulates appetite and increases the likelihood of obesity in humans. In mice will increases food intake, but decreases the body weight due to high activity in mice. The objective of this study was to examine the effect of sleep deprivation 24 hours, 48 hours and 72 hours on body weight in male Wistar rats. This type of research was a true experimental design research with post randomized control group on 14 Wistar rats were divided into control group, treatment group 24 hours, 48 hours, and 72 hours. Rats conditioned paradoxycal sleep deprivation experienced by the modified multiple platform method. Given ad libitum food intake and body weight were measured after sleep deprivation for 24 hours, 48 hours, and 72 hours. Analysis of the data using the Shapiro-Wilk Test and One-Way ANOVA. The mean of body weight after 24 hour sleep deprivation was 193.6±17.9 g, after 48 hours was 179.6±17.3 g, and after 72 hours was 176.7±15.9 g compared with control was 219.6±11.3 g. Sleep deprivation 48 hours and 72 hours compared with controls was significant (p<0.05). It can be concluded there was reduction of body weight on sleep deprivation for 48 hours and 72 hours.Keywords: sleep deprivation, weight, rats


Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 421-431 ◽  
Author(s):  
Michael Koban ◽  
Wei Wei Le ◽  
Gloria E. Hoffman

Chronic rapid eye movement (paradoxical) sleep deprivation (REM-SD) of rats leads to two conspicuous pathologies: hyperphagia coincident with body weight loss, prompted by elevated metabolism. Our goals were to test the hypotheses that 1) as a stressor, REM-SD would increase CRH gene expression in the hypothalamus and that 2) to account for hyperphagia, hypothalamic gene expression of the orexigen neuropeptide Y (NPY) would increase, but expression of the anorexigen proopiomelanocortin (POMC) would decrease. Enforcement of REM-SD of adult male rats for 20 d with the platform (flowerpot) method led to progressive hyperphagia, increasing to approximately 300% of baseline; body weight steadily declined by approximately 25%. Consistent with changes in food intake patterns, NPY expression rapidly increased in the hypothalamic arcuate nucleus by d 5 of REM-SD, peaking at d 20; by contrast, POMC expression decreased progressively during REM-SD. CRH expression was increased by d 5, both in mRNA and ability to detect neuronal perikaryal staining in paraventricular nucleus with immunocytochemistry, and it remained elevated thereafter with modest declines. Taken together, these data indicate that changes in hypothalamic neuropeptides regulating food intake are altered in a manner consistent with the hyperphagia seen with REM-SD. Changes in CRH, although indicative of REM-SD as a stressor, suggest that the anorexigenic actions of CRH are ineffective (or disabled). Furthermore, changes in NPY and POMC agree with current models of food intake behavior, but they are opposite to their acute effects on peripheral energy metabolism and thermogenesis.


1973 ◽  
Author(s):  
William W. Beatty ◽  
Thomas R. Vilberg ◽  
Paul B. Revland

2007 ◽  
Vol 2 (S 1) ◽  
Author(s):  
L Plum ◽  
M Matsumoto ◽  
D Accili
Keyword(s):  

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