Sleep deprivation affects inflammatory marker expression in adipose tissue

Neto, José Cesar Rosa; Lira, Fábio Santos; Venâncio, Daniel Paulino; Cunha, Carolina; Oyama, Lila Missae; Pimentel, Gustavo D.; Tufik, Sérgio; Nascimento, Cláudia Maria Oller do; Santos, Ronaldo Vagner Thomatieli dos; Mello, Marco Túlio de

doi:10.1186/1476-511x-9-125

Cited by 34 publications

(22 citation statements)

References 41 publications

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“…In addition, it has been shown previously that TNF-α stimulates secretion of IL-6 via a NF-κB-dependent pathway. However, the opposite regulation of TNF-α and IL-6 has also been demonstrated in a recent study in rats [59], where OSA caused an increase in serum corticosterone levels, which was associated with up-regulation of IL-6 in retroperitoneal adipose tissue and down-regulation of TNF-α in mesenteric adipose tissue [21]. Recently, it is reported that the inflammatory cytokines of TNF-α and IL-6 are elevated in sleep apnea and obesity and might play a role in the pathogenesis and pathological sequelae of both disorders.…”

Section: Discussionmentioning

confidence: 75%

Effects of Varying Degrees of Intermittent Hypoxia on Proinflammatory Cytokines and Adipokines in Rats and 3T3-L1 Adipocytes

Yang

Zhou

et al. 2014

PLoS ONE

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ObjectivesIntermittent hypoxia (IH), resulted from recurring episodes of upper airway obstruction, is the hallmark feature and the most important pathophysiologic pathway of obstructive sleep apnea (OSA). IH is believed to be the most important factor causing systemic inflammation. Studies suggest that insulin resistance (IR) is positively associated with OSA. In this study, we hypothesized that the recurrence of IH might result in cellular and systemic inflammation, which was manifested through the levels of proinflammatory cytokines and adipokines after IH exposure, and because IR is linked with inflammation tightly, this inflammatory situation may implicate an IR status.MethodsWe developed an IH 3T3-L1 adipocyte and rat model respectively, recapitulating the nocturnal oxygen profile in OSA. In IH cells, nuclear factor kappa B (NF-κB) DNA binding reactions, hypoxia-inducible factor-1α (HIF-1α), glucose transporter-1 (Glut-1), necrosis factor alpha (TNF-α), interleukin (IL) -6, leptin, adiponectin mRNA transcriptional activities and protein expressions were measured. In IH rats, blood glucose, insulin, TNF-α, IL-6, leptin and adiponectin levels were analyzed.ResultsThe insulin and blood glucose levels in rats and NF-κB DNA binding activities in cells had significantly statistical results described as severe IH>moderate IH>mild IH>sustained hypoxia>control. The mRNA and protein levels of HIF-1α and Glut-1 in severe IH group were the highest. In cellular and animal models, both the mRNA and protein levels of TNF-α, IL-6 and leptin were the highest in severe IH group, when the lowest in severe IH group for adiponectin.ConclusionsOxidative stress and the release of pro-inflammatory cytokines/adipokines, which are the systemic inflammatory markers, are associated with IH closely and are proportional to the severity of IH. Because IR and glucose intolerance are linked with inflammation tightly, our results may implicate the clinical relationships between OSA and IR.

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Section: Discussionmentioning

confidence: 75%

Effects of Varying Degrees of Intermittent Hypoxia on Proinflammatory Cytokines and Adipokines in Rats and 3T3-L1 Adipocytes

Yang

Zhou

et al. 2014

PLoS ONE

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“…On the other hand, when the animals were tested 24 h after DOXO treatment a reduced rearing number was observed, suggesting that DOXO can interfere with exploratory behavior. Several studies have previously shown that sleep alterations and sleep-deprived rats exhibit body weight loss and elevated corticosterone levels [25], [26], [27]. The immediate purpose of glucocorticoid release during stress situations is to provide readily usable energy (i.e., glucose to the central nervous system).…”

Section: Discussionmentioning

confidence: 99%

Sleep pattern and locomotor activity are impaired by doxorubicin in non-tumor-bearing rats

et al. 2016

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PurposeWe sought explore the effects of doxorubicin on sleep patterns and locomotor activity. To investigate these effects, two groups were formed: a control group and a Doxorubicin (DOXO) group.MethodsSixteen rats were randomly assigned to either the control or DOXO groups. The sleep patterns were examined by polysomnographic recording and locomotor activity was evaluated in an open-field test.ResultsIn the light period, the total sleep time and slow wave sleep were decreased, while the wake after sleep onset and arousal were increased in the DOXO group compared with the control group (p<0.05). In the dark period, the total sleep time, arousal, and slow wave sleep were increased, while the wake after sleep onset was decreased in the DOXO group compared with the control group (p<0.05). Moreover, DOXO induced a decrease of crossing and rearing numbers when compared control group (p<0.05).ConclusionsTherefore, our results suggest that doxorubicin induces sleep pattern impairments and reduction of locomotor activity.

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“…Another study in rats, however, did show that sleep restriction lasting up to 4 weeks resulted in consistently lower leptin levels and concominant food intake [66]. Similarly, Rosa Neto and colleagues showed leptin decreases due to sleep deprivation [67], as did Martins and colleagues [68]. A study in rats showed that exogenous leptin suppresses rapid eye movement (REM) but enhances slow wave sleep [69].…”

Section: Potential Physiologic Mechanisms Linking Sleep Loss and Diabmentioning

confidence: 99%

Sleep Duration and Diabetes Risk: Population Trends and Potential Mechanisms

et al. 2016

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Sleep is important for regulating many physiologic functions that relate to metabolism. Because of this, there is substantial evidence to suggest that sleep habits and sleep disorders are related to diabetes risk. In specific, insufficient sleep duration and/or sleep restriction in the laboratory, poor sleep quality, and sleep disorders such as insomnia and sleep apnea have all been associated with diabetes risk. This research spans epidemiologic and laboratory studies. Both physiologic mechanisms such as insulin resistance, decreased leptin, and increased ghrelin and inflammation and behavioral mechanisms such as increased food intake, impaired decision-making, and increased likelihood of other behavioral risk factors such as smoking, sedentary behavior, and alcohol use predispose to both diabetes and obesity, which itself is an important diabetes risk factor. This review describes the evidence linking sleep and diabetes risk at the population and laboratory levels.

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Sleep deprivation affects inflammatory marker expression in adipose tissue

Cited by 34 publications

References 41 publications

Effects of Varying Degrees of Intermittent Hypoxia on Proinflammatory Cytokines and Adipokines in Rats and 3T3-L1 Adipocytes

Effects of Varying Degrees of Intermittent Hypoxia on Proinflammatory Cytokines and Adipokines in Rats and 3T3-L1 Adipocytes

Sleep pattern and locomotor activity are impaired by doxorubicin in non-tumor-bearing rats

Sleep Duration and Diabetes Risk: Population Trends and Potential Mechanisms

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