Leptin: A biomarker for sleep disorders?

Pan, Weihong; Kastin, Abba J.

doi:10.1016/j.smrv.2013.07.003

Cited by 75 publications

(64 citation statements)

References 84 publications

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“…[2][3][4][5][6] Secreted frizzled-related protein 5 (SFRP5) is a recently described adipokine, which has the effects of antiinflammation and reducing insulin resistance. 7 SFRP5…”

Section: Chinese Medical Sciences Journal December 2017mentioning

confidence: 99%

阻塞性睡眠呼吸暂停与分泌性卷曲蛋白5（sfrp5）的相关性研究

Zhang

Huang

Xiao

et al. 2017

cmsj

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Key words: secreted frizzled-related protein 5 (SFRP5); obstructive sleep apnea (OSA); obesity Objective Obstructive sleep apnea (OSA) is closely related to obesity, insulin resistance and inflammation. Secreted frizzled-related protein 5 (SFRP5) is a recently discovered adipokine. It is involved in insulin resistance and inflammation in obesity. This study aimed at evaluating the association between SFRP5 and sleeping characteristics as well as biochemical parameters of OSA patients.Methods This was a prospective case control study. Nondiabetic OSA patients and controls were consecutively recruited and divided into three groups: OSA group, apnea-hypopnea Index (AHI)≥5/h; healthy controls with normal body mass index (BMI); obese controls without OSA, and BMI > 24.0 kg/m 2 . All participants underwent polysomnography (PSG). Plasma SFRP5 was examined using enzyme-linked immunosorbent assay (ELISA). Blood biochemical examinations, including fasting blood glucose (FBG), lipid profile, hypersensitive Creactive protein (hsCRP), were performed early in the morning after PSG. Patients with severe OSA were treated with nasal continuous positive airway pressure (nCPAP), and plasma SFRP5 was repeatedly measured for comparison.Results Sixty-eight subjects were enrolled in the study, including 38 patients of OSA, whose medium AHI was 58.70 /h (36.63, 71.15), 20 obese controls, and 10 healthy controls. The plasma SFRP5 level of OSA patients was not significantly different from that of healthy controls or obese controls. In OSA patients, SFRP5 level correlated positively with triglyceride level (r=0.447, P=0.005) and negatively with LDL-cholesterol level and HDLcholesterol level (r=−0.472 and P=0.003; r=−0.478 and P=0.002; respectively). SFRP5 level was not found correlating with FBG, AHI, or any of nocturnal hypoxia parameters. After overnight nCPAP treatment, plasma SFRP5 levels of OSA patients did not change significantly (t=1.557, P = 0.148) compared to that of pretreatment.Conclusions In nondiabetic OSA patients, plasma SFRP5 is associated with the lipid profile. However, no correlation was observed between SFRP5 and FBG or sleep parameters. The SFRP5 level of OSA patients did not differ from that of non-OSA individuals in our study.

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“…[2][3][4][5][6] Secreted frizzled-related protein 5 (SFRP5) is a recently described adipokine, which has the effects of antiinflammation and reducing insulin resistance. 7 SFRP5…”

Section: Chinese Medical Sciences Journal December 2017mentioning

confidence: 99%

阻塞性睡眠呼吸暂停与分泌性卷曲蛋白5（sfrp5）的相关性研究

Zhang

Huang

Xiao

et al. 2017

cmsj

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“…Despite the presence of hyperleptinemia, POKO mice do not respond to leptin with any increase of phosphorylated Signal Transducer and Activator of Transcription-3. Although SF protocols show variable effects on leptin concentrations (Pan and Kastin, 2014), leptin does not appear to play a major role in the increased sleep and attenuated physical activity of the POKO mice. Rather, the decreased locomotion may be mainly explained by increased hypersomnolence (Wang et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Sleep Fragmentation Has Differential Effects on Obese and Lean Mice

Kastin

Wang

et al. 2014

J Mol Neurosci

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Summary Chronic sleep fragmentation (SF), common in patients with sleep apnea, correlates with the development of obesity. We hypothesized that SF differentially affects neurobehavior in lean wildtype (WT) and obese pan-leptin receptor knockout (POKO) mice fed the same normal diet. First we established an SF paradigm by interrupting sleep every 2 min during the inactive light span. The maneuver was effective in decreasing sleep duration and bout length, and in increasing sleep state transition and waking, without significant rebound sleep in the dark span. Changes of sleep architecture were evident in the light span and consistent across days 1–10 of SF. There was reduced NREM, shortened sleep latency, and increased state transitions. During the light span of the first day of SF, there also was reduction of REM and increased delta power of slow wave sleep. Potential effects of SF on thermal pain threshold, locomotor activity, and anxiety were then tested. POKO mice had a lower circadian amplitude of pain latency than WT mice in the hot plate test, and both groups had lowest tolerance at 4 pm (ZT 10) and longest latency at 4 am (ZT 22). SF increased the pain threshold in WT but not POKO mice when tested at 8 am (ZT 2). Both the POKO mutation and SF resulted in reduced physical activity and increased anxiety, but there was no additive effect of these two factors. Overall, SF and the POKO mutation differentially regulate mouse behavior. The results suggest that obesity can blunt neurobehavioral responses to SF.

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“…OSA is an inflammatory process that leads to hyperleptinemia and increased proinflammatory cytokines in the circulation (Alberti et al, 2003;Pan and Kastin, 2014). Since sleep regulates both innate and acquired immunity, sleep disturbance and hypoxia further exacerbate neuroimmune dysfunction.…”

Section: Sleep Disruption and Intermittent Hypoxia Alter A␤ Processinmentioning

confidence: 99%