Research Article, J Sleep Disord Treat Care Vol: 6 Issue: 1
The Impact of Sleep Deprivation on Plasma Leptin and Ghrelin Levels in Narcoleptic Patients
Korkmaz S1*, Aksu M1, Tuna M2, Baskol G2, Bayram F2 and Hallett M3 | |
1Department of Neurology, Acibadem Kayseri Hospital, Acibadem University Faculty of Medicine, Istanbul, Turkey | |
2Erciyes University Faculty of Medicine, Kayseri, Turkey | |
3Chief, Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, USA | |
Corresponding author : Selda Korkmaz, MD Assistant Professor, Department of Neurology, Acibadem Kayseri Hospital, Acibadem University Faculty of Medicine, Istanbul, Turkey, NIH/NINDS Human Motor Control Section, Bethesda, Maryland, US Tel: +1 240-801-0674 E-mail: korkmazs78@gmail.com |
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Received: September 29, 2016 Accepted: October 13, 2016 Published: January 04, 2017 | |
Citation: Korkmaz S, Aksu M, Tuna M, Baskol G, Bayram F , et al. (2017) The Impact of Sleep Deprivation on Plasma Leptin and Ghrelin Levels in Narcoleptic Patients. J Sleep Disor: Treat Care 6:1. doi: 10.4172/2325-9639.1000188 |
Abstract
Background: Narcoleptic patients have an increased rate of comorbid conditions such as obesity, type 2-diabetes. Those conditions have been thought to be associated with altered feeding regulating hormones including leptin, ghrelin and impaired glucose tolerance in narcoleptic patients. Therefore, the current study aimed to characterize basal plasma leptin and ghrelin levels and to assess glucose metabolism in narcoleptic patients and to determine whether the biologic effects of sleep deprivation seen in healthy population would be the same as those in narcoleptic patients.
Method: Following usual night's sleep, 24 hours sleep deprivation was performed on ten narcolepsy patients (five men, five women) and age, sex and body mass index (BMI) matched ten healthy controls. Plasma levels of leptin and ghrelin were measured, and oral glucose tolerance test (OGTT) was performed before and after sleep deprivation.
Results: At baseline, there was no difference in leptin, ghrelin, and glucose tolerance in patients and controls. After 24 h sleep deprivation, patients had increased leptin (p=0.015), reduced ghrelin (p=0.043) and unchanged glucose tolerance, whereas controls had an impaired glucose tolerance.
Conclusion: The metabolic parameters regulating appetite are not different in narcoleptic patients and healthy controls at baseline examination. Hence, they cannot be relevant to increasing the risk of obesity in narcoleptic patients. Unexpectedly, the present study has shown that in narcolepsy, sleep deprivation leads to a metabolic response in a direction to reduced food intake. This awaits further investigation and confirmation.