Glucose and Fat Metabolism in Narcolepsy: Effect of Sodium Oxybate

نویسندگان

  • Claire E. H. M. Donjacour
  • Gert Jan Lammers
چکیده

795 Glucose and Fat Metabolism in Narcolepsy—Donjacour et al INTRODUCTION Narcolepsy is a sleep disorder that is characterized by excessive daytime sleepiness, cataplexy, hypnagogic hallucinations, sleep paralysis, disturbed nocturnal sleep and obesity.1 Both obesity and disturbed nocturnal sleep are important risk factors for the development of type 2 diabetes mellitus (T2DM).2 Narcolepsy is caused by a loss of hypocretin (orexin) neurons in the hypothalamus.3,4 Hypocretins are neuropeptides known to be involved in sleep-wake regulation, feeding behavior as well as body weight and temperature regulation.5,6 Furthermore hypocretins are important hypothalamic regulators of glucose homeostasis. Disturbed activation of hypocretin neurons during sleep deprivation may lead to increased basal endogenous glucose production and a decreased insulin sensitivity in rats.7 Moreover, hypocretin deficiency leads to an age-related defective glucose tolerance and insulin resistance.8 Intracerebroventricular infusions of hypocretin-1 increase hepatic glucose GLUCOSE AND FAT METABOLISM IN NARCOLEPSY: EFFECT OF SODIUM OXYBATE

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تاریخ انتشار 2014