Peripheral leptin levels in narcoleptic patients.

Department of Psychiatry, University of Mainz, Mainz, Germany.
Diabetes Technology &amp Therapeutics (Impact Factor: 2.29). 09/2007; 9(4):348-53. DOI: 10.1089/dia.2006.0037
Source: PubMed

ABSTRACT Narcolepsy is a severe sleep disorder that in most patients is characterized by the deficiency of central orexin. Clinically, narcolepsy is associated with obesity. Currently, there is a literature controversy about the potential alteration of leptin levels in narcoleptic patients. Theoretically, diminished leptin levels could partially contribute to the observed overweight of patients. Two studies have reported decreased leptin levels, whereas a larger, recent study failed to detect differences between patients and controls.
To help settle the controversy, we have measured peripheral leptin levels in 42 narcoleptic patients and in 31 body mass index-matched controls.
No significant differences in leptin levels between the groups were observed. Mean leptin levels were 16.0 +/- 14.9 ng/mL in the narcoleptic men and 30.4 +/- 17.8 ng/mL in the narcoleptic women. The corresponding values for the controls were 21.2 +/- 17.0 ng/mL (P = 0.49, men) and 33.9 +/- 16.9 ng/mL (P = 0.31, women). In addition, no correlation was found between leptin levels and clinical symptomatology in the narcoleptic patients.
Taken together, the data argue against a major deterioration of leptin secretion in narcoleptic patients.

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    ABSTRACT: Patients with narcolepsy may suffer from a host of other comorbid medical and psychiatric conditions. These include eating disorders and obesity, diabetes, schizophrenia, depression, fibromyalgia, migraine headaches, cognitive dysfunction and psychosocial impairment. The associations between narcolepsy and many of these comorbid medical problems have not been clearly defined, and there are often conflicting data in the medical literature. Nevertheless, it is important to be aware of possible associated medical comorbidities when caring for patients with narcolepsy, to facilitate early diagnosis and treatment of these disorders.
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    ABSTRACT: Narcolepsy is caused by a selective loss of hypocretin neurons and is associated with obesity. Ghrelin and leptin interact with hypocretin neurons to influence energy homeostasis. Here, we evaluated whether human hypocretin deficiency, or the narcolepsy therapeutic agent sodium oxybate, alter the levels of these hormones. Eight male, medication free, hypocretin deficient, narcolepsy with cataplexy patients, and 8 healthy controls matched for age, sex, body mass index (BMI), waisttohip ratio, and body fat percentage were assessed. Blood samples of total ghrelin and leptin were collected over 24 hours at 60 and 20-min intervals, respectively, during 2 study occasions: baseline, and during the last night of 5 consecutive nights of sodium oxybate administration (2 × 3.0 g/night). At baseline, mean 24-h total ghrelin (936 ± 142 vs. 949 ± 175 pg/mL, p = 0.873) and leptin (115 ± 5.0 vs. 79.0 ± 32 mg/L, p = 0.18) levels were not different between hypocretin deficient narcolepsy patients and controls. Furthermore, sodium oxybate did not significantly affect the plasma concentration of either one of these hormones. The increased BMI of narcolepsy patients is unlikely to be mediated by hypocretin deficiency-mediated alterations in total ghrelin or leptin levels. Thus, the effects of these hormones on hypocretin neurons may be mainly unidirectional. Although sodium oxybate may influence body weight, the underlying mechanism is unlikely to involve changes in total ghrelin or leptin secretion. Donjacour CEHM; Pardi D; Aziz NA; Frölich M; Roelfsema F; Overeem S; Pijl H; Lammers GJ. Plasma total ghrelin and leptin levels in human narcolepsy and matched healthy controls: basal concentrations and response to sodium oxybate. J Clin Sleep Med 2013;9(8):797-803.
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    ABSTRACT: The profound influences of sleep and circadian rhythms on endocrine systems have already been discovered in the late 1960s. Growth hormone secretion, for example, is closely linked to the first hours of sleep, when slow-wave sleep (SWS) dominates [1] and sleep deprivation almost completely suppresses its release [2]. In contrast, circulating levels of cortisol, the effector hormone of the hypothalamo–pituitary–adrenal (HPA) axis, are the highest in the second half of the night and the early morning, but this time course is not affected by sleep deprivation, indicating circadian rather than sleep-dependent regulation [3]. KeywordsNarcolepsy-Hypothalamus-Metabolism-Energy homeostasis-Endocrine systems-Orexin-Hypocretin-Obesity
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