Glucose tolerance in patients with narcolepsy

Beitinger, PA; Fulda, Stephany; Dalal, MA; Wehrle, R.; Keckeis, Marietta; Wetter, T. C.; Pollmächer, Thomas; Schuld, Andreas

doi:10.1055/s-0030-1267025

Cited by 2 publications

(3 citation statements)

References 19 publications

(24 reference statements)

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“…We did not find any significant differences between patients with narcolepsy and controls according to standard measurements of the OGTT. These results are in line with OGTT data from Beitinger et al (2012) and data on insulin sensitivity from Engel et al (2011), suggesting that narcolepsy is not directly associated with disturbances of glucose metabolism. In these studies and in ours, patients with narcolepsy and controls were matched for BMI.…”

Section: Discussionsupporting

confidence: 87%

“…After an oral standard load of 75 g glucose, blood samples were taken at 30, 60, 120, 180 and 240 min. The prolonged OGTT protocol was adapted from an earlier study of Beitinger and colleagues in patients with narcolepsy to also ascertain potential postprandial hypoglycaemia (Beitinger et al, 2012). Glucose was immediately measured using the glucose oxidase method.…”

Section: Procedures and Measurementsmentioning

confidence: 99%

“…Therefore, narcolepsy is likely to be a complex neuroendocrine disorder. Indeed, patients with narcolepsy are obese, show obesity-dependent disturbances in glucose metabolism (Beitinger et al, 2012;Poli et al, 2009) and have been reported to be at increased risk of diabetes (Honda et al, 1986). Moreover, abnormalities in numerous endocrine variables have been described, although the respective studies are somewhat inconsistent (Pollmächer et al, 2011) and subtle abnormalities in systemic immune parameters have been found, mainly changes in the levels of inflammatory cytokines.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hypothalamo–pituitary–adrenal axis, glucose metabolism and TNF‐α in narcolepsy

Maurovich-Horvat

Keckeis

Lattová

et al. 2014

Journal of Sleep Research

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SUMMARYNarcolepsy with cataplexy is caused by a deficiency in the production of hypocretin/orexin, which regulates sleep and wakefulness, and also influences appetite, neuroendocrine functions and metabolism. In this case-control study, 11 patients with narcolepsy with cataplexy and 11 healthy adults underwent an oral glucose tolerance test, and dexamethasone suppression/corticotropin-releasing hormone stimulation test. The average age of patients and controls was 35.1 AE 13.2 and 41.0 AE 2.9 years, respectively, body mass index was 28.1 AE 6.6 and 25.5 AE 4.7 kg m À2. We did not find evidence of a significantly increased prevalence of disturbed glucose tolerance in patients with narcolepsy. After hypothalamo-pituitary-adrenal axis suppression, the number of non-suppressors did not differ between the groups, indicating normal negative feedback sensitivity. The level of cortisol after dexamethasone suppression was significantly lower in patients with narcolepsy, suggesting a slight basal downregulation and/or a slightly increased negative feedback sensitivity of the major endocrine stress system in narcolepsy. Following corticotropin-releasing hormone stimulation, there were no significant differences in levels of adrenocorticotropic hormone or cortisol, and in adrenocortical responsivity to adrenocorticotropic hormone. Finally, patients with narcolepsy displayed significantly higher plasma levels of tumour necrosis factor alpha, soluble tumour necrosis factor receptor p55, soluble tumour necrosis factor receptor p75 and interleukin 6 after adjustment for body mass index. The present study confirms that narcolepsy by itself is not associated with disturbances of glucose metabolism, but goes along with a subtle dysregulation of inflammatory cytokine production. We also found that dynamic hypothalamo-pituitary-adrenal system response is not altered, whereas negative feedback to dexamethasone might be slightly enhanced. IN TROD UCTI ONNarcolepsy is a rare, chronic sleep disorder characterized by excessive daytime sleepiness, cataplexy, hypnagogic hallucinations and sleep paralysis. Low cerebral spinal fluid hypocretin/orexin levels, caused by selective loss of hypocretin-producing neurons in the prefornical hypothalamus, due to possible autoimmune mechanisms, are reported in 95% of patients with narcolepsy with cataplexy (NC) (Baumann and Bassetti, 2005).In addition to their crucial role as regulators of sleep and wakefulness, hypocretin neurons have been shown to play an important role in energy homeostasis. For example, hypocretins increase food intake, and are involved in glucose metabolism and insulin sensitivity. Furthermore, they have a stimulatory role on the major stress system and can activate

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Section: Discussionsupporting

confidence: 87%

Section: Procedures and Measurementsmentioning

confidence: 99%