Investigation of insulin resistance in narcoleptic patients: dependent or independent of body mass index?

Engel, Alice; Helfrich, Jana; Manderscheid, Nina; Musholt, Petra B.; Forst, Thomas; Pfützner, Andreas; Dahmen, Norbert

doi:10.2147/ndt.s18455

Cited by 13 publications

(8 citation statements)

References 44 publications

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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: 88%

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: 88%

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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“…As treated and untreated patients had similar BMI, it was hypothesized that elevated BMI resulted from the pathophysiology of narcolepsy itself (e.g., loss of orexin peptide) or disease behavior such as reduced physical activity. More recently, blood glucose regulation and T2D was investigated in two studies of patients with narcolepsy using BMI matched controls (71, 72). Findings from both of these studies showed that narcoleptic patients did not have elevated risk of developing T2D or blood glucose dysregulation independent of BMI.…”

Section: Narcolepsymentioning

confidence: 99%

Metabolic Consequences of Sleep and Circadian Disorders

2014

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Sleep and circadian rhythms modulate or control daily physiological patterns with importance for normal metabolic health. Sleep deficiencies associated with insufficient sleep schedules, insomnia with short-sleep duration, sleep apnea, narcolepsy, circadian misalignment, shift work, night eating syndrome and sleep-related eating disorder may all contribute to metabolic dysregulation. Sleep deficiencies and circadian disruption associated with metabolic dysregulation may contribute to weight gain, obesity, and type 2 diabetes potentially by altering timing and amount of food intake, disrupting energy balance, inflammation, impairing glucose tolerance and insulin sensitivity. Given the rapidly increasing prevalence of metabolic diseases, it is important to recognize the role of sleep and circadian disruption in the development, progression, and morbidity of metabolic disease. Some findings indicate sleep treatments and countermeasures improve metabolic health, but future clinical research investigating prevention and treatment of chronic metabolic disorders through treatment of sleep and circadian disruption is needed.

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“…Honda et al found that narcolepsy was associated with increased frequency of type 2 diabetes [70]. However, subsequent studies have failed to find evidence that narcolepsy increases the risk of insulin resistance or glucose intolerance (and consequently of type 2 diabetes) independently of BMI [71 72]. …”

Section: Introductionmentioning

confidence: 99%

The Relationship and Potential Mechanistic Pathways Between Sleep Disturbances and Maternal Hyperglycemia

Izci‐Balserak

Pien

2014

Curr Diab Rep

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This paper reviews recent work investigating the influence of sleep disturbances on maternal hyperglycemia, particularly gestational diabetes mellitus (GDM). The incidence and prevalence of hyperglycemia are increasing worldwide, which is cause for concern because GDM and even mild hyperglycemia are associated with adverse pregnancy outcomes. A better understanding of sleep-related risk factors for maternal hyperglycemia is an important health matter. Evidence demonstrates associations between sleep disturbances, especially sleep-disordered breathing, and hyperglycemia, but causal effects and the underlying mechanisms linking these conditions have not been fully elucidated. Subjective sleep assessments show associations between sleep disturbances and maternal hyperglycemia. There are, however, few studies using objective measures to support these findings. Large prospective studies are required to examine causal relationships between sleep disturbances and maternal hyperglycemia. There is also a need for smaller mechanistic studies to understand the pathophysiology. Furthermore, interventional studies are required to address whether improvement of sleep parameters can prevent/decrease the risk of developing maternal hyperglycemia. Taken together, the data suggests that sleep disturbances during pregnancy are important to identify and manage in order to minimize maternal hyperglycemia and GDM, and improve maternal and fetal well-being.

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Investigation of insulin resistance in narcoleptic patients: dependent or independent of body mass index?

Cited by 13 publications

References 44 publications

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

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

Metabolic Consequences of Sleep and Circadian Disorders

The Relationship and Potential Mechanistic Pathways Between Sleep Disturbances and Maternal Hyperglycemia

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