Hypothalamo-pituitary-adrenal axis, glucose metabolism and TNF-α in narcolepsy
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24650212
DOI
10.1111/jsr.12138
Knihovny.cz E-zdroje
- Klíčová slova
- cytokines, glucose, immune system, metabolism, stress system,
- MeSH
- adrenokortikotropní hormon krev MeSH
- dexamethason farmakologie MeSH
- dospělí MeSH
- glukózový toleranční test MeSH
- hormon uvolňující kortikotropin farmakologie MeSH
- hydrokortison krev MeSH
- index tělesné hmotnosti MeSH
- interleukin-6 metabolismus MeSH
- kataplexie krev komplikace metabolismus MeSH
- krevní glukóza metabolismus MeSH
- lidé MeSH
- narkolepsie krev komplikace metabolismus MeSH
- studie případů a kontrol MeSH
- systém hypofýza - nadledviny účinky léků metabolismus MeSH
- systém hypotalamus-hypofýza účinky léků metabolismus MeSH
- TNF-alfa krev MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adrenokortikotropní hormon MeSH
- dexamethason MeSH
- hormon uvolňující kortikotropin MeSH
- hydrokortison MeSH
- interleukin-6 MeSH
- krevní glukóza MeSH
- TNF-alfa MeSH
Narcolepsy 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 ± 13.2 and 41.0 ± 2.9 years, respectively, body mass index was 28.1 ± 6.6 and 25.5 ± 4.7 kg m(-2) . 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.
Citace poskytuje Crossref.org