-
Something wrong with this record ?
Hypothalamo-pituitary-adrenal axis, glucose metabolism and TNF-α in narcolepsy
E. Maurovich-Horvat, M. Keckeis, Z. Lattová, D. Kemlink, TC. Wetter, A. Schuld, K. Sonka, T. Pollmächer,
Language English Country England, Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
NT13238
MZ0
CEP Register
Digital library NLK
Full text - Article
Source
NLK
Free Medical Journals
from 1992 to 1 year ago
Wiley Free Content
from 1997 to 1 year ago
PubMed
24650212
DOI
10.1111/jsr.12138
Knihovny.cz E-resources
- MeSH
- Adrenocorticotropic Hormone blood MeSH
- Dexamethasone pharmacology MeSH
- Adult MeSH
- Glucose Tolerance Test MeSH
- Corticotropin-Releasing Hormone pharmacology MeSH
- Hydrocortisone blood MeSH
- Body Mass Index MeSH
- Interleukin-6 metabolism MeSH
- Cataplexy blood complications metabolism MeSH
- Blood Glucose metabolism MeSH
- Humans MeSH
- Narcolepsy blood complications metabolism MeSH
- Case-Control Studies MeSH
- Pituitary-Adrenal System drug effects metabolism MeSH
- Hypothalamo-Hypophyseal System drug effects metabolism MeSH
- Tumor Necrosis Factor-alpha blood MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't 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.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc15008176
- 003
- CZ-PrNML
- 005
- 20181023090844.0
- 007
- ta
- 008
- 150306s2014 enk f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1111/jsr.12138 $2 doi
- 035 __
- $a (PubMed)24650212
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a enk
- 100 1_
- $a Maurovich Horvat, Eszter $u Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine and General University Hospital, Charles University, Prague, Czech Republic; Centre of Mental Health, Klinikum Ingolstadt, Ingolstadt, Germany; Max Planck Institute of Psychiatry, Munich, Germany. $7 xx0208396
- 245 10
- $a Hypothalamo-pituitary-adrenal axis, glucose metabolism and TNF-α in narcolepsy / $c E. Maurovich-Horvat, M. Keckeis, Z. Lattová, D. Kemlink, TC. Wetter, A. Schuld, K. Sonka, T. Pollmächer,
- 520 9_
- $a 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.
- 650 _2
- $a adrenokortikotropní hormon $x krev $7 D000324
- 650 _2
- $a dospělí $7 D000328
- 650 _2
- $a krevní glukóza $x metabolismus $7 D001786
- 650 _2
- $a index tělesné hmotnosti $7 D015992
- 650 _2
- $a studie případů a kontrol $7 D016022
- 650 _2
- $a kataplexie $x krev $x komplikace $x metabolismus $7 D002385
- 650 _2
- $a hormon uvolňující kortikotropin $x farmakologie $7 D003346
- 650 _2
- $a dexamethason $x farmakologie $7 D003907
- 650 _2
- $a ženské pohlaví $7 D005260
- 650 _2
- $a glukózový toleranční test $7 D005951
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a hydrokortison $x krev $7 D006854
- 650 _2
- $a systém hypotalamus-hypofýza $x účinky léků $x metabolismus $7 D007030
- 650 _2
- $a interleukin-6 $x metabolismus $7 D015850
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a narkolepsie $x krev $x komplikace $x metabolismus $7 D009290
- 650 _2
- $a systém hypofýza - nadledviny $x účinky léků $x metabolismus $7 D010913
- 650 _2
- $a TNF-alfa $x krev $7 D014409
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Keckeis, Marietta
- 700 1_
- $a Lattová, Zuzana $7 xx0070969
- 700 1_
- $a Kemlink, David $7 xx0081396
- 700 1_
- $a Wetter, Thomas-Christian
- 700 1_
- $a Schuld, Andreas
- 700 1_
- $a Šonka, Karel, $d 1957- $7 jn99240001644
- 700 1_
- $a Pollmächer, Thomas
- 773 0_
- $w MED00002940 $t Journal of sleep research $x 1365-2869 $g Roč. 23, č. 4 (2014), s. 425-431
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/24650212 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20150306 $b ABA008
- 991 __
- $a 20181023091351 $b ABA008
- 999 __
- $a ok $b bmc $g 1065449 $s 890976
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2014 $b 23 $c 4 $d 425-431 $i 1365-2869 $m Journal of sleep research $n J Sleep Res $x MED00002940
- GRA __
- $a NT13238 $p MZ0
- LZP __
- $a Pubmed-20150306