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Unexpected Fat Distribution in Adolescents With Narcolepsy
Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för radiologiska vetenskaper. Linköpings universitet, Medicinska fakulteten.
Linköpings universitet, Institutionen för medicinsk teknik. Linköpings universitet, Tekniska fakulteten. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. AMRA Med AB, Linkoping, Sweden.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Neurologiska kliniken. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Uppsala Univ, Sweden.
Univ Gothenburg, Sweden.
Vise andre og tillknytning
2018 (engelsk)Inngår i: Frontiers in Endocrinology, ISSN 1664-2392, E-ISSN 1664-2392, Vol. 9, artikkel-id 728Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Narcolepsy type 1 is a chronic sleep disorder with significantly higher BMI reported in more than 50% of adolescent patients, putting them at a higher risk for metabolic syndrome in adulthood. Although well-documented, the body fat distribution and mechanisms behind weight gain in narcolepsy are still not fully understood but may be related to the loss of orexin associated with the disease. Orexin has been linked to the regulation of brown adipose tissue (BAT), a metabolically active fat involved in energy homeostasis. Previous studies have used BMI and waist circumference to characterize adipose tissue increases in narcolepsy but none have investigated its specific distribution. Here, we examine adipose tissue distribution in 19 adolescent patients with narcolepsy type 1 and compare them to 17 of their healthy peers using full body magnetic resonance imaging (MRI). In line with previous findings we saw that the narcolepsy patients had more overall fat than the healthy controls, but contrary to our expectations there were no group differences in supraclavicular BAT, suggesting that orexin may have no effect at all on BAT, at least under thermoneutral conditions. Also, in line with previous reports, we observed that patients had more total abdominal adipose tissue (TAAT), however, we found that they had a lower ratio between visceral adipose tissue (VAT) and TAAT indicating a relative increase of subcutaneous abdominal adipose tissue (ASAT). This relationship between VAT and ASAT has been associated with a lower risk for metabolic disease. We conclude that while weight gain in adolescents with narcolepsy matches that of central obesity, the lower VAT ratio may suggest a lower risk of developing metabolic disease.

sted, utgiver, år, opplag, sider
FRONTIERS MEDIA SA , 2018. Vol. 9, artikkel-id 728
Emneord [en]
orexin; hypocretin; brown adipose tissue; visceral adipose tissue; subcutaneous adipose tissue; BMI; magnetic resonance imaging (MRI); obesity
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-153502DOI: 10.3389/fendo.2018.00728ISI: 000452268600001OAI: oai:DiVA.org:liu-153502DiVA, id: diva2:1274647
Merknad

Funding Agencies|Research Council of South East Sweden [FORSS-480551]; Knut and Alice Wallenberg foundation [KAW 2013.0076]

Tilgjengelig fra: 2019-01-02 Laget: 2019-01-02 Sist oppdatert: 2019-06-14
Inngår i avhandling
1. Brain Networks and Dynamics in Narcolepsy
Åpne denne publikasjonen i ny fane eller vindu >>Brain Networks and Dynamics in Narcolepsy
2018 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Narcolepsy is a chronic sleep disorder, characterised by excessive daytime sleepiness with frequent uncontrollable sleep attacks. In addition to sleeprelated problems, changes in cognition have also been observed in patients with narcolepsy and has been linked to the loss of Orexin-A in a number of studies. Results from previous functional and structural neuroimaging studies would suggest that the loss of Orexin-A has numerous downstream effects in terms of both resting state glucose metabolism and perfusion and reduction in cortical grey matter.

Specifically, studies investigating narcolepsy with positron emission tomography (PET) and single photon emission computed tomography (SPECT) have observed aberrant perfusion and glucose metabolism in the hypothalamus and thalamus, as well as in prefrontal cortex. A very recent PET study in a large cohort of adolescents with type 1 narcolepsy further observed that the hypoand hypermetabolism in many of these cortico-frontal and subcortical brain regions also exhibited significant correlations with performance on a number of neurocognitive tests. These findings parallel those found in structural neuroimaging studies, where a reduction of cortical grey matter in frontotemporal areas has been observed.

The Aim of this thesis was to investigate mechanisms and aetiology behind the symptoms in narcolepsy through the application of different neuroimaging techniques. I present in this thesis evidence supporting that the complaints about subjective memory deficits in narcolepsy are related to a misallocation of resources.

I further describe how this has its seat in defective default mode network activation, possibly involving alterations to GABA and Glutamate signaling. In addition to this, I present our findings of a structural deviation in an area of the brainstem previously not described in the aetiology of narcolepsy.

This finding may have implications for further understanding the aetiology of the disease and the specific neuronal populations involved.

In addition to this, I show evidence from adipose tissue measurements in specific compartments, confirming that weight gain in narcolepsy is characterized by centrally located weight gain and may be specifically related to OX changes, but maybe not brown adipose tissue volume.

The findings presented in this thesis provides new insights to the pathophysiology of narcolepsy beyond the well-known depletion of OX producing neurons in the hypothalamus.

sted, utgiver, år, opplag, sider
Linköping: Linköping University Electronic Press, 2018. s. 54
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1651
HSV kategori
Identifikatorer
urn:nbn:se:liu:diva-153629 (URN)10.3384/diss.diva-153629 (DOI)9789176851814 (ISBN)
Disputas
2019-01-25, Hugo Theorells sal, Campus US, Linköping, 09:15 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2019-01-04 Laget: 2019-01-04 Sist oppdatert: 2019-09-30bibliografisk kontrollert

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