• Je něco špatně v tomto záznamu ?

Obstructive sleep apnoea increases lipolysis and deteriorates glucose homeostasis in patients with type 2 diabetes mellitus

MD. Trinh, A. Plihalova, J. Gojda, K. Westlake, J. Spicka, Z. Lattova, M. Pretl, J. Polak

. 2021 ; 11 (1) : 3567. [pub] 20210211

Jazyk angličtina Země Velká Británie

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc22004617

Obstructive sleep apnoea (OSA) is associated with type 2 diabetes mellitus (T2DM). However, mechanisms mediating association between these two conditions remain unclear. This study investigated, whether the OSA-associated changes in adipose tissue lipolysis might contribute to impaired glucose homeostasis in patient with T2DM. Thirty-five matched subjects were recruited into three groups: T2DM + severe OSA (T2DM + OSA, n = 11), T2DM with mild/no OSA (T2DM, n = 10) and healthy controls (n = 14). Subcutaneous abdominal adipose tissue microdialysis assessed spontaneous, epinephrine- and isoprenaline-stimulated lipolysis. Glucose metabolism was assessed by intravenous glucose tolerance test. Spontaneous lipolysis was higher in the T2DM + OSA compared with the T2DM (60.34 ± 23.40 vs. 42.53 ± 10.16 μmol/L, p = 0.013), as well as epinephrine-stimulated lipolysis (236.84 ± 103.90 vs. 167.39 ± 52.17 µmol/L, p < 0.001). Isoprenaline-stimulated lipolysis was unaffected by the presence of OSA (p = 0.750). The α2 anti-lipolytic effect was decreased in T2DM + OSA by 59% and 315% compared with T2DM and controls (p = 0.045 and p = 0.007, respectively). The severity of OSA (AHI) was positively associated with spontaneous (p = 0.037) and epinephrine-stimulated (p = 0.026) lipolysis. The α2-adrenergic anti-lipolytic effect (p = 0.043) decreased with increasing AHI. Spontaneous lipolysis was positively associated with Insulin resistance (r = 0.50, p = 0.002). Epinephrine-stimulated lipolysis was negatively associated with the Disposition index (r =  - 0.34, p = 0.048). AHI was positively associated with Insulin resistance (p = 0.017) and negatively with the Disposition index (p = 0.038). Severe OSA in patients with T2DM increased adipose tissue lipolysis, probably due to inhibition of the α2-adrenergic anti-lipolytic effect. We suggest that dysregulated lipolysis might contribute to OSA-associated impairments in insulin secretion and sensitivity.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc22004617
003      
CZ-PrNML
005      
20220127145119.0
007      
ta
008      
220113s2021 xxk f 000 0|eng||
009      
AR
024    7_
$a 10.1038/s41598-021-83018-1 $2 doi
035    __
$a (PubMed)33574418
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxk
100    1_
$a Trinh, Minh Duc $u Department of Pathophysiology, Third Faculty of Medicine, Charles University, Ruska 87, 100 00, Prague 10, Czech Republic $u Department of Cardiology, University Hospital Královské Vinohrady, Prague, Czech Republic
245    10
$a Obstructive sleep apnoea increases lipolysis and deteriorates glucose homeostasis in patients with type 2 diabetes mellitus / $c MD. Trinh, A. Plihalova, J. Gojda, K. Westlake, J. Spicka, Z. Lattova, M. Pretl, J. Polak
520    9_
$a Obstructive sleep apnoea (OSA) is associated with type 2 diabetes mellitus (T2DM). However, mechanisms mediating association between these two conditions remain unclear. This study investigated, whether the OSA-associated changes in adipose tissue lipolysis might contribute to impaired glucose homeostasis in patient with T2DM. Thirty-five matched subjects were recruited into three groups: T2DM + severe OSA (T2DM + OSA, n = 11), T2DM with mild/no OSA (T2DM, n = 10) and healthy controls (n = 14). Subcutaneous abdominal adipose tissue microdialysis assessed spontaneous, epinephrine- and isoprenaline-stimulated lipolysis. Glucose metabolism was assessed by intravenous glucose tolerance test. Spontaneous lipolysis was higher in the T2DM + OSA compared with the T2DM (60.34 ± 23.40 vs. 42.53 ± 10.16 μmol/L, p = 0.013), as well as epinephrine-stimulated lipolysis (236.84 ± 103.90 vs. 167.39 ± 52.17 µmol/L, p < 0.001). Isoprenaline-stimulated lipolysis was unaffected by the presence of OSA (p = 0.750). The α2 anti-lipolytic effect was decreased in T2DM + OSA by 59% and 315% compared with T2DM and controls (p = 0.045 and p = 0.007, respectively). The severity of OSA (AHI) was positively associated with spontaneous (p = 0.037) and epinephrine-stimulated (p = 0.026) lipolysis. The α2-adrenergic anti-lipolytic effect (p = 0.043) decreased with increasing AHI. Spontaneous lipolysis was positively associated with Insulin resistance (r = 0.50, p = 0.002). Epinephrine-stimulated lipolysis was negatively associated with the Disposition index (r =  - 0.34, p = 0.048). AHI was positively associated with Insulin resistance (p = 0.017) and negatively with the Disposition index (p = 0.038). Severe OSA in patients with T2DM increased adipose tissue lipolysis, probably due to inhibition of the α2-adrenergic anti-lipolytic effect. We suggest that dysregulated lipolysis might contribute to OSA-associated impairments in insulin secretion and sensitivity.
650    _2
$a tuková tkáň $x účinky léků $x metabolismus $7 D000273
650    _2
$a senioři $7 D000368
650    _2
$a diabetes mellitus 2. typu $x komplikace $x epidemiologie $x metabolismus $x patologie $7 D003924
650    _2
$a adrenalin $x aplikace a dávkování $7 D004837
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a glukosa $x metabolismus $7 D005947
650    _2
$a homeostáza $x fyziologie $7 D006706
650    _2
$a lidé $7 D006801
650    _2
$a inzulin $x metabolismus $7 D007328
650    _2
$a inzulinová rezistence $x fyziologie $7 D007333
650    _2
$a isoprenalin $x aplikace a dávkování $7 D007545
650    _2
$a lipolýza $x účinky léků $x genetika $7 D008066
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a lidé středního věku $7 D008875
650    _2
$a obstrukční spánková apnoe $x komplikace $x epidemiologie $x metabolismus $x patologie $7 D020181
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Plihalova, Andrea $u Department of Internal Medicine, University Hospital Královské Vinohrady, Prague, Czech Republic $u Centre for Research on Diabetes, Metabolism and Nutrition, Third Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Gojda, Jan $u Department of Internal Medicine, University Hospital Královské Vinohrady, Prague, Czech Republic $u Centre for Research on Diabetes, Metabolism and Nutrition, Third Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Westlake, Katerina $u Department of Pathophysiology, Third Faculty of Medicine, Charles University, Ruska 87, 100 00, Prague 10, Czech Republic
700    1_
$a Spicka, Jan $u Department of Laboratory Diagnostics, University Hospital Královské Vinohrady, Prague, Czech Republic
700    1_
$a Lattova, Zuzana $u Department of Pathophysiology, Third Faculty of Medicine, Charles University, Ruska 87, 100 00, Prague 10, Czech Republic
700    1_
$a Pretl, Martin $u Neurology and Sleep Laboratory, INSPAMED S.R.O., Prague, Czech Republic
700    1_
$a Polak, Jan $u Department of Pathophysiology, Third Faculty of Medicine, Charles University, Ruska 87, 100 00, Prague 10, Czech Republic. jan.polak@lf3.cuni.cz $u Department of Internal Medicine, University Hospital Královské Vinohrady, Prague, Czech Republic. jan.polak@lf3.cuni.cz
773    0_
$w MED00182195 $t Scientific reports $x 2045-2322 $g Roč. 11, č. 1 (2021), s. 3567
856    41
$u https://pubmed.ncbi.nlm.nih.gov/33574418 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y p $z 0
990    __
$a 20220113 $b ABA008
991    __
$a 20220127145115 $b ABA008
999    __
$a ok $b bmc $g 1751929 $s 1155766
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2021 $b 11 $c 1 $d 3567 $e 20210211 $i 2045-2322 $m Scientific reports $n Sci Rep $x MED00182195
LZP    __
$a Pubmed-20220113

Najít záznam

Citační ukazatele

    Možnosti archivace