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.

• MeSH
• adrenalin aplikace a dávkování   MeSH
• diabetes mellitus 2. typu komplikace   epidemiologie   metabolismus   patologie   MeSH
• glukosa metabolismus   MeSH
• homeostáza fyziologie   MeSH
• inzulin metabolismus   MeSH
• inzulinová rezistence fyziologie   MeSH
• isoprenalin aplikace a dávkování   MeSH
• lidé středního věku MeSH
• lidé MeSH
• lipolýza účinky léků   genetika   MeSH
• obstrukční spánková apnoe komplikace   epidemiologie   metabolismus   patologie   MeSH
• senioři MeSH
• tuková tkáň účinky léků   metabolismus   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adrenalin MeSH
• glukosa MeSH
• inzulin MeSH
• isoprenalin MeSH

AIMS/HYPOTHESIS: The aim of this study was to investigate whether dynamic strength training modifies the control of lipolysis, with particular attention paid to the involvement of the antilipolytic adrenergic alpha 2A receptor (ADRA2A) pathway. METHODS: Twelve obese men (age: 47.4+/-2.8 years; BMI: 32.7+/-0.9) were investigated during a 210-min euglycaemic-hyperinsulinaemic clamp conducted before and after 3 months of dynamic strength training. Before and during the third hour of the clamp, the lipolytic effect of a perfusion of isoproterenol or adrenaline (epinephrine) alone or associated with the ADRA2A antagonist phentolamine was evaluated using the microdialysis method of measuring extracellular glycerol concentration (EGC) in subcutaneous abdominal adipose tissue (SCAAT). In addition, biopsies of SCAAT were carried out before and after training to determine mRNA levels RESULTS: The training increased insulin sensitivity in adipose tissue. The decrease of EGC was more pronounced during the clamp conducted after the training period than during the clamp done in pre-training conditions. Before and after the training, catecholamines induced an increase in EGC, the increase being lower during the clamp on each occasion. The isoproterenol-induced increase in EGC was higher after the training. Adrenaline-induced lipolysis was potentiated by phentolamine after but not before the training. There were no training-induced changes in mRNA levels of key genes of the lipolytic pathway in SCAAT. CONCLUSIONS/INTERPRETATION: In obese subjects, dynamic strength training improves whole-body and adipose tissue insulin responsiveness. It increases responsiveness to the adrenergic beta receptor stimulation of lipolysis and to the antilipolytic action of catecholamines mediated by ADRA2As.

• MeSH
• adrenalin farmakologie   MeSH
• agonisté beta-2-adrenergních receptorů MeSH
• alfa-2-adrenergní receptory - agonisté MeSH
• alfa-2-adrenergní receptory - antagonisté MeSH
• alfa-2-adrenergní receptory genetika   metabolismus   MeSH
• beta-2-adrenergní receptory genetika   metabolismus   MeSH
• cAMP-fosfodiesterasy genetika   fyziologie   MeSH
• cvičení fyziologie   MeSH
• cyklické nukleotidfosfodiesterasy, typ 3 MeSH
• dospělí MeSH
• fentolamin farmakologie   MeSH
• glycerol analýza   krev   MeSH
• glykemický clamp MeSH
• inzulin fyziologie   MeSH
• inzulinová rezistence fyziologie   MeSH
• isoprenalin farmakologie   MeSH
• kyseliny mastné neesterifikované krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• lipolýza MeSH
• messenger RNA analýza   MeSH
• metabolismus lipidů MeSH
• obezita metabolismus   patofyziologie   MeSH
• podkožní břišní tuk chemie   metabolismus   MeSH
• sterolesterasa genetika   fyziologie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• klinické zkoušky MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adrenalin MeSH
• agonisté beta-2-adrenergních receptorů MeSH
• alfa-2-adrenergní receptory - agonisté MeSH
• alfa-2-adrenergní receptory - antagonisté MeSH
• alfa-2-adrenergní receptory MeSH
• beta-2-adrenergní receptory MeSH
• cAMP-fosfodiesterasy MeSH
• cyklické nukleotidfosfodiesterasy, typ 3 MeSH
• fentolamin MeSH
• glycerol MeSH
• inzulin MeSH
• isoprenalin MeSH
• kyseliny mastné neesterifikované MeSH
• messenger RNA MeSH
• sterolesterasa MeSH