Muscle Lipid Oxidation Is Not Affected by Obstructive Sleep Apnea in Diabetes and Healthy Subjects
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články
Grantová podpora
AZV NU21-01-00259
Ministry of Health of the Czech Republic
Programme EXCELES, ID Project No. LX22NPO5104
National Institute for Research of Metabolic and Cardiovascular Diseases, European Union - Next Generation EU
PubMed
36982383
PubMed Central
PMC10048979
DOI
10.3390/ijms24065308
PII: ijms24065308
Knihovny.cz E-zdroje
- Klíčová slova
- IVGTT, free fatty acids, glucose intolerance, hypoxia, lipid utilization, muscle metabolism, obstructive sleep apnea, type 2 diabetes mellitus,
- MeSH
- diabetes mellitus 2. typu * komplikace metabolismus MeSH
- glukosa metabolismus MeSH
- inzulinová rezistence * MeSH
- inzuliny * MeSH
- lidé MeSH
- lipidy MeSH
- obstrukční spánková apnoe * metabolismus MeSH
- polysomnografie MeSH
- svaly metabolismus MeSH
- zdraví dobrovolníci pro lékařské studie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- glukosa MeSH
- inzuliny * MeSH
- lipidy MeSH
The molecular mechanisms linking obstructive sleep apnea (OSA) with type 2 diabetes mellitus (T2DM) remain unclear. This study investigated the effect of OSA on skeletal muscle lipid oxidation in nondiabetic controls and in type 2 diabetes (T2DM) patients. Forty-four participants matched for age and adiposity were enrolled: nondiabetic controls (control, n = 14), nondiabetic patients with severe OSA (OSA, n = 9), T2DM patients with no OSA (T2DM, n = 10), and T2DM patients with severe OSA (T2DM + OSA, n = 11). A skeletal muscle biopsy was performed; gene and protein expressions were determined and lipid oxidation was analyzed. An intravenous glucose tolerance test was performed to investigate glucose homeostasis. No differences in lipid oxidation (178.2 ± 57.1, 161.7 ± 22.4, 169.3 ± 50.9, and 140.0 ± 24.1 pmol/min/mg for control, OSA, T2DM, and T2DM+OSA, respectively; p > 0.05) or gene and protein expressions were observed between the groups. The disposition index, acute insulin response to glucose, insulin resistance, plasma insulin, glucose, and HBA1C progressively worsened in the following order: control, OSA, T2DM, and T2DM + OSA (p for trend <0.05). No association was observed between the muscle lipid oxidation and the glucose metabolism variables. We conclude that severe OSA is not associated with reduced muscle lipid oxidation and that metabolic derangements in OSA are not mediated through impaired muscle lipid oxidation.
Department of Internal Medicine University Hospital Kralovske Vinohrady 100 34 Prague Czech Republic
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