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肌肉脂质氧化不受糖尿病和健康受试者阻塞性睡眠呼吸暂停的影响。

Muscle Lipid Oxidation Is Not Affected by Obstructive Sleep Apnea in Diabetes and Healthy Subjects.

机构信息

Department of Pathophysiology, Third Faculty of Medicine, Charles University, 100 00 Prague, Czech Republic.

Department of Internal Medicine, University Hospital Kralovske Vinohrady, 100 34 Prague, Czech Republic.

出版信息

Int J Mol Sci. 2023 Mar 10;24(6):5308. doi: 10.3390/ijms24065308.

DOI:10.3390/ijms24065308
PMID:36982383
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10048979/
Abstract

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, = 14), nondiabetic patients with severe OSA (OSA, = 9), T2DM patients with no OSA (T2DM, = 10), and T2DM patients with severe OSA (T2DM + OSA, = 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; > 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 HBAC progressively worsened in the following order: control, OSA, T2DM, and T2DM + OSA ( 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.

摘要

阻塞性睡眠呼吸暂停(OSA)与 2 型糖尿病(T2DM)之间的分子机制尚不清楚。本研究旨在探讨 OSA 对非糖尿病对照者和 2 型糖尿病(T2DM)患者骨骼肌脂质氧化的影响。共纳入 44 名年龄和体脂相匹配的参与者:非糖尿病对照组(对照组,n=14)、非糖尿病伴严重 OSA 组(OSA 组,n=9)、无 OSA 的 T2DM 患者组(T2DM 组,n=10)和严重 OSA 的 T2DM 患者组(T2DM+OSA 组,n=11)。进行骨骼肌活检;测定基因和蛋白表达,并分析脂质氧化。进行静脉葡萄糖耐量试验以研究血糖稳态。脂质氧化(178.2±57.1、161.7±22.4、169.3±50.9 和 140.0±24.1 pmol/min/mg,分别为对照组、OSA 组、T2DM 组和 T2DM+OSA 组; > 0.05)或基因和蛋白表达在各组之间无差异。处置指数、葡萄糖刺激的急性胰岛素反应、胰岛素抵抗、血浆胰岛素、血糖和 HBAC 逐渐恶化,顺序为:对照组、OSA 组、T2DM 组和 T2DM+OSA 组(趋势检验,P<0.05)。肌肉脂质氧化与葡萄糖代谢变量之间无相关性。我们的结论是,严重的 OSA 与肌肉脂质氧化减少无关,OSA 中的代谢紊乱不是通过肌肉脂质氧化受损介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca4c/10048979/01b29ca3df95/ijms-24-05308-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca4c/10048979/8d583ebd226a/ijms-24-05308-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca4c/10048979/6464507df4f3/ijms-24-05308-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca4c/10048979/01b29ca3df95/ijms-24-05308-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca4c/10048979/8d583ebd226a/ijms-24-05308-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca4c/10048979/6464507df4f3/ijms-24-05308-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca4c/10048979/01b29ca3df95/ijms-24-05308-g003.jpg

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