Mahat Bimit, Chassé Étienne, Mauger Jean-François, Imbeault Pascal
Behavioral and Metabolic Research Unit, School of Human Kinetics, Faculty of Health, Sciences, University of Ottawa, 125, University Street (room 350), Ottawa, ON, K1N 6N5, Canada.
J Transl Med. 2016 Jul 15;14(1):212. doi: 10.1186/s12967-016-0965-y.
Adipose tissue regulates postprandial lipid metabolism by storing dietary fat through lipoprotein lipase-mediated hydrolysis of exogenous triglycerides, and by inhibiting delivery of endogenous non-esterified fatty acid to nonadipose tissues. Animal studies show that acute hypoxia, a model of obstructive sleep apnea, reduces adipose tissue lipoprotein lipase activity and increases non-esterified fatty acid release, adversely affecting postprandial lipemia. These observations remain to be tested in humans.
We used differentiated human preadipocytes exposed to acute hypoxia as well as adipose tissue biopsies obtained from 10 healthy men exposed for 6 h to either normoxia or intermittent hypoxia following an isocaloric high-fat meal.
In differentiated preadipocytes, acute hypoxia induced a 6-fold reduction in lipoprotein lipase activity. In humans, the rise in postprandial triglyceride levels did not differ between normoxia and intermittent hypoxia. Non-esterified fatty acid levels were higher during intermittent hypoxia session. Intermittent hypoxia did not affect subcutaneous abdominal adipose tissue lipoprotein lipase activity. No differences were observed in lipolytic responses of isolated subcutaneous abdominal adipocytes between normoxia and intermittent hypoxia sessions.
Acute hypoxia strongly inhibits lipoprotein lipase activity in differentiated human preadipocytes. Acute intermittent hypoxia increases circulating plasma non-esterified fatty acid in young healthy men, but does not seem to affect postprandial triglyceride levels, nor subcutaneous abdominal adipose tissue lipoprotein lipase activity and adipocyte lipolysis.
脂肪组织通过脂蛋白脂肪酶介导的外源性甘油三酯水解来储存膳食脂肪，并通过抑制内源性非酯化脂肪酸向非脂肪组织的输送来调节餐后脂质代谢。动物研究表明，急性缺氧（一种阻塞性睡眠呼吸暂停模型）会降低脂肪组织脂蛋白脂肪酶活性并增加非酯化脂肪酸释放，对餐后血脂产生不利影响。这些观察结果仍有待在人体中进行验证。
我们使用了暴露于急性缺氧的分化人脂肪前体细胞，以及从10名健康男性身上获取的脂肪组织活检样本，这些男性在摄入等热量高脂餐后分别暴露于常氧或间歇性缺氧环境6小时。
在分化的脂肪前体细胞中，急性缺氧导致脂蛋白脂肪酶活性降低了6倍。在人体中，常氧和间歇性缺氧条件下餐后甘油三酯水平的升高没有差异。间歇性缺氧期间非酯化脂肪酸水平较高。间歇性缺氧不影响腹部皮下脂肪组织脂蛋白脂肪酶活性。常氧和间歇性缺氧期间，分离的腹部皮下脂肪细胞的脂解反应没有差异。
急性缺氧强烈抑制分化的人脂肪前体细胞中的脂蛋白脂肪酶活性。急性间歇性缺氧会增加年轻健康男性循环血浆中非酯化脂肪酸水平，但似乎不影响餐后甘油三酯水平，也不影响腹部皮下脂肪组织脂蛋白脂肪酶活性和脂肪细胞脂解。
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