Increasing dietary fat elicits similar changes in fat oxidation and markers of muscle oxidative capacity in lean and obese humans.

Increasing dietary fat elicits similar changes in fat oxidation and markers of muscle oxidative capacity in lean and obese humans.
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DOI:
10.1371/journal.pone.0030164
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Melanson EL
Melanson EL
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Bergouignan A;Gozansky WS;Barry DW;Leitner W;MacLean PS;Hill JO;Draznin B;Melanson EL

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在瘦人中,增加饮食脂肪摄入量会导致全身脂肪氧化增加,并导致骨骼肌中调节脂肪氧化的基因发生变化,但这种情况是否会发生在肥胖人群中尚不清楚。我们比较了瘦(LN)和肥胖(OB)成年人暴露于2天高脂肪(HF)饮食后全身脂肪氧化和肌肉氧化能力标志物的变化。10例LN (BMI = 22.5±2.5 kg/m2,年龄= 30±8岁)和9例OB (BMI = 35.9±4.93 kg/m2, 38±5岁,Mean±SD)在室内量热仪中进行了24小时的研究,同时食用等热量低脂(LF, 20%能量)和HF(50%能量)饮食。禁食一晚后,第二天早上进行肌肉活检。LN(0.91±0.01)和OB(0.92±0.01)两组在LF期间的24h呼吸商(RQ)无显著差异,而LN(0.86±0.01)和OB(0.85±0.01)两组在HF期间的24h呼吸商(RQ)也有相似的降低。在HF期间,LN和OB中丙酮酸脱氢酶激酶4 (PDK4)和脂肪酸转运蛋白CD36的表达均增加。未观察到mRNA或蛋白的其他变化。然而,在LN和OB中,乙酰化过氧化物酶体增殖体激活受体γ共激活因子-1-α (PGC1-α)的数量显著减少,磷酸化5- amp激活蛋白激酶(AMPK)的数量显著增加。作为对膳食脂肪等能增加的反应,LN和OB的全身脂肪氧化也同样增加,这与骨骼肌向氧化代谢的转变有关,这表明适应膳食脂肪急性增加的能力并未因肥胖而受损。
In lean humans, increasing dietary fat intake causes an increase in whole-body fat oxidation and changes in genes that regulate fat oxidation in skeletal muscle, but whether this occurs in obese humans is not known. We compared changes in whole-body fat oxidation and markers of muscle oxidative capacity differ in lean (LN) and obese (OB) adults exposed to a 2-day high-fat (HF) diet. Ten LN (BMI = 22.5±2.5 kg/m2, age = 30±8 yrs) and nine OB (BMI = 35.9±4.93 kg/m2, 38±5 yrs, Mean±SD) were studied in a room calorimeter for 24hr while consuming isocaloric low-fat (LF, 20% of energy) and HF (50% of energy) diets. A muscle biopsy was obtained the next morning following an overnight fast. 24h respiratory quotient (RQ) did not significantly differ between groups (LN: 0.91±0.01; OB: 0.92±0.01) during LF, and similarly decreased during HF in LN (0.86±0.01) and OB (0.85±0.01). The expression of pyruvate dehydrogenase kinase 4 (PDK4) and the fatty acid transporter CD36 increased in both LN and OB during HF. No other changes in mRNA or protein were observed. However, in both LN and OB, the amounts of acetylated peroxisome proliferator-activated receptor γ coactivator-1-α (PGC1-α) significantly decreased and phosphorylated 5-AMP-activated protein kinase (AMPK) significantly increased. In response to an isoenergetic increase in dietary fat, whole-body fat oxidation similarly increases in LN and OB, in association with a shift towards oxidative metabolism in skeletal muscle, suggesting that the ability to adapt to an acute increase in dietary fat is not impaired in obesity.
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