Pendergast D R, Fisher N M, Meksawan K, Doubrava M, Vladutiu G D
Department of Physiology, University at Buffalo, Buffalo, New York 14214, USA.
J Inherit Metab Dis. 2004;27(1):89-99. doi: 10.1023/B:BOLI.0000016637.43041.a3.
Fat oxidation is important for maintaining health and for supplying energy for exercise. We have proposed that the predisposition for individual rates of fat oxidation is determined genetically but may be modulated by acute exercise or exercise training. The purpose of this study was to examine cellular fat oxidation in white blood cells (WBC) using [9,10-3H]palmitic acid. Sedentary controls free of symptoms (SED-C, n=32), were compared with known carnitine palmitoyltransferase (CPT) II-deficient patients (n =2), patients with fatiguing diseases (chronic fatigue syndrome, CFS, n=6; multiple sclerosis, MS, n=31), obesity (OB, n=5), eating disorders (ED, n=16), sedentary individuals prior to and after exercise (SED-Ex, n=12), exercise-trained sedentary individuals (SED-Tr, n=12), and elite runners (ER, n=5). Fat oxidation in WBC for all subjects was normally distributed (mean=0.270 +/- 0.090 nmol/h per 10(9) WBC) and ranged from 0.09 nmol/h per 10(9) WBC in CPT II-deficient patients to 0.59 nmol/h per 10(9) WBC in ER. There were no significant sex or acute exercise effects on WBC fat oxidation. Patients with MS, OB or ED were not different from SED-C; however, in CPT II-deficient patients, fat oxidation was low, while that of CFS patients was high. Exercise training in SED-C resulted in a 16% increase in fat oxidation but in ER it was still 97% higher than in SED-C. We propose that while WBC fat oxidation is not significantly affected by sex or acute exercise, and only by 15-20% with training, genetic factors play a role in determining both high and low fat oxidation in certain groups of individuals. The genetic predisposition for individual rates of fat oxidation may be easily measured using WBC fat oxidation, as has been shown for CPT II-deficient patients and for elite runners. Ranges of WBC fat oxidation that are abnormally low (<20 nmol/h per 10(9) WBC, normal 20-35) or high (>35 nmol/h per 10(9) WBC) are proposed based on genetic factors evaluated in this study.
脂肪氧化对于维持健康以及为运动提供能量都很重要。我们提出，个体脂肪氧化速率的易感性由基因决定，但可能会受到急性运动或运动训练的调节。本研究的目的是使用[9,10-3H]棕榈酸检测白细胞（WBC）中的细胞脂肪氧化。将无症状的久坐对照组（SED-C，n = 32）与已知的肉碱棕榈酰转移酶（CPT）II缺乏症患者（n = 2）、患有疲劳性疾病的患者（慢性疲劳综合征，CFS，n = 6；多发性硬化症，MS，n = 31）、肥胖症患者（OB，n = 5）、饮食失调患者（ED，n = 16）、运动前后的久坐个体（SED-Ex，n = 12）、经过运动训练的久坐个体（SED-Tr，n = 12）以及精英跑步者（ER，n = 5）进行比较。所有受试者白细胞中的脂肪氧化呈正态分布（平均值 = 0.270 +/- 0.090 nmol/小时每10(9)个白细胞），范围从CPT II缺乏症患者的0.09 nmol/小时每10(9)个白细胞到精英跑步者的0.59 nmol/小时每10(9)个白细胞。性别或急性运动对白细胞脂肪氧化没有显著影响。MS、OB或ED患者与SED-C没有差异；然而，CPT II缺乏症患者的脂肪氧化较低，而CFS患者的脂肪氧化较高。对SED-C进行运动训练导致脂肪氧化增加16%，但精英跑步者的脂肪氧化仍比SED-C高97%。我们提出，虽然白细胞脂肪氧化不受性别或急性运动的显著影响，训练只会使其增加15 - 20%，但遗传因素在某些个体组中高低脂肪氧化的决定中起作用。个体脂肪氧化速率的遗传易感性可以很容易地通过白细胞脂肪氧化来测量，如CPT II缺乏症患者和精英跑步者所示。基于本研究评估的遗传因素，提出了白细胞脂肪氧化异常低（<20 nmol/小时每10(9)个白细胞，正常为20 - 35）或高（>35 nmol/小时每10(9)个白细胞）的范围。
