Liver fat and lipid oxidation in humans
Liver fat and lipid oxidation in humans
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DOI：
10.1111/j.1478-3231.2009.02076.x
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发表时间：
2009-10-01
影响因子：
6.7
通讯作者：
Yki-Javinen, Hannele
中科院分区：
文献类型：
--
作者：
Kotronen, Anna;Seppala-Lindroos, Anneli;Yki-Javinen, Hannele
背景：动物研究表明，肝脏脂肪酸氧化的变化会改变肝脏脂肪含量。关于全身和肝脏脂质氧化的人体数据存在争议，并且仅基于少数受试者的研究。目的：我们检查了与对照组相比，非酒精性脂肪肝病 (NAFLD) 受试者的全身和肝脏脂质氧化是否发生改变。方法：对 NAFLD 受试者 [平均肝脂肪 14.0%（四分位距 7.5-20.5%），n = 29] 和对照受试者 [1.6%（1.0-3.0%），n = 29] 进行体内底物氧化率和胰岛素敏感性（使用正常血糖高胰岛素钳夹技术结合间接量热法和输注 [3-H-3] 葡萄糖）。使用质子磁共振波谱法测量肝脏脂肪。测量 3-羟基丁酸 (3-OHB) 的血浆浓度作为肝脂质氧化的标志物。结果：在基础状态下，患有和不患有 NAFLD 的受试者的底物氧化率和血清 3-OHB 浓度相当。两组中血浆 3-OHB 浓度均受到胰岛素类似的抑制。在胰岛素输注过程中，全身脂质氧化与胰岛素刺激的葡萄糖处理呈负相关（r = -0.48，P < 0.0001），NAFLD 受试者 [3.7 +/- 0.2 mg/（kg 无脂质量分钟）] 低于对照组 [5.0 +/- 0.3 mg/（kg 无脂肪质量分钟），P = 0.0008]。结论：NAFLD 中肝脂质氧化没有变化。由于外周胰岛素抵抗，全身脂质氧化增加。这些数据意味着肝脏脂肪酸氧化的改变不会影响人类肝脏脂肪含量。
Background: Studies in animals show that changes in hepatic fatty acid oxidation alter liver fat content. Human data regarding whole-body and hepatic lipid oxidation are controversial and based on studies of only a few subjects. Aims: We examined whether whole-body and hepatic lipid oxidation are altered in subjects with non-alcoholic fatty liver disease (NAFLD) compared with controls. Methods: In vivo measurements of rates of substrate oxidation and insulin sensitivity (using the euglycaemic hyperinsulinaemic clamp technique in combination with indirect calorimetry and infusion of [3-H-3] glucose) were performed in subjects with NAFLD [mean liver fat 14.0% (interquartile range 7.5-20.5%), n = 29] and in control subjects [1.6% (1.0-3.0%), n = 29]. Liver fat was measured using proton magnetic resonance spectroscopy. Plasma concentrations of 3-hydroxybutyrate (3-OHB) were measured as markers of hepatic lipid oxidation. Results: In the basal state, substrate oxidation rates and serum 3-OHB concentrations were comparable in subjects with and without NAFLD. Plasma 3-OHB concentrations were similarly suppressed by insulin in both the groups. During the insulin infusion, whole-body lipid oxidation was inversely correlated with insulin-stimulated glucose disposal (r = -0.48, P < 0.0001), which was lower in subjects with NAFLD [3.7 +/- 0.2 mg/(kg fat-free mass min)] than in the control subjects [5.0 +/- 0.3 mg/(kg fat-free mass min), P = 0.0008]. Conclusions: Hepatic lipid oxidation is unchanged in NAFLD. Whole-body lipid oxidation is increased because of peripheral insulin resistance. These data imply that alterations in hepatic fatty acid oxidation do not contribute to liver fat content in humans.