From the Departments of Radiology (LL, CIN, JEW, and VBS-H), Human Biology (LL, PS, and VBS-H), and Human Movement Sciences (CIN and MKCH), NUTRIM, Maastricht University Medical Center, Maastricht, The Netherlands, and Top Institute Food and Nutrition (LL, CIN, PS, and VBS-H), Wageningen, The Netherlands.
Am J Clin Nutr. 2015 Jan;101(1):65-71. doi: 10.3945/ajcn.114.094730. Epub 2014 Nov 5.
Fat accumulation in nonadipose tissue is linked to insulin resistance and metabolic diseases. Earlier studies have shown that hepatic lipid accumulation can occur after 4 d of a high-fat diet in humans, and this fat accumulation can be blunted by the ingestion of additional proteins.
In this study, we explored whether a single high-fat meal increased the lipid content in liver and skeletal muscle as measured by using in vivo proton magnetic resonance spectroscopy (¹H-MRS) and whether the addition of protein can modulate the postprandial ectopic lipid storage.
Intrahepatic lipid (IHL) and intramyocellular lipid (IMCL) concentrations were determined by using ¹H-MRS before and 3 and 5 h after a high-fat with added protein meal (61.5% of energy from fat) or a high-fat without added protein meal (mean ± SEM: 51.1 ± 7.9 g of protein; 191.9 ± 9.9 kcal added) in a randomized crossover study. IHL and IMCL concentrations were converted to absolute concentrations (g/kg wet weight) by using water as an internal reference.
Nine lean, healthy subjects [6 men and 3 women; mean (±SD) age: 22.7 ± 3.0 y; mean body mass index (in kg/m²): 21.8 ± 1.8] were included in this study. IHL concentrations increased ∼20% (P < 0.01) at 3 h after the meal and did not further increase after 5 h. In contrast, IMCL concentrations were not altered during the postprandial period (P = 0.74). The addition of protein to a single high-fat meal did not change the postprandial accumulation of fat in the liver (P = 0.93) or skeletal muscle (P = 0.84).
In this study, we showed that a single energy-dense, high-fat meal induced net lipid accumulation in the liver, which was detected by using in vivo ¹H-MRS. This noninvasive approach might bring new opportunities to study postprandial hepatic lipid dynamics. The addition of protein did not change the ectopic lipid retention after a single high-fat meal.
非脂肪组织中的脂肪堆积与胰岛素抵抗和代谢性疾病有关。早期的研究表明,人类在高脂肪饮食 4 天后会发生肝脏脂质堆积,而额外摄入蛋白质可以减轻这种脂肪堆积。
本研究旨在通过体内质子磁共振波谱(¹H-MRS)来探讨单次高脂肪餐是否会导致肝脏和骨骼肌中的脂质含量增加,以及额外添加蛋白质是否可以调节餐后异位脂质储存。
在一项随机交叉研究中,9 名健康的瘦人(6 名男性和 3 名女性;平均年龄为 22.7 ± 3.0 岁;平均体重指数为 21.8 ± 1.8kg/m²)分别摄入高脂肪添加蛋白质餐(61.5%的能量来自脂肪)或高脂肪不添加蛋白质餐(平均±标准差:51.1 ± 7.9g 蛋白质;191.9 ± 9.9kcal 热量)。在这项研究中,使用¹H-MRS 分别在餐前和餐后 3 小时和 5 小时测量肝内脂质(IHL)和肌内脂质(IMCL)浓度。IHL 和 IMCL 浓度通过以水作为内参转换为绝对浓度(g/kg 湿重)。
9 名受试者中,IHL 浓度在餐后 3 小时增加了约 20%(P < 0.01),5 小时后不再增加。相比之下,IMCL 浓度在餐后期间没有改变(P = 0.74)。在单次高脂肪餐中添加蛋白质并没有改变肝脏(P = 0.93)或骨骼肌(P = 0.84)中的脂肪餐后积累。
在这项研究中,我们发现单次高能量、高脂肪餐会导致肝脏中的净脂质积累,这可以通过体内¹H-MRS 检测到。这种非侵入性的方法可能为研究餐后肝脏脂质动力学带来新的机会。在单次高脂肪餐后添加蛋白质并没有改变异位脂质的保留。