Krygsman A, Roux C R, Muller C, Louw J
Medical Research Council, Diabetes Discovery Platform, Parow Valley, South Africa.
Exp Clin Endocrinol Diabetes. 2010 Jul;118(7):434-41. doi: 10.1055/s-0030-1247544. Epub 2010 Feb 25.
BACKGROUND/AIMS: Both dietary fat content and fatty acid composition play a role in the development of glucose intolerance and insulin resistance. In this study we investigated the effect of moderate increases in dietary fat (10-30% of fat as total calories) and associated differences in fatty acid content, on the development of metabolic perturbations in the Wistar rat.
Eighteen normal male Wistar rats were randomly divided into 3 groups (n=6 each) at weaning, and fed different diets for 10 months: D10-10% fat as energy; D20-20% fat as energy and D30-30% fat as energy ad libitum.
Compared with D10, rats fed D20 and D30 exhibited increased body weight from as early as 1 month of the study (p<0.01). None of the diets resulted in hyperglycemia, but glucose intolerance developed as early as 1 month in the D20 and D30 groups (p<0.01) following intravenous glucose tolerance test. Over time, the glucose stimulated insulin secretion rate (GSIS) became more blunted in the D20 and D30 groups, but by 10 months the D20 group regained some insulin responsiveness. D30 showed very poor GSIS at 10 months indicating glucose intolerance. Plasma omega6 and omega3 fatty acid profiles mostly reflected the dietary content, but the ratio of omega6:omega3 in plasma deteriorated over time in D30, whereas that of D10 and D20 improved.
A moderate increase in dietary fat (20%), within the recommended nutritional range, and an unfavourable omega6:omega3 ratio resulted in glucose intolerance in this Wistar rat model, which was exacerbated with a further increase in dietary fat (30%).
背景/目的：膳食脂肪含量和脂肪酸组成在葡萄糖耐受不良和胰岛素抵抗的发展过程中均发挥作用。在本研究中，我们调查了膳食脂肪适度增加（脂肪占总热量的10 - 30%）以及脂肪酸含量的相关差异对Wistar大鼠代谢紊乱发展的影响。
18只正常雄性Wistar大鼠在断奶时随机分为3组（每组n = 6），并随意喂食不同饮食10个月：D10 - 脂肪占能量的10%；D20 - 脂肪占能量的20%；D30 - 脂肪占能量的30%。
与D10组相比，喂食D20和D30的大鼠早在研究第1个月时体重就有所增加（p < 0.01）。所有饮食均未导致高血糖，但在静脉葡萄糖耐量试验后，D20和D30组早在第1个月时就出现了葡萄糖耐受不良（p < 0.01）。随着时间推移，D20和D30组的葡萄糖刺激胰岛素分泌率（GSIS）变得更加迟钝，但到10个月时，D20组恢复了一些胰岛素反应性。D30组在10个月时显示出非常差的GSIS，表明存在葡萄糖耐受不良。血浆ω6和ω3脂肪酸谱大多反映了饮食含量，但D30组血浆中ω6:ω3的比例随时间恶化，而D10和D20组的该比例有所改善。
在推荐的营养范围内，膳食脂肪适度增加（20%）以及不利的ω6:ω3比例导致了该Wistar大鼠模型出现葡萄糖耐受不良，随着膳食脂肪进一步增加（30%），这种情况会加剧。
