Lee Ying-Chung, Ko Ya-Hui, Hsu Yung-Pei, Ho Low-Tone
Department of Physiology, School of Medicine, National Yang-Ming University, Taiwan, ROC.
Life Sci. 2006 Feb 9;78(11):1155-62. doi: 10.1016/j.lfs.2005.06.009. Epub 2006 Jan 24.
The aim of this study was to compare the postprandial leptin response in rats with and without metabolic syndrome induced by a fructose-enriched diet. The effect of aging and the association between variations in metabolic substrates was also evaluated. Oral glucose tolerance test (OGTT) and fasting/re-feeding test were used to evaluate the responses of leptin and to explore the dynamic relationship between endogenous leptin and metabolic substrates, including glucose, insulin and triglycerides (TG). At the 7th week, plasma leptin was unchanged in control rats after oral glucose loading. However, plasma leptin levels increased in fructose-fed rats with insulin resistant OGTT curves. At the 11th month, plasma leptin level was reduced during starvation and returned to the level prior to starvation during re-feeding in control rats. In contrast, the starvation-induced reduction in leptin showed a potentially larger rebound effect during re-feeding in fructose-fed rats. Analysis of covariance demonstrated that there alone was no interactive effect of dietary manipulation between leptin and TG, suggesting that fructose diet-induced insulin resistance-related metabolic syndrome may concomitantly elevate leptin and TG. Furthermore, multiple regression analysis suggests TG was the primary correlative determinant of endogenous leptin concentration. Our data showed that there are different patterns of leptin response to OGTT and fasting/re-feeding tests in rats with and without metabolic syndrome. The results suggest that these effects may be related to a TG-mediated impairment of leptin function and a protective mechanism to reduce lipid-induced tissue damage in patients with metabolic syndrome.
本研究的目的是比较喂食富含果糖饮食诱导的代谢综合征大鼠和未诱导代谢综合征大鼠的餐后瘦素反应。还评估了衰老的影响以及代谢底物变化之间的关联。采用口服葡萄糖耐量试验（OGTT）和禁食/再喂食试验来评估瘦素反应，并探索内源性瘦素与包括葡萄糖、胰岛素和甘油三酯（TG）在内的代谢底物之间的动态关系。在第7周时，口服葡萄糖负荷后，对照大鼠的血浆瘦素水平未发生变化。然而，胰岛素抵抗OGTT曲线的果糖喂养大鼠的血浆瘦素水平升高。在第11个月时，对照大鼠在饥饿期间血浆瘦素水平降低，再喂食期间恢复到饥饿前的水平。相比之下，果糖喂养大鼠在再喂食期间，饥饿诱导的瘦素降低显示出潜在的更大反弹效应。协方差分析表明，单独来看，饮食干预对瘦素和TG之间没有交互作用，这表明果糖饮食诱导的胰岛素抵抗相关代谢综合征可能会同时升高瘦素和TG。此外，多元回归分析表明TG是内源性瘦素浓度的主要相关决定因素。我们的数据表明，有代谢综合征和无代谢综合征的大鼠对OGTT和禁食/再喂食试验的瘦素反应模式不同。结果表明，这些效应可能与TG介导的瘦素功能损害以及代谢综合征患者减少脂质诱导的组织损伤的保护机制有关。
