Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype
Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype
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DOI：
10.1152/ajpendo.00515.2009
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发表时间：
2010-02-01
影响因子：
5.1
通讯作者：
Weickert, M. O.
中科院分区：
文献类型：
--
作者：
Isken, F.;Klaus, S.;Weickert, M. O.
伊斯肯·F，克劳斯·S，佩茨克·KJ，洛登肯珀·C，菲弗·AF，魏克特·莫。高VS下脂肪氧化损伤。低血糖指数饮食发生在肥胖表型形成之前。Am J生理学内分泌代谢酶298：e287-e295,2010。2009年11月24日首次出版；DOI：10.1152/ajpeno.00515.2009。-暴露于高血糖指数(GI)饮食和低血糖指数(GI)饮食会增加肥胖倾向C57BL/6J小鼠的脂肪质量和胰岛素抵抗。然而，更长期的影响和可能涉及的机制在很大程度上是未知的。我们将四组雄性C57BL/6J小鼠(每组10只)分别给予长期(20wk)或短期(6wk)等能量和常量营养素匹配的饲料，只是淀粉类型和GI不同。对所有四组小鼠的身体成分、肝脏脂肪、脂代谢的分子因素以及胰岛素敏感性和代谢灵活性的标志物进行了调查。喂食高GI饮食的小鼠表现出(从第5周开始)体内脂肪质量和肝脏脂肪的迅速显著增加，肝脏中的基因表达谱与脂肪生成的增加一致，并且在长期暴露后，葡萄糖负荷后的葡萄糖清除显著减少。长期的高GI饮食也导致了餐后状态下碳水化合物和脂肪氧化的延迟，这表明代谢灵活性降低。相反，在短期高强度运动后，碳水化合物的氧化作用没有观察到差异。低GI暴露。然而，早在高GI干预开始后3wk，脂肪酸氧化就显著减弱，而此时包括体脂质量在内的大多数测量的表型标记物在两组之间是相似的。因此，长期高GI喂养导致肥胖倾向的C57BL/6J小鼠出现肥胖、胰岛素抵抗和代谢不灵活的表型。在这些变化之前，早期发病和显著受损的脂肪酸氧化，因此表明潜在的因果关系。
Isken F, Klaus S, Petzke KJ, Loddenkemper C, Pfeiffer AF, Weickert MO. Impairment of fat oxidation under high-vs. low-glycemic index diet occurs before the development of an obese phenotype. Am J Physiol Endocrinol Metab 298: E287-E295, 2010. First published November 24, 2009; doi:10.1152/ajpendo.00515.2009.-Exposure to high vs. low glycemic index (GI) diets increases fat mass and insulin resistance in obesity-prone C57BL/6J mice. However, the longer-term effects and potentially involved mechanisms are largely unknown. We exposed four groups of male C57BL/6J mice (n = 10 per group) to long-term (20 wk) or short-term (6 wk) isoenergetic and macronutrient matched diets only differing in starch type and as such GI. Body composition, liver fat, molecular factors of lipid metabolism, and markers of insulin sensitivity and metabolic flexibility were investigated in all four groups of mice. Mice fed the high GI diet showed a rapid-onset (from week 5) marked increase in body fat mass and liver fat, a gene expression profile in liver consistent with elevated lipogenesis, and, after long-term exposure, significantly reduced glucose clearance following a glucose load. The long-term high-GI diet also led to a delayed switch to both carbohydrate and fat oxidation in the postprandial state, indicating reduced metabolic flexibility. In contrast, no difference in carbohydrate oxidation was observed after short-term high-vs. low-GI exposure. However, fatty acid oxidation was significantly blunted as early as 3 wk after beginning of the high-GI intervention, at a time where most measured phenotypic markers including body fat mass were comparable between groups. Thus long-term high-GI feeding resulted in an obese, insulin-resistant, and metabolically inflexible phenotype in obesity-prone C57BL/6J mice. Early onset and significantly impaired fatty acid oxidation preceded these changes, thereby indicating a potentially causal involvement.