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首页> 外文期刊>European journal of clinical nutrition >Role of insulin in age-related changes in macronutrient metabolism.
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Role of insulin in age-related changes in macronutrient metabolism.

机译：胰岛素在与年龄有关的常量营养素代谢变化中的作用。

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Age is associated with an increase in body fat mass and a decrease of protein mass. As body substrate turnover is under insulin control, defects in insulin secretion and/or action may in part account for these changes. As regards secretion, current evidence suggest that no clear defect in insulin secretion is found in the aged. The wide spectrum of glucose tolerance of the elderly may be associated with different patterns of insulin secretion. Insulin sensitivity to glucose metabolism is more or less normal in the aged, despite subtle delays in the onset of its action. Normalization of the data by either body weight or lean body mass is important in defining the insulin sensitivity of the elderly. Increased rates of free fatty acid (FFA) flux and oxidation rates have been found in healthy elderly subjects, both when post-absorptive and during hyperinsulinemia. These differences however disappeared following normalization by fat mass, suggesting that FFA kinetics reflect the established changes in fat mass. Thus, the mechanism(s) leading to an increase in the fat mass in elderly cannot simply be derived from studies of fat kinetics. The operation of the Randle cycle (ie, inverse relationships between fat and glucose oxidation) in the elderly has also been suggested. Finally, the insulin effects on whole-body amino acid and protein metabolism do not seem to be impaired in the aged. However, in the human muscle a decreased synthesis of contractile as well as mitochondrial proteins was found, in association with decreased specific gene expression. The degree of physical activity probably interacts with these changes, possibly playing a causative role. The possible interaction between insulin and exercise in the maintenance of muscle mass in the elderly needs to be studied further.
机译：年龄与体内脂肪量增加和蛋白质量减少有关。由于身体底物更新受胰岛素控制，胰岛素分泌和/或作用的缺陷可能部分解释了这些变化。关于分泌，目前的证据表明在老年人中没有发现胰岛素分泌的明显缺陷。老年人广泛的葡萄糖耐量可能与胰岛素分泌的不同模式有关。尽管老年人的胰岛素作用迟缓，但其对葡萄糖代谢的敏感性或多或少是正常的。通过体重或瘦体重对数据进行归一化对于定义老年人的胰岛素敏感性很重要。在吸收后和高胰岛素血症期间，在健康的老年受试者中都发现游离脂肪酸（FFA）的通量和氧化率增加。但是，这些差异在通过脂肪量归一化之后消失了，这表明FFA动力学反映了脂肪量的确定变化。因此，导致老年人脂肪量增加的机理不能简单地从脂肪动力学研究中得出。还提出了老年人的兰德尔循环操作（即脂肪和葡萄糖氧化之间的反比关系）。最后，在老年人中，胰岛素对全身氨基酸和蛋白质代谢的影响似乎并未受到损害。然而，在人类肌肉中，发现收缩蛋白以及线粒体蛋白的合成减少，同时特异性基因表达降低。身体活动的程度可能与这些变化相互作用，可能起着致病作用。胰岛素与运动之间可能相互作用的维持老年人的肌肉质量需要进一步研究。

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