Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 (n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 (n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased (P < 0.000003) and TBARS (P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status (P < 0.05; r = 0.434) and a negative correlation for TBARS and age (P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging.

Impact statement

Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.

中文翻译：

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胰岛素抵抗和氧化应激是衰老的原因还是结果。

胰岛素抵抗 (IR) 可能与氧化应激有关并导致心血管疾病。目前的研究集中在有或没有胰岛素抵抗的老年人中胰岛素抵抗指数和氧化-抗氧化标志物之间的相互作用。评估涉及人体测量数据（体重、身高、BMI、体脂百分比 (FAT)）和生化测试（葡萄糖、脂质、血清胰岛素和血浆氧化-抗氧化标志物：硫代巴比妥酸反应物质 (TBARS)、Cu、Zn-超氧化物歧化酶 (SOD-1) 和总抗氧化状态）。假设截止点为 0.3 的胰岛素抵抗指数 (IR) 允许将组划分为：胰岛素敏感组 (InsS) IR < 0,3 ( n  = 35，中位年龄 69.0 岁) 和胰岛素抵抗组 (InsR) IR ≥ 0.3 ( n = 51，中位年龄 71.0 岁）。脂质和抗氧化防御系统标记没有区分所研究的组。InsR老年组 与InsS组相比，FAT增加（P  <0.000003），TBARS（P =0.008）浓度降低。SOD-1 与总抗氧化状态呈正相关（P  < 0.05; r = 0.434），TBARS 与年龄呈负相关（P < 0.05 与 r = -0.421) 在 InsR 个体中计算。在老年人中，无论胰岛素抵抗状态如何，氧化应激都会持续存在。我们认为氧化应激增加可能是老年的结果。胰岛素作用通过与氧化应激和细胞外和细胞内抗氧化防御系统的一致关联来识别动脉粥样硬化高危人群。因此，我们认为胰岛素抵抗不是衰老的原因。

影响陈述

胰岛素抵抗与导致心血管疾病的氧化应激有关。然而，很少有研究检查有或没有胰岛素抵抗的老年人。我们证明单独的抗氧化防御系统不能消除动脉粥样硬化高风险老年人的胰岛素作用，而组合的氧化-抗氧化标志物（硫代巴比妥酸反应物质（TBARS）、Cu、Zn-超氧化物歧化酶（SOD-1） ) 和总抗氧化状态 (TAS)) 可能更有效，并可能产生更好的临床结果。事实上，只有在胰岛素抵抗的老年人中才能看到氧化应激的减少和抗氧化防御之间的强烈相互作用。在我们看来，这对临床医生来说是有价值的信息，