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代谢综合征患者的结构化生活方式干预可减轻氧化应激,但不能改善心血管自主神经病变的测量指标。

Structured lifestyle intervention in patients with the metabolic syndrome mitigates oxidative stress but fails to improve measures of cardiovascular autonomic neuropathy.

机构信息

Department of Internal Medicine and Molecular and Integrative Physiology, Division of Nephrology, University of Michigan, Ann Arbor, MI, United States.

Department of Neurology, University of Michigan, Ann Arbor, MI, United States.

出版信息

J Diabetes Complications. 2017 Sep;31(9):1437-1443. doi: 10.1016/j.jdiacomp.2017.03.008. Epub 2017 May 2.

Abstract

AIMS

To assess the role of oxidative stress in mediating adverse outcomes in metabolic syndrome (MetS) and resultant cardiovascular autonomic neuropathy (CAN), and to evaluate the effects of lifestyle interventions on measures of oxidative stress and CAN in subjects with MetS.

METHODS

Pilot study in 25 non-diabetic subjects with MetS (age 49±10years, 76% females) participating in a 24-week lifestyle intervention (supervised aerobic exercise/Mediterranean diet), and 25 age-matched healthy controls. CAN was assessed by cardiovascular reflex tests, heart rate variability (HRV) and PET imaging with sympathetic analog [C] meta-hydroxyephedrine ([C]HED). Specific oxidative fingerprints were measured by liquid-chromatography/mass-spectrometry (LC/MS).

RESULTS

At baseline, MetS subjects had significantly higher oxidative stress markers [3-nitrotyrosine (234±158 vs. 54±47μmol/mol tyrosine), ortho-tyrosine (59±38 vs. 18±10μmol/molphenylalanine, all P<0.0001], and impaired HRV at rest and during deep breathing (P=0.039 and P=0.021 respectively) compared to controls. Twenty-four-week lifestyle intervention significantly reduced all oxidative stress markers (all P<0.01) but did not change any of the CAN measures.

CONCLUSIONS

Subjects with MetS present with signs of CAN and increased oxidative stress in the absence of diabetes. The 24-week lifestyle intervention was effective in ameliorating oxidative stress, but did not improve measures of CAN. Larger clinical trials with longer duration are required to confirm these findings.

摘要

目的

评估氧化应激在代谢综合征(MetS)及其导致的心血管自主神经病变(CAN)不良结局中的作用,并评估生活方式干预对 MetS 患者氧化应激和 CAN 测量指标的影响。

方法

对 25 名非糖尿病 MetS 患者(年龄 49±10 岁,76%为女性)进行了一项为期 24 周的生活方式干预(监督有氧运动/地中海饮食)的试点研究,并纳入了 25 名年龄匹配的健康对照者。通过心血管反射测试、心率变异性(HRV)和使用交感神经类似物 [C]meta-羟基苯丙胺 ([C]HED)的 PET 成像评估 CAN。通过液相色谱/质谱(LC/MS)测量特定的氧化指纹。

结果

基线时,MetS 患者的氧化应激标志物 [3-硝基酪氨酸(234±158 比 54±47μmol/mol 酪氨酸)、邻-酪氨酸(59±38 比 18±10μmol/mol 苯丙氨酸]显著升高(所有 P<0.0001),并且在休息和深呼吸时 HRV 受损(分别为 P=0.039 和 P=0.021)。24 周的生活方式干预显著降低了所有氧化应激标志物(均 P<0.01),但没有改变任何 CAN 测量指标。

结论

患有 MetS 的患者在没有糖尿病的情况下出现 CAN 迹象和氧化应激增加。24 周的生活方式干预在改善氧化应激方面是有效的,但不能改善 CAN 测量指标。需要更大规模、更长时间的临床试验来证实这些发现。

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