Abraham N G, Brunner E J, Eriksson J W, Robertson R P
New York Medical College, Department of Pharmacology, Valhalla, NY 10595. USA.
Ann N Y Acad Sci. 2007 Oct;1113:256-75. doi: 10.1196/annals.1391.015. Epub 2007 May 18.
This article summarizes some aspects of stress in the metabolic syndrome at the psychosocial, tissue, and cellular levels. The metabolic syndrome is a valuable research concept for studying population health and social-biological translation. The cluster of cardiovascular risk factors labeled the metabolic syndrome is linked with low socioeconomic status. Systematic differences in diet and physical activity contribute to social patterning of the syndrome. In addition, psychosocial factors including chronic work stress are linked with its development. Psychosocial factors could lead to metabolic perturbations and increase cardiovascular risk via activation of neuroendocrine responses, for example, in the autonomic nervous system and in several hormonal pathways. High glucocorticoid levels will promote lipid storage in visceral rather than subcutaneous adipose tissue. Adipocytes secrete several proinflammatory cytokines, which considered major contributors to increase in oxidants and cell injury. Upregulation of heme oxygenase 1 (HO-1) and peroxidase in the early development of diabetes produces a decrease in oxidative-mediated injury. Increased HO activity is associated with a significant decrease in superoxide, endothelial cell shedding and blood pressure. Finally, it is proposed that overexpression of glutathione peroxidase in beta cells may protect beta cell deterioration from oxidative stress during development of diabetes and hyperglycemia and this may result in attenuation of beta cell failure. If this proves to be the case, then the scene will be set to develop glutathione peroxidase mimetics for use in preclinical and clinical trials.
本文总结了代谢综合征在心理社会、组织和细胞水平上压力的一些方面。代谢综合征是研究人群健康和社会生物学转化的一个有价值的研究概念。被标记为代谢综合征的心血管危险因素集群与社会经济地位低下有关。饮食和身体活动的系统性差异导致了该综合征的社会模式。此外，包括慢性工作压力在内的心理社会因素与其发展有关。心理社会因素可通过激活神经内分泌反应，例如自主神经系统和几种激素途径，导致代谢紊乱并增加心血管风险。高糖皮质激素水平会促进脂质在内脏而非皮下脂肪组织中的储存。脂肪细胞分泌几种促炎细胞因子，这些细胞因子被认为是氧化剂增加和细胞损伤的主要促成因素。糖尿病早期血红素加氧酶1（HO-1）和过氧化物酶的上调可减少氧化介导的损伤。HO活性增加与超氧化物、内皮细胞脱落和血压的显著降低有关。最后，有人提出β细胞中谷胱甘肽过氧化物酶的过表达可能在糖尿病和高血糖发展过程中保护β细胞免受氧化应激导致的细胞恶化，这可能导致β细胞功能衰竭的减轻。如果事实如此，那么将为开发用于临床前和临床试验的谷胱甘肽过氧化物酶模拟物奠定基础。
