Carvalho Livia A, Urbanova Livia, Hamer Mark, Hackett Ruth A, Lazzarino Antonio I, Steptoe Andrew
Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, Rm356a, London WC1E 6BR, UK.
Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, Rm356a, London WC1E 6BR, UK.
Psychoneuroendocrinology. 2015 Jan;51:209-18. doi: 10.1016/j.psyneuen.2014.09.023. Epub 2014 Sep 30.
Psychological stress may contribute to type 2 diabetes but mechanisms are still poorly understood. In this study, we examined whether stress responsiveness is associated with glucocorticoid and mineralocorticoid sensitivity in a controlled experimental comparison of people with type 2 diabetes and non-diabetic participants. Thirty-seven diabetes patients and 37 healthy controls underwent psychophysiological stress testing. Glucocorticoid (GR) and mineralocorticoid sensitivity (MR) sensitivity were measured by dexamethasone- and prednisolone-inhibition of lipopolysaccharide (LPS)-induced interleukin (IL) 6 levels, respectively. Blood pressure (BP) and heart rate were monitored continuously, and we periodically assessed salivary cortisol, plasma IL-6 and monocyte chemotactic protein (MCP-1). Following stress, both glucocorticoid and mineralocorticoid sensitivity decreased among healthy controls, but did not change in people with diabetes. There was a main effect of group on dexamethasone (F(1,74)=6.852, p=0.013) and prednisolone (F(1,74)=7.295, p=0.010) sensitivity following stress at 45 min after tasks. People with diabetes showed blunted stress responsivity in systolic BP, diastolic BP, heart rate, IL-6, MCP-1, and impaired post-stress recovery in heart rate. People with Diabetes had higher cortisol levels as measured by the total amount excreted over the day and increased glucocorticoid sensitivity at baseline. Our study suggests that impaired stress responsivity in type-2 diabetes is in part due to a lack of stress-induced changes in mineralocorticoid and glucocorticoid sensitivity.
心理压力可能会导致2型糖尿病,但其中的机制仍知之甚少。在本研究中,我们在2型糖尿病患者和非糖尿病参与者的对照实验比较中,检验了应激反应性是否与糖皮质激素和盐皮质激素敏感性相关。37名糖尿病患者和37名健康对照者接受了心理生理应激测试。分别通过地塞米松和泼尼松龙抑制脂多糖(LPS)诱导的白细胞介素(IL)6水平来测量糖皮质激素(GR)和盐皮质激素敏感性(MR)。持续监测血压(BP)和心率,并定期评估唾液皮质醇、血浆IL - 6和单核细胞趋化蛋白(MCP - 1)。应激后,健康对照者的糖皮质激素和盐皮质激素敏感性均下降,但糖尿病患者没有变化。在任务后45分钟应激时,组间对地塞米松(F(1,74)=6.852,p = 0.013)和泼尼松龙(F(1,74)=7.295,p = 0.010)敏感性有主要影响。糖尿病患者在收缩压、舒张压、心率、IL - 6、MCP - 1方面的应激反应迟钝,且心率在应激后的恢复受损。通过一天内排泄的总量测量,糖尿病患者的皮质醇水平较高,且基线时糖皮质激素敏感性增加。我们的研究表明,2型糖尿病患者应激反应受损部分是由于缺乏应激诱导的盐皮质激素和糖皮质激素敏感性变化。