Diabetes:精神紧张可导致高血糖和高脂血症
新华网 · 2012/03/26
高血糖和高脂血症是常见的生活方式病,而精神状态被认为与生活方式病有很深的关系。日本名古屋大学研究人员日前宣布,他们在动物实验中发现精神紧张状态可引起内脏脂肪炎症,导致高血糖和高脂血症。

导读:高血糖和高脂血症是常见的生活方式病,而精神状态被认为与生活方式病有很深的关系。日本名古屋大学研究人员日前宣布,他们在动物实验中发现精神紧张状态可引起内脏脂肪炎症,导致高血糖和高脂血症。

研究人员让小鼠在直径3厘米的狭小圆筒内每天待2个小时,连续两周时间让小鼠经常处于精神紧张状态。结果发现,小鼠肾上腺皮质等分泌的激素导致内脏脂肪出现分解、萎缩,细胞内和血液中引起炎症的“MCP-1”蛋白质的量增加,产生内脏脂肪炎症。与正常小鼠相比,精神紧张的小鼠分泌胰岛素功能降低,难以将血液中的糖分吸收到细胞中,血液容易凝固而出现血栓。

研究人员还发现,如果向精神紧张的小鼠体内注入能够遏制“MCP-1”蛋白质功能的脂肪干细胞,脂肪炎症和分泌胰岛素的功能都得到改善。相关论文刊登在美国《糖尿病》杂志网络版上。


Stress Augments Insulin Resistance and Prothrombotic State

Role of Visceral Adipose-Derived Monocyte Chemoattractant Protein-1

Yasuhiro Uchida, Kyosuke Takeshita, Koji Yamamoto, Ryosuke Kikuchi, Takayuki Nakayama, Mieko Nomura, Xian Wu Cheng, Kensuke Egashira, Tadashi Matsushita, Hideo Nakamura and Toyoaki Murohara

Stressors contribute to thrombosis and insulin resistance. Since obesity-related adipose inflammation is also involved in these pathological states, we assumed that stress correlates with adipose inflammation. Male mice were subjected to 2-week intermittent restraint stress. Expression of plasma lipids, monocyte/macrophage markers (CD11b, CD68, and F4/80), proinflammatory cytokines (monocyte chemoattractant protein-1 [MCP-1], tumor necrosis factor-α, and interleukin-6), adiponectin, heat shock protein 70.1 (HSP70.1), and coagulation factors (plasminogen activation inhibitor-1 [PAI-1] and tissue factor [TF]) in blood and inguinal white adipose tissue (WAT) was determined using immunohistochemistry, enzyme-linked immunosorbent assay, and RT-PCR, respectively. Glucose metabolism was assessed by glucose tolerance tests (GTTs) and insulin tolerance tests, and expression of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in WAT. To examine effects of MCP-1 blockade, animals were treated with control or neutralizing antibody, or transplanted with control or 7ND (dominant-negative form of MCP-1)-overexpressing adipose-derived stromal cells (ADSCs). Stress increased monocyte accumulation, free fatty acids, proinflammatory cytokine, and HSP70.1 and reduced adiponectin. Adipose stromal cells highly expressed MCP-1. The stress-induced adipose inflammation increased PAI-1 and TF but did not give rise to thrombus formation. Without any changes in GTT, stress worsened insulin sensitivity and decreased IRS-1 and GLUT4 in WAT. Neutralizing antibody and 7ND-ADSCs reversed stress-induced adipose inflammation, procoagulant state, and insulin resistance. Stress evoked adipose inflammation to increase coagulation factors and impair insulin sensitivity, through adipose-derived MCP-1.

文献链接http://diabetes.diabetesjournals.org/content/early/2012/02/27/db11-0828.abstract

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