Sjöstrand Mikaela, Eriksson Jan W
The Lundberg Laboratory for Diabetes Research, Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
Mol Cell Endocrinol. 2009 Jan 15;297(1-2):104-11. doi: 10.1016/j.mce.2008.05.010. Epub 2008 May 27.
Dysregulated hormonal, metabolic and neural signalling within and between organs can contribute to development of metabolic diseases including type 2 diabetes. Insulin-antagonistic effects of hormones, cytokines and excess metabolic substrates such as glucose and fatty acids may be exerted via common mechanisms involving for example reactive oxygen species (ROS) accumulation and associated inflammatory responses. Visceral adiposity is a central component of the metabolic syndrome and it is also strongly associated with insulin resistance. Both visceral obesity and insulin resistance are important risk factors for the development of type 2 diabetes. In the development of insulin resistance, it is likely that intra-abdominal adipose tissue plays a critical role in a complex endocrine and neural network involving several tissues. This review paper focuses on neuroendocrine 'stress' factors that target insulin-responsive tissues, in particular adipose tissue. We propose that there are common pathways by which dysregulation in different endocrine systems may contribute to the development of type 2 diabetes.
器官内部以及器官之间激素、代谢和神经信号的失调会促使包括2型糖尿病在内的代谢性疾病的发展。激素、细胞因子以及葡萄糖和脂肪酸等过量代谢底物的胰岛素拮抗作用可能通过常见机制发挥作用，例如活性氧（ROS）积累及相关炎症反应。内脏肥胖是代谢综合征的核心组成部分，并且与胰岛素抵抗也密切相关。内脏肥胖和胰岛素抵抗都是2型糖尿病发展的重要危险因素。在胰岛素抵抗的发展过程中，腹内脂肪组织很可能在涉及多个组织的复杂内分泌和神经网络中发挥关键作用。这篇综述文章聚焦于针对胰岛素反应性组织（尤其是脂肪组织）的神经内分泌“应激”因素。我们认为，不同内分泌系统的失调可能通过共同途径促使2型糖尿病的发展。
