Surwit R S, Williams P G
Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, North Carolina 27710, USA.
Psychosom Med. 1996 Nov-Dec;58(6):582-9. doi: 10.1097/00006842-199611000-00006.
To review the literature regarding the use of animal models in research addressing psychosomatic aspects of diabetes.
We examine the key findings in animal model vs. human research in the area of stress and diabetes. Previous research has suggested that stress is a potential contributor to chronic hyperglycemia in diabetes. Stress affects metabolic activity via the stimulation of a variety of hormones that can result in elevated blood glucose levels. In patients with diabetes, due to a relative or absolute lack of insulin, stress-induced increases in glucose cannot be properly metabolized. Additionally, regulation of these stress hormones may be abnormal in diabetes.
Human studies on the role of stress in the onset and course of type II diabetes are few and are limited by the constraints and logistics of examining life stress in humans. However, animal research allows for tight experimental control and the manipulation of factors that may contribute to the development and/or course of diabetes, such as stress, eating behavior, the nutrient content of food, and physical activity. Disease processes can be examined at a mechanistic level in animals which is typically limited in human research.
There is a large body of animal work to support the notion that stress reliably produces hyperglycemia in type II diabetes. Furthermore, there is evidence that the autonomic nervous system plays a role in the pathophysiology of this condition in both animals and humans. Examination of eating behavior and nutrient content of food in animal models of diabetes has shed light on the role of these factors in the development of diabetes, as well as obesity. Finally, genetic research using animal models of diabetes will provide new directions for research in humans to delineate the genetic contribution to the development of diabetes.
回顾关于在研究糖尿病心身方面中使用动物模型的文献。
我们研究了应激与糖尿病领域中动物模型研究和人类研究的关键发现。先前的研究表明，应激是糖尿病慢性高血糖的一个潜在促成因素。应激通过刺激多种激素来影响代谢活动，这些激素可导致血糖水平升高。在糖尿病患者中，由于相对或绝对缺乏胰岛素，应激诱导的血糖升高无法得到适当代谢。此外，糖尿病患者中这些应激激素的调节可能异常。
关于应激在2型糖尿病发病和病程中作用的人体研究很少，并且受到研究人类生活应激的限制和实际困难的制约。然而，动物研究允许进行严格的实验控制，并能操控可能导致糖尿病发生和/或病程发展的因素，如应激、饮食行为、食物的营养成分和身体活动。在动物身上可以从机制层面研究疾病过程，而这在人体研究中通常受到限制。
有大量动物研究工作支持应激确实会在2型糖尿病中导致高血糖这一观点。此外，有证据表明自主神经系统在动物和人类的这种病症的病理生理学中都起作用。在糖尿病动物模型中对饮食行为和食物营养成分的研究揭示了这些因素在糖尿病以及肥胖症发生过程中的作用。最后，使用糖尿病动物模型的基因研究将为人类研究提供新方向，以阐明基因对糖尿病发生的影响。
